| + |
PLK3 | up-regulates 
phosphorylation
|
BCL2L1 |
0.391 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-172230 |
Ser49 |
ESEMETPsAINGNPS |
Homo sapiens |
|
| pmid |
sentence |
| 21336504 |
Polo kinase 3 (plk3) was implicated in bcl-xl(ser49) phosphorylation. These data indicate that, during g2 checkpoint, phospho-bcl-xl(ser49) is another downstream target of plk3, acting to stabilize g2 arrest. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK8 | down-regulates 
phosphorylation
|
BCL2L1 |
0.776 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-99219 |
Ser62 |
PSWHLADsPAVNGAT |
Homo sapiens |
Prostate Gland Cancer Cell |
| pmid |
sentence |
| 12633850 |
By site-directed mutagenesis studies, we have identified that serine 62 is the necessary site for taxol- or 2-me-induced bcl-xl phosphorylation in prostate cancer cells. Further studies with the inhibitor of jun kinase (jnk) and phosphorylation mutant of bcl-xl reveal the augmentative role of jnk-mediated bcl-xl phosphorylation in apoptosis of prostate cancer cells. In summary, our studies suggest that the phosphorylation of bcl-xl by stress response kinase signaling might oppose the anti-apoptotic function of bcl-xl to permit prostate cancer cells to die by apoptosis |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML |
| + |
JNK | down-regulates
phosphorylation
|
BCL2L1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-99215 |
Ser62 |
PSWHLADsPAVNGAT |
Homo sapiens |
Prostate Gland Cancer Cell |
| pmid |
sentence |
| 12633850 |
We have identified that serine 62 is the necessary site for taxol- or 2-me-induced bcl-xl phosphorylation in summary, our studies suggest that the phosphorylation of bcl-xl by stress response kinase signaling might oppose the anti-apoptotic function of bcl-xl |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-73638 |
Thr115 |
LTSQLHItPGTAYQS |
Homo sapiens |
|
| pmid |
sentence |
| 10617621 |
Sapk phosphorylates bcl-x(l) on threonine 47 (thr-47) and threonine 115 (thr-115) in vitro and in vivo. In contrast to wild-type bcl-x(l), a mutant bcl-x(l) with the two threonines substituted by alanines (ala-47, ala-115) is a more potent inhibitor of ionizing radiation-induced apoptosis |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-73642 |
Thr47 |
GTESEMEtPSAINGN |
Homo sapiens |
|
| pmid |
sentence |
| 10617621 |
Sapk phosphorylates bcl-x(l) on threonine 47 (thr-47) and threonine 115 (thr-115) in vitro and in vivo. In contrast to wild-type bcl-x(l), a mutant bcl-x(l) with the two threonines substituted by alanines (ala-47, ala-115) is a more potent inhibitor of ionizing radiation-induced apoptosis |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network |
| + |
CDK2 | up-regulates activity
phosphorylation
|
BCL2L1 |
0.499 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278242 |
Ser73 |
NGATGHSsSLDAREV |
Homo sapiens |
|
| pmid |
sentence |
| 27239332 |
Our findings show that Cdk2 phosphorylation of Bcl-xL at Ser73, but not the Bcl-xL cleavage products, is necessary and sufficient to induce cell death. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BCL2L1 | down-regulates
binding
|
BAK1 |
0.745 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-55549 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9463381 |
Bcl-xl bind to bax or five other pro-apoptotic relatives (bak, bad, bik, bid or bim) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-152983 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17289999 |
Bax is held in check by mcl1, bcl-2, and either bcl2l1 or bcl2l2, or by all four. They bind a primed conformer of bak or bax |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Malignant Melanoma |
| + |
BCL2L1 | down-regulates
binding
|
BECN1 |
0.915 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-154480 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17446862 |
The anti-apoptotic proteins bcl-2 and bcl-x(l) bind and inhibit beclin-1, an essential mediator of autophagy. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FLT3 | up-regulates quantity by expression 
transcriptional regulation
|
BCL2L1 |
0.338 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261549 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 15626738 |
FLT3-ITD-TKD dual mutants induce hyperactivation of STAT5 and up-regulation of its downstream targets Bcl-x(L) and RAD51 in Ba/F3 cells |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
N-[4-(2-tert-butylphenyl)sulfonylphenyl]-2,3,4-trihydroxy-5-[(2-propan-2-ylphenyl)methyl]benzamide | down-regulates
chemical inhibition
|
BCL2L1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-207462 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
4-[4-[[2-(4-chlorophenyl)-5,5-dimethyl-1-cyclohexenyl]methyl]-1-piperazinyl]-N-[4-[[(2R)-4-(4-morpholinyl)-1-(phenylthio)butan-2-yl]amino]-3-(trifluoromethylsulfonyl)phenyl]sulfonylbenzamide | down-regulates
chemical inhibition
|
BCL2L1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-189153 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BCL2L1 | down-regulates activity
binding
|
VDAC1 |
0.568 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249614 |
|
|
|
|
| pmid |
sentence |
| 10365962 |
The anti-apoptotic protein Bcl-x(L) closes VDAC by binding to it directly |
|
| Publications: |
1 |
| + |
BCL2L1 | down-regulates activity
binding
|
CASP9 |
0.683 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-56402 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9539746 |
Bcl2l1 associates with casp9 and apaf-1 in mammalian cells.Bcl-XL interacts with Apaf-1 and inhibits Apaf-1-dependent caspase-9 activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
chelerythrine | down-regulates
chemical inhibition
|
BCL2L1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-100670 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12702731 |
Chelerythrine inhibited the bclxl-bak bh3 peptide binding with ic50 of 1.5 micro m and displaced bax, a bh3-containing protein, from bclxl. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Obatoclax mesylate | down-regulates activity
chemical inhibition
|
BCL2L1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262023 |
|
|
in vitro |
|
| pmid |
sentence |
| 23515850 |
Obatoclax and its predecessor analogs bind to BCL-2, BCL-XL, BCL-w, BCL-B, BFL-1, and MCL-1 in vitro |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
EIF3E | up-regulates quantity
translation regulation
|
BCL2L1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259156 |
|
|
Homo sapiens |
MDA-MB-231 Cell, U2-OS Cell |
| pmid |
sentence |
| 20453879 |
Validated mRNA targets regulated positively at the translational level by eIF3e included urokinase-type plasminogen activator and apoptotic regulator BCL-XL, whereas synthesis of proteins including the mitotic checkpoint component MAD2L1 was negatively regulated. Taken together, our study data suggest that eIF3e has a positive role in breast cancer progression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ABT-737 | down-regulates
chemical inhibition
|
BCL2L1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-189171 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-151784 |
|
|
Homo sapiens |
Leukemia Cell, B-lymphocyte, Lymphoma Cell |
| pmid |
sentence |
| 17200714 |
A cell-permeant compound, abt-737, binds with high affinity to bcl2, bcl2l1, and bcl2l2, antagonizes their antiapoptotic function, and induces apoptosis in select human tumor cell lines, primary patient-derived cells. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
BBC3 | down-regulates activity
binding
|
BCL2L1 |
0.76 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-133811 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 15694340 |
Only bimbh3 and bbc3 had comparable strong affinities for all the prosurvival proteins. The members that promote cell survival, including mammalian bcl-2, bcl-xl,bcl-w, mcl-1, and a1.Puma promotes bax translocation by both by directly interacting with bax and by competitive binding to bcl-x(l) in uv-induced apoptosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Mitochondrial Control of Apoptosis |
| + |
BCL2L11 | down-regulates activity
binding
|
BCL2L1 |
0.956 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-178679 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 18498746 |
Bim can induce apoptosis by interacting with anti-apoptotic members of the bcl2 family, including bcl2, bcl-xl and mcl-1.Bim binds bcl-2, bcl2l1, bcl2l2, mcl1 and a1 tightly. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
BAD | down-regulates activity
binding
|
BCL2L1 |
0.847 |
| 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. |
|
| 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 |
|
| 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 |
| + |
CD79A | down-regulates quantity by repression 
transcriptional regulation
|
BCL2L1 |
0.27 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-93481 |
|
|
Homo sapiens |
B-lymphocyte |
| pmid |
sentence |
| 12324477 |
Bcr ligation activated mitochondrial apoptotic pathways including down-regulation of bcl-x(l). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CDK1 | down-regulates activity
phosphorylation
|
BCL2L1 |
0.539 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267986 |
|
|
Homo sapiens |
KB-3-1 Cell |
| pmid |
sentence |
| 19917720 |
Cyclin-Dependent Kinase 1-Mediated Bcl-xL/Bcl-2 Phosphorylation Acts as a Functional Link Coupling Mitotic Arrest and Apoptosis|These findings suggest a model whereby a switch in the duration of CDK1 activation, from transient during mitosis to sustained during mitotic arrest, dramatically increases the extent of Bcl-xL/Bcl-2 phosphorylation, resulting in inactivation of their antiapoptotic function. Thus, phosphorylation of antiapoptotic Bcl-2 proteins acts as a sensor for CDK1 signal duration and as a functional link coupling mitotic arrest to apoptosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, KIT in AML |
| + |
RNF183 | down-regulates quantity by destabilization
ubiquitination
|
BCL2L1 |
0.387 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278595 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29507230 |
As an E3 ligase, RNF183 ubiquitinates Bcl-xL, causing its degradation and subsequent apoptosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BID | down-regulates activity
binding
|
BCL2L1 |
0.857 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-209675 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 22464442 |
Overexpression of antiapoptotic proteins including Bcl-XL and/or Bcl-2 contributes to tumor initiation, progression, and resistance to therapy by direct interactions with proapoptotic BH3 proteins. Release of BH3 proteins from antiapoptotic proteins kills some cancer cells and sensitizes others to chemotherapy. Binding of Bcl-XL and Bcl-2 to the BH3 proteins Bad, Bid, and the three major isoforms of Bim was measured for fluorescent protein fusions in live cells using fluorescence lifetime imaging microscopy and fluorescence resonance energy transfer. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
SH2B3 | down-regulates quantity by repression
transcriptional regulation
|
BCL2L1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-177485 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22101255 |
Our results indicated that lnk/sh2b3 constrains expression of bcl-xl and participates in the regulation of hsc homeostasis by maintaining proper responses against various proapoptotic stimuli. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, KIT in AML |
| + |
BCL2L1 | down-regulates
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261683 |
|
|
Mus musculus |
FL5.12 Cell |
| pmid |
sentence |
| 9393856 |
Bcl-xL Expression Prevents Cytochrome c Redistribution and Subsequent Mitochondrial Depolarization during Apoptosis. Bcl-xL expression prevented both cytochrome c redistribution and mitochondrial membrane depolarization. In contrast, zVAD treatment could not prevent either cytochrome c redistribution or mitochondrial membrane depolarization in control transfectants withdrawn from IL-3. Thus, cytochrome c redistribution from mitochondria is an early apoptotic event that precedes mitochondrial membrane depolarization. Bcl-xL expression functions to inhibit both of these events. In at least some forms of cell death, the ability of Bcl-xL to regulate these mitochondrial events cannot be mimicked by caspase inhibition |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, KIT in AML, COVID-19 Causal Network, FLT3-ITD in AML, Mitochondrial Control of Apoptosis, Malignant Melanoma, SARS-COV APOPTOSIS |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
BCL2L1 |
0.655 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261551 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 15626738 |
FLT3-ITD-TKD dual mutants induce hyperactivation of STAT5 and up-regulation of its downstream targets Bcl-x(L) and RAD51 in Ba/F3 cells |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, KIT in AML, FLT3-ITD in AML |
| + |
IKBKB | down-regulates quantity
phosphorylation
|
BCL2L1 |
0.341 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279529 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19488402 |
We present evidence for a signaling network that involves phosphorylation and reduction of Bcl-xL by IKKbeta, and subsequent activation of caspases, which can cleave Htt.|We propose that IKKbeta reduces Bcl-xL levels by phosphorylation (XREF_FIG), a modification known to promote Bcl-xL degradation . |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LGALS3 | up-regulates quantity by stabilization
|
BCL2L1 |
0.279 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261906 |
|
|
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 |
| + |
CREB1 | up-regulates quantity by expression
transcriptional regulation
|
BCL2L1 |
0.362 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-140911 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16205321 |
The results showed that the nuclear pkcalpha was significantly decreased in the liver during sepsis, which was accompanied by decreases in phospho-creb content, dna-binding activity of creb, and bcl-xl expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Malignant Melanoma |
| + |
BCL2L1 | up-regulates activity
binding
|
BAD |
0.847 |
| 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 |
| + |
hsa-miR-491-5p | down-regulates quantity by repression
post transcriptional regulation
|
BCL2L1 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277947 |
|
|
Homo sapiens |
IGROV-1 Cell |
| pmid |
sentence |
| 25299770 |
We found that miR-491-5p efficiently induces apoptosis in IGROV1-R10 cells by directly inhibiting BCL-XL expression and by inducing BIM accumulation in its dephosphorylated form. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PRKN | down-regulates quantity by destabilization
ubiquitination
|
BCL2L1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278661 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 28038320 |
In cells, we found BCL-XL levels were reduced by overexpression of PARK2, but this catalytic activity was blocked by the proteasome inhibitor MG132, suggesting degradation of BCL-XL protein by PARK2 is dependent on the proteasome system (XREF_FIG A).|PARK2 directly binds to and ubiquitinates BCL-XL. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BCL2L1 | down-regulates activity
binding
|
APAF1 |
0.842 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-56399 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9539746 |
These experiments demonstrate that bcl-xl associates with caspase-9 and apaf-1, and show that bcl-xl inhibits the maturation of caspase-9 mediated by apaf-1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
7a | down-regulates activity
binding
|
BCL2L1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261075 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17428862 |
In this study, we show that the overexpression of Bcl-XL, a prosurvival member of the Bcl-2 family, blocks 7a-induced apoptosis, suggesting that the mechanism for apoptosis induction by 7a is at the level of or upstream from the Bcl-2 family. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-COV APOPTOSIS |
| + |
E | down-regulates activity
|
BCL2L1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260586 |
|
|
Homo sapiens |
JURKAT Cell |
| pmid |
sentence |
| 16048439 |
SARS-CoV E protein induces apoptosis by ‘sequestering’ Bcl-xL to the membranes of ER and Golgi, where the SARS-CoV E protein is located. As a consequence, the existing balance between pro-survival protein Bcl-xL and pro-apoptotic proteins, including Bax and BH3-domain-only proteins, is tipped by SARS CoV E protein, so that sequestered Bcl-xL could not fulfil its normal function in inhibition of apoptosis. | This result implied that SARS-CoV E protein might induce T-cell apoptosis via a pathway antagonistic to the mitochondrion-dependent mechanism of Bcl-xL. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-COV APOPTOSIS |
| + |
CD40 | up-regulates quantity by expression
transcriptional regulation
|
BCL2L1 |
0.429 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-93387 |
|
|
Homo sapiens |
B-lymphocyte |
| pmid |
sentence |
| 12324477 |
Cd40 ligation up-regulated bcl-2 and bcl-xl as much as 9.7- (p < 0.01) and 6.8-fold (p < 0.01), respectively (fig. 2, b and c). Under similar conditions, cd27 ligation also up-regulated bcl-2 and bcl-xl as much as 5.0- (p < 0.01) and 3.9-fold (p < 0.01), respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CD27 | up-regulates quantity by expression
transcriptional regulation
|
BCL2L1 |
0.323 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-93320 |
|
|
Homo sapiens |
B-lymphocyte |
| pmid |
sentence |
| 12324477 |
Cd40 ligation up-regulated bcl-2 and bcl-xl as much as 9.7- (p < 0.01) and 6.8-fold (p < 0.01), respectively (fig. 2, b and c). Under similar conditions, cd27 ligation also up-regulated bcl-2 and bcl-xl as much as 5.0- (p < 0.01) and 3.9-fold (p < 0.01), respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BIK | down-regulates
binding
|
BCL2L1 |
0.808 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-26453 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 7478623 |
We have identified a novel cellular protein, bik, that interacts with the cellular survival-promoting proteins, bcl-2 and bcl-xl in transient transfection assays, bik promotes cell death in a manner similar to the death-promoting members of the bcl-2 family, bax and bak. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BCL2L1 | down-regulates
binding
|
BAX |
0.742 |
| 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 |
| + |
BCL2L11 | down-regulates
binding
|
BCL2L1 |
0.956 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-133829 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15694340 |
Bim can induce apoptosis by interacting with anti-apoptotic members of the bcl2 family, including bcl2, bcl-xl and mcl-1.Bim binds bcl-2, bcl2l1, bcl2l2, mcl1 and a1 tightly. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
HRK | down-regulates
binding
|
BCL2L1 |
0.605 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-47797 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9130713 |
Hrk, physically interacts with the death-repressor proteins bcl2 and bcl2l1. Hrk activates cell death at least in part by interacting with and inhibiting the protection afforded by bcl2 and bcl2l1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BCL2L1 | down-regulates
|
HIP1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-82460 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11007801 |
Hip-1 activity was found to be independent of the ded-containing caspase 8 but was significantly inhibited by the antiapoptotic protein bcl-x(l), implicating the intrinsic pathway of apoptosis in hip-1-induced cell death. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
4.0
BCL2L1
- 
- 