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Symbol BCL2L1 contributors: mct/npt - updated : 29-09-2017
HGNC name BCL2-like 1
HGNC id 992
  • including BH1, BH2, BH3, BH4 domains
  • C-terminal transmembrane domain, that can by itself direct protein oligomerization, which could be related to its previously reported role in mitochondrial morphology alterations and apoptosis inhibition , C-terminal tail forms a transmembrane alpha-helix that retains a significant degree of conformational dynamics and the presence of the intact C-terminus destabilizes the soluble state of the protein
  • mono polymer homomer , heteromer , dimer
    interspecies homolog to murine Bcl2l1 (97.85 pc)
  • BCL2-like apoptosis inhibitors family
  • CATEGORY regulatory
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,nuclear envelope
    basic FUNCTION
  • involved in regulation of cell death by blocking the voltage dependent anion channel (VDAC)
  • has a role in preventing BAX activation at the mitochondrial membrane
  • inhibits p53-induced apoptosis in head and neck neoplasms
  • anti/pro-apoptotic regulatory activity
  • dispensable for germinal center formation
  • MCL1 and BCL2L1 function in the same apoptotic pathway
  • suppress serum deprivation-induced cell death, while ROMO1 is responsible for a serum deprivation-induced increase in reactive oxygen species (ROS)
  • can bind pro-apoptotic members of this family preventing them from activating the execution phase of apoptosis
  • ensures the survival of both developing and peripheral T cells, which is essential for a functional immune system
  • combination of BCL2L1 and MCL1 is essential for the viability of the megakaryocyte lineage
  • BCL2L1, and PMAIP1 co-ordinately regulate oxidative stress-induced apoptosis
  • permeabilize the outer mitochondrial membrane of cells and inhibit the regulation of apoptosis, tumor genesis and cellular responses to anti-cancer therapy
  • BCL2L1 regulates neuronal outgrowth during development and protects neurites from hypoxic insult, as opposed by TNFRSF21
  • is an anti-apoptotic BCL2 family protein found both in the cytosol and bound to intracellular membranes
  • despite its role in BAX inhibition, BL2L1 also likely primes mitochondria to permeabilization and cytochrome c release
  • critical role of BL2L1, an anti-apoptotic protein, during brain development
  • unanticipated functions for BCL2 proteins as transcriptional regulators
  • CELLULAR PROCESS cell life, cell death/apoptosis
    cell life, antiapoptosis
    a component
  • BCLXL dimerizing with BAX and BAK
  • BCLXS dimerizing with BCL2
    small molecule
  • 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
  • cell & other
    inhibited by by overexpression of TARDBP
    Other regulated by HIV-Tat
    proteolytically cleaved by caspase during apoptosis
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein 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
  • parkinson disease
  • non-Hodgkin lymphoma
  • polycythemia vera
  • Variant & Polymorphism
    Candidate gene
    Therapy target
    neuromuscularspinal muscular atrophy 
    potential target in SMA therapeutics
  • selective loss of these Bcl-xL-dependent neurons results in mice exhibiting severe neurobehavioral abnormalities, including self-injurious and risk-taking behaviors, hyperactivity, and learning and memory defects