protein
| binding to APAF1 |
|
interacting with BNIP3 (critically regulates the apoptosis of terminally differentiated chondrocytes) |
|
interacting with PLK1 (regulator of its phosphorylation and controling its anti-apoptotic function under certain specific conditions) ((Tamura 2009) |
|
BCL2L1 and BIRC5 can critically contribute in a cooperative, nonredundant manner to augment the accumulation and persistence of CD8(+) T cells following encounter with Antigen  |
|
recruited by ROMO1 to reduce the mitochondrial membrane potential, resulting in ROS production and apoptotic cell death  |
|
TCERG1 regulates alternative splicing of the apoptosis gene BCL2L1 in a promoter-dependent manner  |
|
BAX BH3 domain complexing with the pro-survival proteins MCL1 and BCL2L1  |
|
HEBP2 interacts with the anti-apoptotic protein BCL2L1  |
|
PARK7 protects cells against UVB-induced cell death dependent on its oxidation and its association with mitochondrial BCL2L1  |
|
can bind pro-apoptotic members of BCL2 family, preventing them from activating the execution phase of apoptosis  |
|
plays a critical role in the survival of neuronal populations by regulating the multi-BH domain protein BAX  |
|
interaction with VDAC1, mediating BCL2L1 protection against apoptosis (BCL2L1 acting as antiapoptotic protein, promoting tumor cell survival via binding to VDAC1)  |
|
YAP1, CTNNB1 and TBX5 form a complex that regulates the expression of genes that promote survival, including BIRC5 and BCL2L1  |
|
ATXN3 promotes the interaction between BCL2L1 and BAX, but does not affect the ubiquitination and degradation of BCL2L1  |
|
interaction between BL2L1 and VDAC1, VDAC3 promotes matrix Ca(2+) accumulation by increasing Ca(2+) transfer across the outer mitochondrial membrane  |
|
interaction between BCL2 and BL2L1 with a stress chaperone, mortalin (HSPA9)  |
|
antiapoptotic BCL2L1 opposes this activity by sequestering cytosolic TP53 via association with its DNA-binding domain, an interaction enhanced by TP53 tetramerization  |
|
BCL2L1 protein protects from DDIT3-dependent apoptosis during plasma cell differentiation  |
|
BCL2L1 regulates CD1D-mediated Ag processing and presentation to NKT cells by altering the late endosomal compartment and changing the intracellular localization of CD1D  |
|
SYK binds robustly to nucleolin and phosphorylates it on tyrosine, enhancing its ability to bind the BCL2L1 mRNA  |
|
PI3K/AKT1 regulates survival during differentiation of macrophages by maintaining NFKB1-dependent expression of antiapoptotic BCL2L1  |
|
PACS2 is a mediator of the ATM and NFkB1-dependent induction of BCL2L1 that promotes cell survival in response to DNA damage  |
|
BCL2L1 is an exosomal CASP3 substrate and this processing is required for the uptake of exosomes by recipient cells  |
|
PGAM5 might participate in the degradation of BCL2L1 mediated by KEAP1  |
|
PRKN tumor suppressor controls the apoptotic regulator BCL2L1 and modulates programmed cell death  |
|
BCL2 proteins directly promote SUFU turnover, inhibit SUFU-GLI interaction, and induce the expression of the GLI target genes BCL2, MCL1 and BCL2L1  |
|
HNF1A upregulates transactivation of an anti-apoptotic gene BCL2L1  |
|
|
Other morbid association(s)
|
Type | Gene Modification | Chromosome rearrangement | Protein expression | Protein Function
|
---|
constitutional
| somatic mutation
|  
|  
|  
|
mutated in non-Hodgkin lymphoma | constitutional
|  
|  
| --over
|  
|
increased expression and redistribution of BCLXL in Parkinson disease | constitutional
|  
|  
| --other
|  
|
dysregulated expression in polycythemia vera, contributing to the pathogenesis of this disorder | tumoral
| fusion
|  
|  
|  
|
BACH2-BCL2L1 fusion gene resulting from a t(6;20)(q15;q11.2) chromosomal translocation in Burkitt lymphoma  | constitutional
|  
|  
| --over
|  
|
increased expression, which is observed in many cancer cells, confers resistance to oxidative stress in the cancer cells by suppressing ROMO1-mediated oxidative stress ( | constitutional
|  
|  
| --low
|  
|
in SMA  | |