Bud13 BUD13 homolog [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Bud13provided by MGI
Official Full Name: BUD13 homologprovided by MGI
Primary source: MGI:MGI:2443443
See related: Ensembl:ENSMUSG00000032077 AllianceGenome:MGI:2443443
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: D030060M11Rik
Summary: Predicted to be involved in mRNA splicing, via spliceosome. Predicted to be located in nucleoplasm. Predicted to be part of RES complex and U2-type precatalytic spliceosome. Orthologous to human BUD13 (BUD13 homolog). [provided by Alliance of Genome Resources, Dec 2024]
Expression: Ubiquitous expression in thymus adult (RPKM 7.4), whole brain E14.5 (RPKM 6.9) and 28 other tissues See more
Orthologs: human all
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Genomic context

Location:: 9 A5.2; 9 25.38 cM

Exon count:: 10

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	9	NC_000075.7 (46194281..46210084)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	9	NC_000075.6 (46282976..46298783)

Chromosome 9 - NC_000075.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

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Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

RNASEH1-AS1 induced by H3K27ac stabilizes ANXA2 mRNA to promote the progression of colorectal cancer through recruiting BUD13.
Title: RNASEH1-AS1 induced by H3K27ac stabilizes ANXA2 mRNA to promote the progression of colorectal cancer through recruiting BUD13.
The mechanism of BUD13 m6A methylation mediated MBNL1-phosphorylation by CDK12 regulating the vasculogenic mimicry in glioblastoma cells.
Title: The mechanism of BUD13 m6A methylation mediated MBNL1-phosphorylation by CDK12 regulating the vasculogenic mimicry in glioblastoma cells.
BUD13 is a protein that has the ability to increase splicing of the Irf7 intron. BUD13 depletion compromises type I interferon response by countering intron retention in Irf7.
Title: BUD13 Promotes a Type I Interferon Response by Countering Intron Retention in Irf7.

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Variation

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Alleles

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

Endonuclease-mediated (4)

Interactions

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Products	Interactant	Other Gene	Complex	Source	Pubs	Description

General gene information

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Markers

G67031 (e-PCR)
- UniSTS:178237

NoName (e-PCR)
- UniSTS:236113

AI303781 (e-PCR)
- UniSTS:179891

AV305342 (e-PCR)
- UniSTS:179892

BB396022 (e-PCR)
- UniSTS:208371

Gene Ontology Provided by MGI

Process	Evidence Code	Pubs
involved_in mRNA splicing, via spliceosome	IBA Inferred from Biological aspect of Ancestor more info
involved_in mRNA splicing, via spliceosome	ISO Inferred from Sequence Orthology more info
involved_in mRNA splicing, via spliceosome	ISS Inferred from Sequence or Structural Similarity more info

Component	Evidence Code	Pubs
part_of U2-type precatalytic spliceosome	ISO Inferred from Sequence Orthology more info
part_of U2-type precatalytic spliceosome	ISS Inferred from Sequence or Structural Similarity more info
part_of U2-type spliceosomal complex	IBA Inferred from Biological aspect of Ancestor more info
located_in nucleoplasm	IEA Inferred from Electronic Annotation more info
located_in nucleoplasm	ISO Inferred from Sequence Orthology more info
located_in nucleus	ISO Inferred from Sequence Orthology more info
located_in nucleus	ISS Inferred from Sequence or Structural Similarity more info

General protein information

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Preferred Names: BUD13 homolog

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.