| + |
AKT2 | down-regulates 
phosphorylation
|
BAD |
0.504 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81110 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-136 is the major phosphoacceptor site for akt;akt can weakly phosphorilate ser-155. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81114 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-136 is the major phosphoacceptor site for akt;akt can weakly phosphorilate ser-155. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PRKACG | down-regulates
phosphorylation
|
BAD |
0.409 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-67392 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 10230396 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81153 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-67396 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 10230396 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81157 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81161 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Publications: |
5 |
Organism: |
Homo Sapiens |
| + |
RPS6KA5 | down-regulates activity
phosphorylation
|
BAD |
0.35 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262990 |
Ser118 |
GRELRRMsDEFVDSF |
|
|
| pmid |
sentence |
| 12213813 |
Phosphorylation of Bad at Ser112 in response to growth factors or cytokines is generally linked to cell survival. Knockdown of MSK1 suppressed Bad phosphorylation after calcium ionophore A23187 treatment in neuronal cells |
|
| Publications: |
1 |
| Pathways: | Malignant Melanoma |
| + |
PRKCE | down-regulates
phosphorylation
|
BAD |
0.346 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163908 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 20179209 |
Pkcs phosphorylate bad under in vitro conditions, and the association of phosphorylated bad with pkc-mu or pkc-epsilon, as shown by immunoprecipitation, indicated direct involvement of pkcs in bad phosphorylation. To confirm these results, cells overexpressing pegfp-n1, wt-bad, or bad with a single site mutated (ser112ala;ser136ala;ser155ala), two sites mutated (ser(112/136)ala;ser(112/155)ala;ser(136/155)ala), or the triple mutant were tested. Igf-i protected completely against rapamycin-induced apoptosis in cells overexpressing wt-bad and mutants having either one or two sites of phosphorylation mutated |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163912 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 20179209 |
Pkcs phosphorylate bad under in vitro conditions, and the association of phosphorylated bad with pkc-mu or pkc-epsilon, as shown by immunoprecipitation, indicated direct involvement of pkcs in bad phosphorylation. To confirm these results, cells overexpressing pegfp-n1, wt-bad, or bad with a single site mutated (ser112ala;ser136ala;ser155ala), two sites mutated (ser(112/136)ala;ser(112/155)ala;ser(136/155)ala), or the triple mutant were tested. Igf-i protected completely against rapamycin-induced apoptosis in cells overexpressing wt-bad and mutants having either one or two sites of phosphorylation mutated |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163916 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
|
| pmid |
sentence |
| 20179209 |
Pkcs phosphorylate bad under in vitro conditions, and the association of phosphorylated bad with pkc-mu or pkc-epsilon, as shown by immunoprecipitation, indicated direct involvement of pkcs in bad phosphorylation. To confirm these results, cells overexpressing pegfp-n1, wt-bad, or bad with a single site mutated (ser112ala;ser136ala;ser155ala), two sites mutated (ser(112/136)ala;ser(112/155)ala;ser(136/155)ala), or the triple mutant were tested. Igf-i protected completely against rapamycin-induced apoptosis in cells overexpressing wt-bad and mutants having either one or two sites of phosphorylation mutated |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
PRKACA | down-regulates
phosphorylation
|
BAD |
0.521 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-180902 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 18794113 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81129 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-67379 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 10230394 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-180906 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 18794113 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81137 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-67387 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
|
| pmid |
sentence |
| 10230394 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Publications: |
6 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network |
| + |
PIM2 | down-regulates
phosphorylation
|
BAD |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-78015 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 10837473 |
Similar to pim1, pim2 phosphorylates bad, which antagonizes the pro-apoptotic function of bax |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIM1 | down-regulates activity
phosphorylation
|
BAD |
0.379 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250390 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 16403219 |
Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-XL. pim kinases are constitutively active when expressed in HEK-293 cells and are able to phosphorylate the Bcl-2 family member Bad on three residues, Ser112, Ser136 and Ser155 in vitro and in cells. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249607 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 16403219 |
All three Pim kinase family members predominantly phosphorylate Bad on Ser112 and in addition are capable of phosphorylating Bad on multiple sites associated with the inhibition of the pro-apoptotic function of Bad in HEK-293 cells. This would be consistent with the proposed function of Pim kinases in promoting cell proliferation and preventing cell death. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250392 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16403219 |
Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-XL. pim kinases are constitutively active when expressed in HEK-293 cells and are able to phosphorylate the Bcl-2 family member Bad on three residues, Ser112, Ser136 and Ser155 in vitro and in cells. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling |
| + |
PRKD1 | down-regulates
phosphorylation
|
BAD |
0.311 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163920 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 20179209 |
Pkcs phosphorylate bad under in vitro conditions, and the association of phosphorylated bad with pkc-mu or pkc-epsilon, as shown by immunoprecipitation, indicated direct involvement of pkcs in bad phosphorylation. To confirm these results, cells overexpressing pegfp-n1, wt-bad, or bad with a single site mutated (ser112ala;ser136ala;ser155ala), two sites mutated (ser(112/136)ala;ser(112/155)ala;ser(136/155)ala), or the triple mutant were tested. Igf-i protected completely against rapamycin-induced apoptosis in cells overexpressing wt-bad and mutants having either one or two sites of phosphorylation mutated |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163924 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 20179209 |
Pkcs phosphorylate bad under in vitro conditions, and the association of phosphorylated bad with pkc-mu or pkc-epsilon, as shown by immunoprecipitation, indicated direct involvement of pkcs in bad phosphorylation. To confirm these results, cells overexpressing pegfp-n1, wt-bad, or bad with a single site mutated (ser112ala;ser136ala;ser155ala), two sites mutated (ser(112/136)ala;ser(112/155)ala;ser(136/155)ala), or the triple mutant were tested. Igf-i protected completely against rapamycin-induced apoptosis in cells overexpressing wt-bad and mutants having either one or two sites of phosphorylation mutated |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163928 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
|
| pmid |
sentence |
| 20179209 |
Pkcs phosphorylate bad under in vitro conditions, and the association of phosphorylated bad with pkc-mu or pkc-epsilon, as shown by immunoprecipitation, indicated direct involvement of pkcs in bad phosphorylation. To confirm these results, cells overexpressing pegfp-n1, wt-bad, or bad with a single site mutated (ser112ala;ser136ala;ser155ala), two sites mutated (ser(112/136)ala;ser(112/155)ala;ser(136/155)ala), or the triple mutant were tested. Igf-i protected completely against rapamycin-induced apoptosis in cells overexpressing wt-bad and mutants having either one or two sites of phosphorylation mutated |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
PRKACB | down-regulates
phosphorylation
|
BAD |
0.403 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81141 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81145 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81149 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
AKT3 | down-regulates
phosphorylation
|
BAD |
0.522 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81118 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-136 is the major phosphoacceptor site for akt;akt can weakly phosphorilate ser-155. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81122 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
Ser-136 is the major phosphoacceptor site for akt;akt can weakly phosphorilate ser-155. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PIM2 | down-regulates activity
phosphorylation
|
BAD |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250395 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16403219 |
Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-XL. pim kinases are constitutively active when expressed in HEK-293 cells and are able to phosphorylate the Bcl-2 family member Bad on three residues, Ser112, Ser136 and Ser155 in vitro and in cells. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249604 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16403219 |
All three Pim kinase family members predominantly phosphorylate Bad on Ser112 and in addition are capable of phosphorylating Bad on multiple sites associated with the inhibition of the pro-apoptotic function of Bad in HEK-293 cells. This would be consistent with the proposed function of Pim kinases in promoting cell proliferation and preventing cell death. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250394 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16403219 |
Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-XL. pim kinases are constitutively active when expressed in HEK-293 cells and are able to phosphorylate the Bcl-2 family member Bad on three residues, Ser112, Ser136 and Ser155 in vitro and in cells. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
PIM | down-regulates activity
phosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259423 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16403219 |
Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-XL. pim kinases are constitutively active when expressed in HEK-293 cells and are able to phosphorylate the Bcl-2 family member Bad on three residues, Ser112, Ser136 and Ser155 in vitro and in cells. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259421 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 16403219 |
All three Pim kinase family members predominantly phosphorylate Bad on Ser112 and in addition are capable of phosphorylating Bad on multiple sites associated with the inhibition of the pro-apoptotic function of Bad in HEK-293 cells. This would be consistent with the proposed function of Pim kinases in promoting cell proliferation and preventing cell death. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259422 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16403219 |
Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-XL. pim kinases are constitutively active when expressed in HEK-293 cells and are able to phosphorylate the Bcl-2 family member Bad on three residues, Ser112, Ser136 and Ser155 in vitro and in cells. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
RAF1 | down-regulates
phosphorylation
|
BAD |
0.644 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-155293 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 17535812 |
The activation of several major anti-apoptotic signaling pathways correlates with an increase in the phosphorylation of bad on ser-112, ser-136, and ser-155. These phosphorylation events result in bad inactivation through sequestration by 14-3-3 proteins |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81165 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 15849194 |
Raf-1 protects cells from apoptosis, independently of its signals to MEK and ERK, by translocating to the mitochondria where it binds Bcl-2 and displaces BAD|Upon phosphorylation by Pak1, Raf-1 translocates to mitochondria and phosphorylates BAD at Ser-112. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network |
| + |
RPS6K | down-regulates activity
phosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252786 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10837486 |
Rsk1, and survival factor signaling stimulate phosphorylation of bad at ser-155, blocking the binding of bad to bcl-xl. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252767 |
Ser153 |
SWTRVFQsWWDRNLG |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10837486 |
We report here that the phosphorylation of BAD at Ser-155 within the BH3 domain is a second phosphorylation-dependent mechanism that inhibits the death-promoting activity of BAD. Protein kinase A, RSK1, and survival factor signaling stimulate phosphorylation of BAD at Ser-155, blocking the binding of BAD to Bcl-XL. RSK1 phosphorylates BAD at both Ser-112 and Ser-155 and rescues BAD-mediated cell death in a manner dependent upon phosphorylation at both sites. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252784 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 18246127 |
To understand the mechanisms underlying B-RAF effects on cell survival we initially analysed the Bcl-2 family protein, Bad, that is phosphorylated by RSK1 at the inhibitory serine-75 residue in a MEK-dependent manner in melanoma cells |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling |
| + |
PIM | down-regulates
phosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259418 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 10837473 |
Similar to pim1, pim2 phosphorylates bad, which antagonizes the pro-apoptotic function of bax |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
PIM3 | down-regulates activity
phosphorylation
|
BAD |
0.353 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250396 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16403219 |
Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-XL. pim kinases are constitutively active when expressed in HEK-293 cells and are able to phosphorylate the Bcl-2 family member Bad on three residues, Ser112, Ser136 and Ser155 in vitro and in cells. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249605 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16403219 |
All three Pim kinase family members predominantly phosphorylate Bad on Ser112 and in addition are capable of phosphorylating Bad on multiple sites associated with the inhibition of the pro-apoptotic function of Bad in HEK-293 cells. This would be consistent with the proposed function of Pim kinases in promoting cell proliferation and preventing cell death. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250399 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16403219 |
Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-XL. pim kinases are constitutively active when expressed in HEK-293 cells and are able to phosphorylate the Bcl-2 family member Bad on three residues, Ser112, Ser136 and Ser155 in vitro and in cells. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
PRKCI | down-regulates
phosphorylation
|
BAD |
0.324 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-172886 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
Glioblastoma Cell |
| pmid |
sentence |
| 21419810 |
In-vitro kinase activity assay showed that pkc-_ directly phosphorylated bad at phospho specific residues, ser-112, ser-136 and ser-155 which in turn induced inactivation of bad and disruption of bad/bcl-xl dimer |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-172890 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
Glioblastoma Cell |
| pmid |
sentence |
| 21419810 |
In-vitro kinase activity assay showed that pkc-_ directly phosphorylated bad at phospho specific residues, ser-112, ser-136 and ser-155 which in turn induced inactivation of bad and disruption of bad/bcl-xl dimer |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-172894 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
Glioblastoma Cell |
| pmid |
sentence |
| 21419810 |
In-vitro kinase activity assay showed that pkc-_ directly phosphorylated bad at phospho specific residues, ser-112, ser-136 and ser-155 which in turn induced inactivation of bad and disruption of bad/bcl-xl dimer |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
RPS6KA2 | down-regulates activity
phosphorylation
|
BAD |
0.381 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249044 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10837486 |
We report here that the phosphorylation of BAD at Ser-155 within the BH3 domain is a second phosphorylation-dependent mechanism that inhibits the death-promoting activity of BAD. Protein kinase A, RSK1, and survival factor signaling stimulate phosphorylation of BAD at Ser-155, blocking the binding of BAD to Bcl-XL. RSK1 phosphorylates BAD at both Ser-112 and Ser-155 and rescues BAD-mediated cell death in a manner dependent upon phosphorylation at both sites. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AKT | down-regulates activity
phosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-244148 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
Neuron |
| pmid |
sentence |
| 9346240 |
Experiments in this study reveal that akt phosphorylates bad both in vitro and in vivo and that akt-mediated phosphorylation of bad effectively blocks bad induced cell death.[...] In addition, these findings implicate a particular phosphorylation site on bad, serine 136, in the suppression of bad-mediated death by akt.[...]The Phosphorylation of bad may lead to the prevention of cell death via a mechanism that involves the selective association of the phosphorylated forms of bad with 14-3-3 protein isoforms. Akt phosphorylates bad in vitro and in vivo we show that growth factor activation of the pi3'k/akt signaling pathway culminates in the phosphorylation of the bcl-2 family member bad, thereby suppressing apoptosis and promoting cell survival. Akt phosphorylates bad in vitro and in vivo erbb-mediated phosphorylation of bad by akt promotes survival by blocking the interaction of this pro-apoptotic molecule with bcl-2 and bcl-x proteins |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251469 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 9381178 |
Active Akt induced a significant increase in BAD phosphorylation. mutant BAD with alanine substitutions at Ser112 and Ser136 was not phosphorylated by active Akt . phosphorylation of BAD by Akt will preclude its binding to membrane-anchored Bcl-xL, leading to increased cell survival. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-244144 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
Neuron |
| pmid |
sentence |
| 9346240 |
Experiments in this study reveal that akt phosphorylates bad both in vitro and in vivo and that akt-mediated phosphorylation of bad effectively blocks bad induced cell death.[...] In addition, these findings implicate a particular phosphorylation site on bad, serine 136, in the suppression of bad-mediated death by akt.[...]The Phosphorylation of bad may lead to the prevention of cell death via a mechanism that involves the selective association of the phosphorylated forms of bad with 14-3-3 protein isoforms. Akt phosphorylates bad in vitro and in vivo we show that growth factor activation of the pi3'k/akt signaling pathway culminates in the phosphorylation of the bcl-2 family member bad, thereby suppressing apoptosis and promoting cell survival. Akt phosphorylates bad in vitro and in vivo erbb-mediated phosphorylation of bad by akt promotes survival by blocking the interaction of this pro-apoptotic molecule with bcl-2 and bcl-x proteins |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251470 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 9381178 |
Active Akt induced a significant increase in BAD phosphorylation. mutant BAD with alanine substitutions at Ser112 and Ser136 was not phosphorylated by active Akt . phosphorylation of BAD by Akt will preclude its binding to membrane-anchored Bcl-xL, leading to increased cell survival. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, FLT3-ITD signaling, Inhibition of Apoptosis, Malignant Melanoma, SARS-COV APOPTOSIS, VEGF Signaling |
| + |
AKT1 | down-regulates activity
phosphorylation
|
BAD |
0.816 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-52859 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
Neuron |
| pmid |
sentence |
| 9346240 |
Experiments in this study reveal that akt phosphorylates bad both in vitro and in vivo and that akt-mediated phosphorylation of bad effectively blocks bad induced cell death.[...] In addition, these findings implicate a particular phosphorylation site on bad, serine 136, in the suppression of bad-mediated death by akt.[...]The Phosphorylation of bad may lead to the prevention of cell death via a mechanism that involves the selective association of the phosphorylated forms of bad with 14-3-3 protein isoforms. Akt phosphorylates bad in vitro and in vivo we show that growth factor activation of the pi3'k/akt signaling pathway culminates in the phosphorylation of the bcl-2 family member bad, thereby suppressing apoptosis and promoting cell survival. Akt phosphorylates bad in vitro and in vivo erbb-mediated phosphorylation of bad by akt promotes survival by blocking the interaction of this pro-apoptotic molecule with bcl-2 and bcl-x proteins |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252562 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 9381178 |
Active Akt induced a significant increase in BAD phosphorylation. mutant BAD with alanine substitutions at Ser112 and Ser136 was not phosphorylated by active Akt . phosphorylation of BAD by Akt will preclude its binding to membrane-anchored Bcl-xL, leading to increased cell survival. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252563 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 9381178 |
Active Akt induced a significant increase in BAD phosphorylation. mutant BAD with alanine substitutions at Ser112 and Ser136 was not phosphorylated by active Akt . phosphorylation of BAD by Akt will preclude its binding to membrane-anchored Bcl-xL, leading to increased cell survival. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-52863 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
Neuron |
| pmid |
sentence |
| 9346240 |
Experiments in this study reveal that akt phosphorylates bad both in vitro and in vivo and that akt-mediated phosphorylation of bad effectively blocks bad induced cell death.[...] In addition, these findings implicate a particular phosphorylation site on bad, serine 136, in the suppression of bad-mediated death by akt.[...]The Phosphorylation of bad may lead to the prevention of cell death via a mechanism that involves the selective association of the phosphorylated forms of bad with 14-3-3 protein isoforms. Akt phosphorylates bad in vitro and in vivo we show that growth factor activation of the pi3'k/akt signaling pathway culminates in the phosphorylation of the bcl-2 family member bad, thereby suppressing apoptosis and promoting cell survival. Akt phosphorylates bad in vitro and in vivo erbb-mediated phosphorylation of bad by akt promotes survival by blocking the interaction of this pro-apoptotic molecule with bcl-2 and bcl-x proteins |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling |
| + |
PRKACA | down-regulates activity
phosphorylation
|
BAD |
0.521 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250338 |
Ser118 |
GRELRRMsDEFVDSF |
Chlorocebus aethiops |
COS-7 Cell |
| pmid |
sentence |
| 10880354 |
Ser(155) is phosphorylated preferentially by PKA in vitro and is the only residue in BAD that becomes phosphorylated when cells are exposed to cAMP-elevating agents. The phosphorylation of BAD at Ser(155) prevents it from binding to Bcl-X(L) and promotes its interaction with 14-3-3 proteins. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-67383 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 10230394 |
Phosphorylation and inactivation of BAD by mitochondria-anchored protein kinase A|Collectively, these results implicate PKA as the principal mitochondria-based S112 kinase. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-180780 |
Ser99 |
PFRGRSRsAPPNLWA |
in vitro |
|
| pmid |
sentence |
| 10949026 |
Survival factors, acting through kinases such as Akt and PKA, induce endogenous BAD phosphorylation at two evolutionarily conserved sites, Ser-112 and Ser-136, which leads to the translocation of BAD from the mitochondria to the cytoplasm and the inhibition of BAD-dependent death |
|
| Publications: |
3 |
Organism: |
Chlorocebus Aethiops, Homo Sapiens, In Vitro |
| Pathways: | COVID-19 Causal Network |
| + |
RPS6KA1 | down-regulates activity
phosphorylation
|
BAD |
0.404 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-78020 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10837486 |
Rsk1, and survival factor signaling stimulate phosphorylation of bad at ser-155, blocking the binding of bad to bcl-xl. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249045 |
Ser153 |
SWTRVFQsWWDRNLG |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10837486 |
We report here that the phosphorylation of BAD at Ser-155 within the BH3 domain is a second phosphorylation-dependent mechanism that inhibits the death-promoting activity of BAD. Protein kinase A, RSK1, and survival factor signaling stimulate phosphorylation of BAD at Ser-155, blocking the binding of BAD to Bcl-XL. RSK1 phosphorylates BAD at both Ser-112 and Ser-155 and rescues BAD-mediated cell death in a manner dependent upon phosphorylation at both sites. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-160635 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 18246127 |
To understand the mechanisms underlying B-RAF effects on cell survival we initially analysed the Bcl-2 family protein, Bad, that is phosphorylated by RSK1 at the inhibitory serine-75 residue in a MEK-dependent manner in melanoma cells |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-180910 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10558990 |
The rsks catalyze the phosphorylation of the pro-apoptotic protein bad at serine 112 to promote cell survival. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling, Inhibition of Apoptosis |
| + |
IKK-complex | down-regulates activity
phosphorylation
|
BAD |
0.266 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-209776 |
Ser25 |
AERGLGPsPAGDGPS |
Mus musculus |
MEF Cell |
| pmid |
sentence |
| 23332762 |
Ikk phosphorylates bad at serine-26 (ser26) and primes it for inactivation. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | COVID-19 Causal Network, FLT3-ITD signaling, Inhibition of Apoptosis |
| + |
PAK1 | down-regulates
phosphorylation
|
BAD |
0.341 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-177271 |
Ser74 |
VEIRSRHsSYPAGTE |
Homo sapiens |
|
| pmid |
sentence |
| 22096607 |
Bad is a pro-apoptotic member of the bcl-2 family of proteins, which can be phosphorylated on numerous sites to modulate binding to bcl-2 and 14-3-3 proteins and inhibit its pro-apoptotic activities. Together, these findings demonstrate that pak1 phosphorylates bad directly at s111, but phosphorylated s112 through raf-1. These two sites of bad serve as redundant regulatory sites for bcl-2 binding |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-73529 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 10611223 |
Pak phosphorylates bad in vitro and in vivo on ser112 and ser136, resulting in a markedly reduced interaction between bad and bcl-2 or bcl-x(l) and the increased association of bad with 14-3-3tau. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-73533 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
|
| pmid |
sentence |
| 10611223 |
Pak phosphorylates bad in vitro and in vivo on ser112 and ser136, resulting in a markedly reduced interaction between bad and bcl-2 or bcl-x(l) and the increased association of bad with 14-3-3tau. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
Calcineurin | up-regulates activity 
dephosphorylation
|
BAD |
0.412 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252324 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10195903 |
Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD|Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252332 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10195903 |
Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD|Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PPP3CC | up-regulates activity
dephosphorylation
|
BAD |
0.372 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248528 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10195903 |
Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD|Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248529 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10195903 |
Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD|Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PPP3CB | up-regulates activity
dephosphorylation
|
BAD |
0.34 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248383 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10195903 |
Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD|Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248384 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10195903 |
Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD|Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
RPS6KA2 | down-regulates
phosphorylation
|
BAD |
0.381 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-184591 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 19282669 |
The rsks catalyze the phosphorylation of the pro-apoptotic protein bad at serine 112 to promote cell survival. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RPS6KA3 | down-regulates
phosphorylation
|
BAD |
0.393 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-184595 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 19282669 |
The rsks catalyze the phosphorylation of the pro-apoptotic protein bad at serine 112 to promote cell survival. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PAK5 | down-regulates activity
phosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250247 |
Ser75 |
EIRSRHSsYPAGTED |
Chlorocebus aethiops |
COS-7 Cell |
| pmid |
sentence |
| 12897128 |
P21-Activated kinase 5 (Pak5) localizes to mitochondria and inhibits apoptosis by phosphorylating BAD. Pak5 phosphorylates BAD Ser-112 |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
PPP3CA | up-regulates activity
dephosphorylation
|
BAD |
0.451 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263739 |
Ser75 |
EIRSRHSsYPAGTED |
in vitro |
|
| pmid |
sentence |
| 10195903 |
Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis.| Bcl-xL did not coimmunoprecipitate with BAD(S75E, S99E) protein (Fig. 2A), regardless of whether it was coexpressed with DCnA/B  |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248694 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10195903 |
Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD|Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248695 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
|
| pmid |
sentence |
| 10195903 |
Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD|Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263740 |
Ser99 |
PFRGRSRsAPPNLWA |
in vitro |
|
| pmid |
sentence |
| 10195903 |
Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis.| Bcl-xL did not coimmunoprecipitate with BAD(S75E, S99E) protein (Fig. 2A), regardless of whether it was coexpressed with DCnA/B  |
|
| Publications: |
4 |
Organism: |
In Vitro, Homo Sapiens |
| + |
CDK1 | up-regulates activity
phosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267921 |
Ser91 |
EGMGEEPsPFRGRSR |
|
|
| pmid |
sentence |
| 24677263 |
CDK1-mediated Bcl-2 serine 70 phosphorylation enhances its pro-apoptotic function, whereas CDK1-mediated Bad serine 128 phosphorylation promotes apoptosis. |
|
| Publications: |
1 |
| Pathways: | Acute Myeloid Leukemia |
| + |
PRKACG | down-regulates activity
phosphorylation
|
BAD |
0.409 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-67400 |
Ser99 |
PFRGRSRsAPPNLWA |
in vitro |
|
| pmid |
sentence |
| 10949026 |
Survival factors, acting through kinases such as Akt and PKA, induce endogenous BAD phosphorylation at two evolutionarily conserved sites, Ser-112 and Ser-136, which leads to the translocation of BAD from the mitochondria to the cytoplasm and the inhibition of BAD-dependent death |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
BAD | down-regulates
binding
|
BCL2L2 |
0.553 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-133805 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15694340 |
Bad, however, bound tightly to bcl-2, bcl2l1, and bcl2l2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BAD | down-regulates activity
relocalization
|
BCL2 |
0.792 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-133756 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 15694340 |
Apoptosis is initiated when Bcl-2 and its prosurvival relatives are engaged by proapoptotic BH3-only proteins via interaction of its BH3 domain with a groove on the Bcl-2-like proteins. These interactions have been considered promiscuous, but our analysis of the affinity of eight BH3 peptides for five Bcl-2-like proteins has revealed that the interactions vary over 10,000-fold in affinity, and accordingly, only certain protein pairs associate inside cells. Bim and Puma potently engaged all the prosurvival proteins comparably. Bad, however, bound tightly to Bcl-2, Bcl-xL, and Bcl-w but only weakly to A1 and not to Mcl-1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD signaling, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, Malignant Melanoma, SARS-COV APOPTOSIS |
| + |
BAD | down-regulates 
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256260 |
|
|
Homo sapiens |
NCI-H292 Cell, NCI-H1299 Cell, A-549 Cell, NCI-H460 Cell, SK-MES-1 Cell |
| pmid |
sentence |
| 23725574 |
Our data suggested that increased expression of BAD enhance apoptosis and has negative influence on cell proliferation and tumor growth in NSCLC. Bad is a new potential target for tumor interventions. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, FLT3-ITD signaling, Malignant Melanoma, VEGF Signaling |
| + |
NPTX1 | up-regulates activity
relocalization
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261483 |
|
|
Mus musculus |
Neuron |
| pmid |
sentence |
| 23069675 |
Immunofluorescence staining and subcellular fractionation analyses revealed increased mitochondrial translocation of Bad and Bax proteins from cytoplasm following OGD (4 h) and simultaneously increased release of Cyt C from mitochondria followed by activation of caspase-3. NP1 protein was immunoprecipitated with Bad and Bax proteins; OGD caused increased interactions of NP1 with Bad and Bax, thereby, facilitating their mitochondrial translocation and dissipation of mitochondrial membrane potential |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
ERK1/2 | down-regulates activity
phosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-244497 |
|
|
in vitro |
|
| pmid |
sentence |
| 8929531 |
The rapid phosphorylation of bad following il-3 connects a proximal survival signal with the bcl-2 family, modulating this checkpoint for apoptosis.phosphorylatedBAD is bound to 14-3-3 within the cytosol, while only nonphosphorylated BAD is heterodimerized with membrane-bound BCL-XL. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, FLT3-ITD signaling, Inhibition of Apoptosis, Malignant Melanoma, VEGF Signaling |
| + |
HMOX1 | up-regulates quantity by expression 
transcriptional regulation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256304 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26722274 |
The results of the present study indicated that knockdown of HMOX-1 significantly enhanced doxorubicin-induced apoptosis and downregulated the expression of Bcl-2 and Bcl-xL in breast cancer cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK3 | down-regulates
phosphorylation
|
BAD |
0.46 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-188172 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 19777442 |
Erk-1 map kinase prevents tnf-induced apoptosis through bad phosphorylation and inhibition of bax translocation in hela cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates
binding
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-44855 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8929531 |
14-3-3 blocks bad activity by promoting ser-155 phosphorylation, which induces the dissociation of bad and bcl-xl. in the presence of survival factor il-3, cells phosphorylated bad on two serine residues embedded in 14-3-3 consensus binding sites. Only the nonphosphorylated bad heterodimerized with bcl-x(l) at membrane sites to promote cell death. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81106 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
14-3-3 blocks bad activity by promoting ser-155 phosphorylation, which induces the dissociation of bad and bcl-xl. in the presence of survival factor il-3, cells phosphorylated bad on two serine residues embedded in 14-3-3 consensus binding sites. Only the nonphosphorylated bad heterodimerized with bcl-x(l) at membrane sites to promote cell death. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
BAD | down-regulates activity
binding
|
BCL2L1 |
0.841 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-133759 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 15694340 |
Bad, however, bound tightly to bcl-2, bcl2l1, and bcl2l2 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249617 |
|
|
|
|
| pmid |
sentence |
| 7834748 |
Bad binds more strongly to Bcl-x, than Bcl-2 in mammalian cells, and it reversed the death repressor activity of Bcl-x,, but not that of Bcl-2. When Bad dimerized with Bcl-x,, Bax was displaced and apoptosis was restored. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens, |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, Mitochondrial Control of Apoptosis, Malignant Melanoma, SARS-COV APOPTOSIS |
| + |
IKBKB | down-regulates
phosphorylation
|
BAD |
0.266 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-192614 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23332762 |
Ikk phosphorylates bad at serine-26 (ser26) and primes it for inactivation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling |
| + |
BCL2L1 | up-regulates activity
binding
|
BAD |
0.841 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81125 |
|
|
in vitro |
|
| pmid |
sentence |
| 10949026 |
Bad dimerizes with bcl-xl at the mitochondrial membrane where it exert its killing effects. Phosphorylation of bad promotes its binding to 14-3-3 protein, which may sequester bad from bcl-xl, thus promoting cell cells survival. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, Mitochondrial Control of Apoptosis, Malignant Melanoma, SARS-COV APOPTOSIS |
| + |
NPTX1 | up-regulates quantity
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260410 |
|
|
Homo sapiens |
MHCC-97 Cell, SMMC-7721 Cell |
| pmid |
sentence |
| 31113871 |
We found that the protein levels of BCL2-associated agonist of cell death (BAD) and BCL2-associated X protein (BAX) were increased in NPTX1-overexpressing SMMC-7721 and MHCC-97h cells relative to control cells. In contrast, decreased levels of myeloid cell leukemia sequence 1 (Mcl-1) and B-cell lymphoma-2 (Bcl-2) were found in NPTX1-overexpressing SMMC-7721 and MHCC-97h cells relative to control |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BAD | up-regulates
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256259 |
|
|
Homo sapiens |
NCI-H292 Cell, NCI-H1299 Cell, A-549 Cell, NCI-H460 Cell, SK-MES-1 Cell |
| pmid |
sentence |
| 23725574 |
Our data suggested that increased expression of BAD enhance apoptosis and has negative influence on cell proliferation and tumor growth in NSCLC. Bad is a new potential target for tumor interventions. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, FLT3-ITD signaling, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, Malignant Melanoma, SARS-COV APOPTOSIS |
| + |
BAD | up-regulates activity
binding
|
TP53 |
0.335 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-149815 |
|
|
Homo sapiens |
NCI-H1299 Cell |
| pmid |
sentence |
| 17000778 |
We also demonstrate that bad physically interacts with cytoplasmic p53. bad is able to direct p53 to the mitochondria and forms a p53/bad complex at the mitochondria. the mitochondrial p53/bad complex promotes apoptosis |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma |
| + |
Gbeta | down-regulates
phosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270037 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 19777442 |
Erk-1 map kinase prevents tnf-induced apoptosis through bad phosphorylation and inhibition of bax translocation in hela cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Survival Factors | down-regulates
|
BAD |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-209693 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 9346240 |
Akt Phosphorylation of BAD Couples Survival Signals to the Cell-Intrinsic Death MachineryAkt phosphorylates BAD in vitro and in vivo, and blocks the BAD-induced death of primary neurons in a site-specific manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Inhibition of Apoptosis, Mitochondrial Control of Apoptosis |
| + |
PI3K | down-regulates activity
phosphorylation
|
BAD |
0.283 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254951 |
|
|
Homo sapiens |
Mast Cell |
| pmid |
sentence |
| 15526160 |
C-Kit promotes survival via PI3-kinase-dependent activation of Akt and phosphorylation of Bad, a pro-apoptotic molecule, at S136 in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, FLT3-ITD signaling, VEGF Signaling |
| + |
PP2B | up-regulates activity
dephosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269992 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10195903 |
Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD|Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PKA | down-regulates
phosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270129 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10230396 |
Ser-155 is the major phosphoacceptor site for pka on bad, but that pka also phosphorylates ser-112 and ser-136. Phosphorylated bad appears to be the inactive moiety. These results implicate pkac as the candidate kinase for s112 phosphorylation in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling |
| + |
MAPK1 | down-regulates activity
phosphorylation
|
BAD |
0.438 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-44858 |
|
|
in vitro |
|
| pmid |
sentence |
| 8929531 |
The rapid phosphorylation of bad following il-3 connects a proximal survival signal with the bcl-2 family, modulating this checkpoint for apoptosis.phosphorylatedBAD is bound to 14-3-3 within the cytosol, while only nonphosphorylated BAD is heterodimerized with membrane-bound BCL-XL. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
Caspase 3 complex | up-regulates activity
cleavage
|
BAD |
0.517 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256455 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 15231831 |
Casp3 cleaves bad at asp-61. In addition, caspases convert bad(l) into a pro-death fragment that resembles the short splice variant. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK8 | down-regulates
phosphorylation
|
BAD |
0.672 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-121940 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14967141 |
Jnk phosphorylates bad at threonine 201, thereby inhibiting bad association with the antiapoptotic molecule bcl-x(l) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML |
| + |
CASP3 | up-regulates activity
cleavage
|
BAD |
0.517 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-126727 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 15231831 |
Casp3 cleaves bad at asp-61. In addition, caspases convert bad(l) into a pro-death fragment that resembles the short splice variant. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
IKK-complex | down-regulates
phosphorylation
|
BAD |
0.266 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216399 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23332762 |
Ikk phosphorylates bad at serine-26 (ser26) and primes it for inactivation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, FLT3-ITD signaling, Inhibition of Apoptosis |
| + |
LGALS3 | up-regulates quantity by stabilization
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261907 |
|
|
Homo sapiens |
K-562 Cell |
| pmid |
sentence |
| 21821001 |
Our study also showed that a number of K562 cells survived despite the apoptotic stimuli. Within these surviving cells, galectin-3 was upregulated through newly synthesized protein. Notably, inducible galectin-3, which stabilized the pro-survival Bcl-2 family proteins Mcl-1, Bcl-xL, and Bcl-2, was essential for anti-apoptosis. Unpredictably, GSK-3β was critical for inducible galectin-3 expression as well as for cell survival. As summarized in Fig. 4C, we not only found inducible galectin-3 has an anti-apoptotic effect, but we also identified a GSK-3β-regulated mechanism for apoptotic resistance in K562 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AVP | down-regulates
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-178197 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 18402937 |
Vp induces phosphorylation of the pro-apoptotic protein bad and prevents cytochrome c release. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Brain |
| + |
BAD | down-regulates
|
Survival |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254953 |
|
|
Homo sapiens |
Mast Cell |
| pmid |
sentence |
| 15526160 |
C-Kit promotes survival via PI3-kinase-dependent activation of Akt and phosphorylation of Bad, a pro-apoptotic molecule, at S136 in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Inhibition of Apoptosis, Malignant Melanoma |
3.0
BAD
- 
- 