BCL2L10

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BCL2-like 10 (apoptosis facilitator)
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
SymbolsBCL2L10; BCL-B; Boo; Diva
External IDsOMIM: 606910 MGI: 1330841 HomoloGene: 8396 ChEMBL: 5988 GeneCards: BCL2L10 Gene
RNA expression pattern
More reference expression data
Orthologs
SpeciesHumanMouse
Entrez1001712049
EnsemblENSG00000137875ENSMUSG00000032191
UniProtQ9HD36Q9Z0F3
RefSeq (mRNA)NM_020396NM_013479
RefSeq (protein)NP_065129NP_038507
Location (UCSC)Chr 15:
52.4 – 52.4 Mb
Chr 9:
75.35 – 75.35 Mb
PubMed search

Bcl-2-like protein 10 is a protein that in humans is encoded by the BCL2L10 gene.[1][2][3]

The protein encoded by this gene belongs to the BCL-2 protein family. BCL-2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. The protein encoded by this gene contains conserved BH4, BH1 and BH2 domains. This protein can interact with other members of BCL-2 protein family including BCL2, BCL2L1/BCL-X(L), and BAX. Overexpression of this gene has been shown to suppress cell apoptosis possibly through the prevention of cytochrome C release from the mitochondria, and thus activating caspase-3 activation. The mouse counterpart of this protein is found to interact with Apaf1 and forms a protein complex with Caspase 9, which suggests the involvement of this protein in APAF1 and CASP9 related apoptotic pathway.[3]

References

  1. Inohara N, Gourley TS, Carrio R, Muniz M, Merino J, Garcia I, Koseki T, Hu Y, Chen S, Nunez G (Jan 1999). "Diva, a Bcl-2 homologue that binds directly to Apaf-1 and induces BH3-independent cell death". J Biol Chem 273 (49): 32479–86. doi:10.1074/jbc.273.49.32479. PMID 9829980. 
  2. Song Q, Kuang Y, Dixit VM, Vincenz C (Feb 1999). "Boo, a novel negative regulator of cell death, interacts with Apaf-1". EMBO J 18 (1): 167–78. doi:10.1093/emboj/18.1.167. PMC 1171112. PMID 9878060. 
  3. 3.0 3.1 "Entrez Gene: BCL2L10 BCL2-like 10 (apoptosis facilitator)". 

Further reading

External links

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