Bcl2l10 Bcl2-like 10 [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Bcl2l10provided by MGI
Official Full Name: Bcl2-like 10provided by MGI
Primary source: MGI:MGI:1330841
See related: Ensembl:ENSMUSG00000032191 AllianceGenome:MGI:1330841
Gene type: protein coding
RefSeq status: PROVISIONAL
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: Boo; Diva
Summary: Enables identical protein binding activity. Involved in microtubule organizing center organization. Acts upstream of or within negative regulation of extrinsic apoptotic signaling pathway in absence of ligand; negative regulation of intrinsic apoptotic signaling pathway; and positive regulation of apoptotic process. Located in membrane and spindle. Is expressed in several structures, including early conceptus; genitourinary system; hemolymphoid system; liver; and meninges. Human ortholog(s) of this gene implicated in multiple myeloma; myelodysplastic syndrome; and stomach carcinoma. Orthologous to human BCL2L10 (BCL2 like 10). [provided by Alliance of Genome Resources, Dec 2024]
Expression: Biased expression in ovary adult (RPKM 8.8) and subcutaneous fat pad adult (RPKM 0.4) See more
Orthologs: human all
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Genomic context

Location:: 9 42.3 cM; 9 D

Exon count:: 2

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	9	NC_000075.7 (75255040..75258922)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	9	NC_000075.6 (75347758..75351640)

Chromosome 9 - NC_000075.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

Go to nucleotide: Graphics FASTA GenBank

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

The knockdown of BCL-B resulted in increased apoptosis and mitophagy in hepatic stellate cells, while the overexpression of BCL-B caused the opposite effects.
Title: The role of the apoptosis-related protein BCL-B in the regulation of mitophagy in hepatic stellate cells during the regression of liver fibrosis.
role for Bcl-B in B cell proliferation and plasmocyte differentiation through its ability to impair B cell death and drive multiple myeloma progression.
Title: BCL-B (BCL2L10) is overexpressed in patients suffering from multiple myeloma (MM) and drives an MM-like disease in transgenic mice.
Bcl2l10, Tpx2, and Aurka co-localized on the meiotic spindles, and Bcl2l10 was present in the same complex with Tpx2.
Title: Bcl2l10, a new Tpx2 binding partner, is a master regulator of Aurora kinase A in mouse oocytes.
Protein-protein interactions involving apoptosis regulator Diva (Boo) and the BH3 domain of proapoptotic Bcl-2 members.
Title: Nuclear magnetic resonance study of protein-protein interactions involving apoptosis regulator Diva (Boo) and the BH3 domain of proapoptotic Bcl-2 members.
analysis of a novel interaction between Bcl-2 members Diva and Harakiri
Title: Characterization of a novel interaction between Bcl-2 members Diva and Harakiri.
Structure and sequence alignment of mouse pro-survival Bcl-2 family members reveals Boo/Diva as a divergent Bcl-2 protein.
Title: The structure of Boo/Diva reveals a divergent Bcl-2 protein.
The role of Bcl2l10 is strongly associated with oocyte maturation, especially at the MI-MII transition.
Title: Role of Bcl2-like 10 (Bcl2l10) in Regulating Mouse Oocyte Maturation.
BCL2L10 is a novel and prime candidate related to oocyte maturation, fertility, and embryo developmental competence
Title: Oocytes and early embryos selectively express the survival factor BCL2L10.

Submit: New GeneRIF Correction

Variation

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Alleles

Alleles of this type are documented at Mouse Genome Informatics (MGI)

Targeted (1) 1 citation

Interactions

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Products	Interactant	Other Gene	Complex	Source	Pubs	Description

General gene information

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Markers

RH127218 (e-PCR)
- UniSTS:208420

RH124541 (e-PCR)
- UniSTS:161363

NoName (e-PCR)
- UniSTS:236201

AU023065 (e-PCR)
- UniSTS:179934

Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables calcium ion binding	ISO Inferred from Sequence Orthology more info
enables calcium ion binding	ISS Inferred from Sequence or Structural Similarity more info
enables caspase binding	ISO Inferred from Sequence Orthology more info
enables channel activity	IBA Inferred from Biological aspect of Ancestor more info
enables identical protein binding	IPI Inferred from Physical Interaction more info	PubMed
enables protein binding	IPI Inferred from Physical Interaction more info	PubMed

Process	Evidence Code	Pubs
involved_in apoptotic process	ISO Inferred from Sequence Orthology more info
involved_in apoptotic process	ISS Inferred from Sequence or Structural Similarity more info
involved_in extrinsic apoptotic signaling pathway in absence of ligand	IBA Inferred from Biological aspect of Ancestor more info
acts_upstream_of extrinsic apoptotic signaling pathway in absence of ligand	IDA Inferred from Direct Assay more info	PubMed
NOT acts_upstream_of_or_within extrinsic apoptotic signaling pathway via death domain receptors	ISO Inferred from Sequence Orthology more info	PubMed
acts_upstream_of intrinsic apoptotic signaling pathway	IDA Inferred from Direct Assay more info	PubMed
involved_in intrinsic apoptotic signaling pathway in response to DNA damage	IBA Inferred from Biological aspect of Ancestor more info
involved_in microtubule organizing center organization	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within negative regulation of apoptotic process	ISO Inferred from Sequence Orthology more info	PubMed
involved_in negative regulation of apoptotic process	ISO Inferred from Sequence Orthology more info
acts_upstream_of_or_within negative regulation of extrinsic apoptotic signaling pathway in absence of ligand	IDA Inferred from Direct Assay more info	PubMed
acts_upstream_of_or_within negative regulation of intrinsic apoptotic signaling pathway	IDA Inferred from Direct Assay more info	PubMed
involved_in positive regulation of apoptotic process	IBA Inferred from Biological aspect of Ancestor more info
acts_upstream_of_or_within positive regulation of apoptotic process	IDA Inferred from Direct Assay more info	PubMed
involved_in release of cytochrome c from mitochondria	IBA Inferred from Biological aspect of Ancestor more info

Component	Evidence Code	Pubs
located_in cytosol	ISO Inferred from Sequence Orthology more info
located_in endoplasmic reticulum	IEA Inferred from Electronic Annotation more info
located_in endoplasmic reticulum	ISO Inferred from Sequence Orthology more info
located_in membrane	IDA Inferred from Direct Assay more info	PubMed
located_in membrane	ISO Inferred from Sequence Orthology more info	PubMed
located_in mitochondria-associated endoplasmic reticulum membrane contact site	ISO Inferred from Sequence Orthology more info
located_in mitochondria-associated endoplasmic reticulum membrane contact site	ISS Inferred from Sequence or Structural Similarity more info
is_active_in mitochondrial outer membrane	IBA Inferred from Biological aspect of Ancestor more info
located_in mitochondrion	ISO Inferred from Sequence Orthology more info
located_in mitochondrion	ISS Inferred from Sequence or Structural Similarity more info
located_in nuclear membrane	IEA Inferred from Electronic Annotation more info
located_in spindle	IDA Inferred from Direct Assay more info	PubMed

General protein information

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Preferred Names: bcl-2-like protein 10

Names: anti-apoptotic protein Boo; apoptosis regulator Bcl-B; bcl-2 homolog Diva; bcl2-L-10

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.