| + |
GSK3B | up-regulates 
phosphorylation
|
BAX |
0.384 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-130141 |
Ser163 |
GGWDGLLsYFGTPTW |
Homo sapiens |
Neuron |
| pmid |
sentence |
| 15525785 |
Glycogen synthase kinase-3beta phosphorylates bax and promotes its mitochondrial localization during neuronal apoptosis. Gsk-3beta directly phosphorylated bax(alpha) on ser163 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, Acute Myeloid Leukemia, FLT3-ITD signaling |
| + |
AKT | down-regulates activity 
phosphorylation
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-209651 |
Ser184 |
VAGVLTAsLTIWKKM |
Homo sapiens |
Polymorphonuclear Neutrophil |
| pmid |
sentence |
| 14766748 |
Phosphorylation of Bax Ser184 by Akt regulates its activity and apoptosis in neutrophilsWe suggest that Bax is regulated by phosphorylation of Ser(184) in an Akt-dependent manner and that phosphorylation inhibits Bax effects on the mitochondria by maintaining the protein in the cytoplasm, heterodimerized with antiapoptotic Bcl-2 family members |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD signaling, Inhibition of Apoptosis, Malignant Melanoma, SARS-COV APOPTOSIS |
| + |
AKT1 | down-regulates activity
phosphorylation
|
BAX |
0.499 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252538 |
Ser184 |
VAGVLTAsLTIWKKM |
Homo sapiens |
Polymorphonuclear Neutrophil |
| pmid |
sentence |
| 14766748 |
Phosphorylation of Bax Ser184 by Akt regulates its activity and apoptosis in neutrophilsWe suggest that Bax is regulated by phosphorylation of Ser(184) in an Akt-dependent manner and that phosphorylation inhibits Bax effects on the mitochondria by maintaining the protein in the cytoplasm, heterodimerized with antiapoptotic Bcl-2 family members |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling |
| + |
PRKCZ | down-regulates activity
phosphorylation
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-155111 |
Ser184 |
VAGVLTAsLTIWKKM |
Homo sapiens |
|
| pmid |
sentence |
| 17525161 |
Protein kinase czeta abrogates the proapoptotic function of bax through phosphorylation. Overexpression of wild type or the constitutively active a119d but not the dominant negative k281w pkczeta mutant results in bax phosphorylation at serine 184. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ING1 | up-regulates quantity by expression 
transcriptional regulation
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254488 |
|
|
Homo sapiens |
U2-OS Cell |
| pmid |
sentence |
| 15662138 |
Ectopic expression of p33ING1b could obviously upregulate p53, p21WAF1 and bax protein levels and activate caspase-3 in taxol-treated U2OS cells. Taken together, our data demonstrate that p33ING1b enhances taxol-induced apoptosis through p53-dependent pathway in human osteosarcoma cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AATF | down-regulates quantity
transcriptional regulation
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259916 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22909821 |
We identify the transcriptional regulator apoptosis-antagonizing transcription factor (AATF)/Che-1 as a critical regulator of the cellular outcome of the p53 response. Upon genotoxic stress, AATF is phosphorylated by the checkpoint kinase MK2. Phosphorylation results in the release of AATF from cytoplasmic MRLC3 and subsequent nuclear translocation where AATF binds to the PUMA, BAX and BAK promoter regions to repress p53-driven expression of these pro-apoptotic genes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BID | up-regulates
binding
|
BAX |
0.819 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-152929 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17289999 |
We find short peptides representing the alpha-helical bh3 domains of bid or bim are capable of inducing oligomerization of bak and bax to release cytochrome cthe first alfa helix of bax plays a necessary role in its ligand-induced activation by the bh3-only proteins bid and puma |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-131442 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15574335 |
We find short peptides representing the alpha-helical bh3 domains of bid or bim are capable of inducing oligomerization of bak and bax to release cytochrome cthe first alfa helix of bax plays a necessary role in its ligand-induced activation by the bh3-only proteins bid and puma |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-73902 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10629050 |
Bid, a bh3-domain-only protein which interacts with bax, was able to trigger a conformational change in bax. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-92945 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12242151 |
We find short peptides representing the alpha-helical bh3 domains of bid or bim are capable of inducing oligomerization of bak and bax to release cytochrome cthe first alfa helix of bax plays a necessary role in its ligand-induced activation by the bh3-only proteins bid and puma |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS, TNF-alpha Signaling |
| + |
MAPK8 | up-regulates
|
BAX |
0.541 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-124012 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15071501 |
We demonstrate that jnk-mediated phosphorylation of 14-3-3 induces the release of bax from 14-3-3 and triggers its translocation to the mitochondria here we demonstrate that activated jnk promotes bax translocation to mitochondria through phosphorylation of 14-3-3, a cytoplasmic anchor of bax. Phosphorylation of 14-3-3 led to dissociation of bax from this protein. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, SAPK/JNK Signaling, TNF-alpha Signaling |
| + |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
BAX |
0.744 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-47541 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9122197 |
P53 can transcriptionally activate bax, a bcl-2 family member that promotes apoptosis |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer |
| + |
BBC3 | up-regulates
binding, relocalization
|
BAX |
0.502 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-20064 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 1557433 |
The first Helix of bax plays a necessary role in its ligand-induced activation by the bh3-only proteins bid and puma |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-185671 |
|
|
Homo sapiens |
Lung Cancer Cell |
| pmid |
sentence |
| 19439449 |
Puma promotes bax translocation by both by directly interacting with bax and by competitive binding to bcl-x(l) in uv-induced apoptosis. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Death Receptor Signaling, Mitochondrial Control of Apoptosis |
| + |
BCL2L1 | down-regulates
binding
|
BAX |
0.736 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-59141 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9670005 |
The presence of an anti-apoptotic molecule such as bcl-2 or bcl-xl can inhibit the activation of bax following a death signal. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, Mitochondrial Control of Apoptosis, Malignant Melanoma, SARS-COV APOPTOSIS |
| + |
MAPK10 | up-regulates
|
BAX |
0.262 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-124001 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15071501 |
Demonstrate that jnk-mediated phosphorylation of 14-3-3 induces the release of bax from 14-3-3 and triggers its translocation to the mitochondria; these results strongly indicate that jnk regulates the activity of bax by phosphorylating 14-3-3 proteins. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BAX | up-regulates
|
CYCS |
0.686 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-160039 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18097445 |
This process of mitochondrial outer membrane permeabilization (momp) results in the release of cycs.it is commonly thought that bax and bak form pores in membranes |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
USP24 | up-regulates quantity by stabilization
deubiquitination
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275606 |
|
|
Homo sapiens |
A-549 Cell |
| pmid |
sentence |
| 27991932 |
In this study, several cancer-related proteins (Bax, p300, E2F4 and securin) have been proven to be substrates of ubiquitin-specific peptidase 24 (USP24), and relevance has been shown between USP24 and its substrates in samples from clinical lung cancer patients. |Knockdown of USP24 decreases Bax and p300 levels |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ETS1 | down-regulates quantity by repression 
transcriptional regulation
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254204 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 17213822 |
Our results suggest that the interaction between ETS1 and GFI1 facilitates their binding to specific sites on the Bax promoter and represses Bax expression in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MCL1 | down-regulates
binding
|
BAX |
0.727 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-151787 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17289999 |
Which of the multiple pro-survival proteins that can bind Bax (fig. S15A) can functionally restrain it? Mcl-1 must, because neutralizing Mcl-1 by enforced Noxa expression rendered MEFs containing only Bax (Bak KO cells) sensitive to the Bad BH3 mimetic ABT-737 (Fig. 4A), which inactivates Bcl-2, Bcl-xL, and Bcl-w |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML, COVID-19 Causal Network, SARS-COV APOPTOSIS |
| + |
BAX | up-regulates activity
binding
|
VDAC1 |
0.574 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249613 |
|
|
|
|
| pmid |
sentence |
| 10365962 |
The recombinant pro-apoptotic proteins Bax and Bak accelerate the opening of VDAC |
|
| Publications: |
1 |
| + |
BCL2L11 | up-regulates activity
binding
|
BAX |
0.827 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-92939 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 12242151 |
We find short peptides representing the alpha-helical BH3 domains of BID or BIM are capable of inducing oligomerization of BAK and BAX to release cytochrome c. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-196935 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22492984 |
Bim, and puma bind with high affinity to all pro-survival proteins |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-87280 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 11997495 |
We have shown that the interaction of the bims and bimad isoforms with bax leads to a conformational change in this protein analogous to that triggered by the bh3-only protein bid.We find short peptides representing the alpha-helical bh3 domains of bid or bim are capable of inducing oligomerization of bak and bax to release cytochrome. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-152986 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17289999 |
Contrary to the direct-activation model, we show that Bax and Bak can mediate apoptosis without discernable association with the putative BH3-only activators (Bim, Bid, and Puma), even in cells with no Bim or Bid and reduced Puma. Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak |
|
| Publications: |
4 |
Organism: |
Mus Musculus, Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, SAPK/JNK Signaling, SARS-COV APOPTOSIS |
| + |
GFI1 | down-regulates quantity by repression
transcriptional regulation
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254203 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 17213822 |
Our results suggest that the interaction between ETS1 and GFI1 facilitates their binding to specific sites on the Bax promoter and represses Bax expression in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TP53 | up-regulates
binding
|
BAX |
0.744 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-121895 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14963330 |
Tp53 directly activated the proapoptotic bcl-2 protein bax in the absence of other proteins to permeabilize mitochondria and engage the apoptotic program |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-140242 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16151013 |
P53 also accumulates in the cytoplasm where it directly activates bax to promote mitochondrial outer membrane permeabilization. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer |
| + |
BAX | up-regulates activity
binding
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-73895 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10629050 |
Following bid-induced conformational change, bax oligomerizes and inserts tightly within the outer mitochondrial membrane. The integration of bax in the outer mitochondrial membrane is followed by cytochrome crelease |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, Acute Myeloid Leukemia, MLL fusion protein in AML, COVID-19 Causal Network, Death Receptor Signaling, FLT3-ITD signaling, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer, SAPK/JNK Signaling, SARS-COV APOPTOSIS, TNF-alpha Signaling |
| + |
BAX | up-regulates
relocalization
|
DIABLO |
0.525 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-87109 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14585074 |
Bax and/or bak-mediated release of pro-apoptotic mediators including smac/diablo and omi |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Death Receptor Signaling |
| + |
WWTR1 | up-regulates quantity by expression
transcriptional regulation
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255606 |
|
|
Homo sapiens |
Colorectal Cancer Cell |
| pmid |
sentence |
| 22470139 |
Efficient knockdown of WWTR1, demonstrated by quantitative real-time PCR, led to upregulation of ASNS and downregulation of SMAD3, LTBR, BAX and BAK1 in WWTR1 knockdown cells, suggesting that these genes may be involved in the repression of cell proliferation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BAX | up-regulates
relocalization
|
HTRA2 |
0.317 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-88590 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14585074 |
Bax and/or bak-mediated release of pro-apoptotic mediators including smac/diablo and omi |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BAX | up-regulates
relocalization
|
CYCS |
0.686 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-73898 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10629050 |
The integration of bax oligomers in the outer mitochondrial membrane is followed by cytochrome crelease |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
BCL2 | down-regulates activity
binding
|
BAX |
0.621 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-36898 |
|
|
Homo sapiens |
B-lymphocyte, Lymphoma Cell |
| pmid |
sentence |
| 8183370 |
Bcl-2 has the unique oncogenic role of extending cell survival by inhibiting a variety of apoptotic deaths. Bcl-2 exerts its action through heterodimerization with bax. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, Acute Myeloid Leukemia, MLL fusion protein in AML, COVID-19 Causal Network, Death Receptor Signaling, FLT3-ITD signaling, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer, SARS-COV APOPTOSIS |
| + |
BAX | down-regulates activity
binding
|
BCL2 |
0.621 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249612 |
|
|
|
|
| pmid |
sentence |
| 8358790 |
Bax shows extensive amino acid homology with Bcl-2 and forms homodimers and heterodimers with Bcl-2 in vivo. When Bax predominates, programed cell death is accelerated, and the death repressor activity of Bcl-2 is countered. |
|
| Publications: |
1 |
| Pathways: | Alzheimer, Acute Myeloid Leukemia, MLL fusion protein in AML, COVID-19 Causal Network, Death Receptor Signaling, FLT3-ITD signaling, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer, SARS-COV APOPTOSIS |
| + |
NR4A3 | up-regulates quantity by expression
transcriptional regulation
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259397 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30455429 |
Over-expression of NR4A3 attenuated proliferation of cancer cells and promoted apoptosis by augmenting the expression of pro-apoptotic genes, PUMA and Bax. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JNK | up-regulates
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269977 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15071501 |
Demonstrate that jnk-mediated phosphorylation of 14-3-3 induces the release of bax from 14-3-3 and triggers its translocation to the mitochondria; these results strongly indicate that jnk regulates the activity of bax by phosphorylating 14-3-3 proteins. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, FLT3-ITD signaling |
| + |
BAX | up-regulates
|
DIABLO |
0.525 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-170969 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21210296 |
Permeabilization of the outer mitochondrial membrane allows the leakage of at least five apoptotic mediators from the mitochondrial intermembrane space, such as cyt c,(diablo/diablo), htra2/omi, apoptosis-inducing factors (aif), and endonuclease g. Such modifications result in their activation and translocation to outer mitochondrial membrane (omm) which helps it to interact with multidomain pro-apototic members, bax/baklike proteins, leading to their oligomerization and formation of pore. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Death Receptor Signaling |
| + |
ENDOG | up-regulates
|
BAX |
0.356 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-170972 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21210296 |
Permeabilization of the outer mitochondrial membrane allows the leakage of at least five apoptotic mediators from the mitochondrial intermembrane space, such as cyt c, (diablo/diablo), htra2/omi, apoptosis-inducing factors (aif), and endonuclease g. Such modifications result in their activation and translocation to outer mitochondrial membrane (omm) which helps it to interact with multidomain pro-apototic members, bax/baklike proteins, leading to their oligomerization and formation of pore. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PPM1D | down-regulates activity
dephosphorylation
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276993 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23907458 |
34 In this study, a novel function of Wip1 was identified, that is, its ability to dephosphorylate directly and thus inactivate apoptotic BAX protein in response to gamma irradiation.|To ascertain whether Wip1 dephosphorylates BAX, recombinant Wip1 was incubated with previously reported BAX-derived phosphopeptides containing Ser87, Ser163, Thr167, and Ser184 in an in vitro phosphatase assay. xref , xref Peptides containing phospho-Thr180 from p38 MAPK and phospho-Thr31 from UNG2 were used as a positive and negative control, respectively. xref As shown in xref , purified Wip1 did not dephosphorylate the four BAX-derived phosphopeptides. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RERE | up-regulates activity
relocalization
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264485 |
|
|
Homo sapiens |
Neuroblastoma Cell Line |
| pmid |
sentence |
| 11331249 |
We detected RERE protein mainly in the nucleus, where it colocalizes with the promyelocytic leukemia protein in promyelocytic leukemia oncogenic domains (PODs). Overexpression of RERE recruits a fraction of the proapoptotic protein BAX to PODS: This observation correlates with RERE-induced apoptosis, which occurs in a caspase-dependent manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TP53 | up-regulates activity
binding
|
BAX |
0.744 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-178690 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14963330 |
Tp53 directly activated the proapoptotic bcl-2 protein bax in the absence of other proteins to permeabilize mitochondria and engage the apoptotic program |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer |
| + |
PYCARD | up-regulates
relocalization
|
BAX |
0.36 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-149522 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16964285 |
Asc directly induces bax-mediated apoptosis. Asc induces the translocation of bax to the mitochondria, bax-dependent cycs release from the mitochondria and casp9 activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MYCT1 | up-regulates quantity by expression
transcriptional regulation
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261734 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30283340 |
MYCT1 overexpression significantly inhibited cell proliferation, arrested cell cycle at G0/G1 phase, and downregulated the expression of cyclins D and E. Moreover, MYCT1 overexpression triggered apoptosis in AML cells, which was accompanied by enhanced cleavage of caspase-3 and -9, upregulated expression of B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), and downregulated Bcl-2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NPTX1 | up-regulates activity
relocalization
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261439 |
|
|
Mus musculus |
|
| 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 |
| + |
BCL2L2 | down-regulates
binding
|
BAX |
0.47 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-154518 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17452531 |
Bcl-w may protect largely via its ability to associate with bax because it could efficiently protect xem from tbid and bid, bad, hrk, and bmf bh3 peptides |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NPTX1 | up-regulates quantity
|
BAX |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260411 |
|
|
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 |
| + |
BAX | up-regulates
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261494 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23567751 |
The mitochondrial pathway of apoptosis proceeds when the outer mitochondrial membrane (OMM) is compromised by the pro-apoptotic BCL-2 family members, BAK and BAX. Once activated, BAK and BAX form proteolipid pores in the OMM leading to mitochondrial outer membrane permeabilization (MOMP), and the release of inner membrane space proteins, such as cytochrome c, which promotes caspase activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, Acute Myeloid Leukemia, MLL fusion protein in AML, COVID-19 Causal Network, Death Receptor Signaling, FLT3-ITD signaling, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer, SARS-COV APOPTOSIS, TNF-alpha Signaling |
| + |
SH3GLB1 | up-regulates
binding
|
BAX |
0.335 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-141166 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 16227588 |
Here, we provide evidence that bif-1 plays a regulatory role in apoptotic activation of not only bax but also bak and appears to be involved in suppression of tumorigenesis. while bif-1 did not directly interact with bak, it heterodimerized with bax on mitochondria in intact cells, and this interaction was enhanced by apoptosis induction and preceded the bax conformational change. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AIFM1 | up-regulates
|
BAX |
0.413 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-170960 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21210296 |
Permeabilization of the outer mitochondrial membrane allows the leakage of at least five apoptotic mediators from the mitochondrial intermembrane space, such as cyt c, (diablo/diablo), htra2/omi, apoptosis-inducing factors (aif), and endonuclease g. Such modifications result in their activation and translocation to outer mitochondrial membrane (omm) which helps it to interact with multidomain pro-apototic members, bax/baklike proteins, leading to their oligomerization and formation of pore. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
BAX |
0.744 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-33922 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 7834749 |
Bax is a p53 primary-response gene, presumably involved in a p53-regulated pathway for induction of apoptosis |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling, Mitochondrial Control of Apoptosis, Malignant Melanoma, p53 in cancer |
| + |
MAPK9 | up-regulates
|
BAX |
0.302 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-124023 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15071501 |
Demonstrate that jnk-mediated phosphorylation of 14-3-3 induces the release of bax from 14-3-3 and triggers its translocation to the mitochondria;these results strongly indicate that jnk regulates the activity of bax by phosphorylating 14-3-3 proteins. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
BAX
- 
- 