Cdk3 cyclin dependent kinase 3 [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Cdk3provided by MGI
Official Full Name: cyclin dependent kinase 3provided by MGI
Primary source: MGI:MGI:1916931
See related: Ensembl:ENSMUSG00000092300 AllianceGenome:MGI:1916931
Gene type: pseudo
RefSeq status: VALIDATED
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: Cdk3-ps; 2310050O10Rik
Summary: Predicted to enable cyclin-dependent protein serine/threonine kinase activity. Predicted to be involved in protein phosphorylation. Predicted to be active in nucleus. Is expressed in several structures, including chondrocranium; heart; hindbrain roof; lung; and nasal cavity. Orthologous to human CDK3 (cyclin dependent kinase 3). [provided by Alliance of Genome Resources, Apr 2022]
Expression: Ubiquitous expression in limb E14.5 (RPKM 2.3), whole brain E14.5 (RPKM 2.2) and 27 other tissues See more
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Genomic context

Location:: 11 E2; 11 81.02 cM

Exon count:: 7

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	11	NC_000077.7 (116106828..116111113)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	11	NC_000077.6 (116216002..116220287)

Chromosome 11 - NC_000077.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

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Expression

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See details

Project title: Mouse ENCODE transcriptome data
Description: RNA profiling data sets generated by the Mouse ENCODE project.
BioProject: PRJNA66167
Publication: PMID 25409824
Analysis date: n/a

Bibliography

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GeneRIFs: Gene References Into Functions

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Variation

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Alleles

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

Spontaneous (2) 1 citation

Interactions

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Products	Interactant	Other Gene	Complex	Source	Pubs	Description

General gene information

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Markers

PMC29317P1 (e-PCR)
- UniSTS:272446

PMC29317P2 (e-PCR)
- UniSTS:272447

NoName (e-PCR)
- UniSTS:492524

Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables cyclin binding	IBA Inferred from Biological aspect of Ancestor more info
enables cyclin-dependent protein serine/threonine kinase activity	IBA Inferred from Biological aspect of Ancestor more info

Process	Evidence Code	Pubs
involved_in G0 to G1 transition	ISO Inferred from Sequence Orthology more info
involved_in G1/S transition of mitotic cell cycle	IBA Inferred from Biological aspect of Ancestor more info
involved_in negative regulation of Notch signaling pathway	ISO Inferred from Sequence Orthology more info
involved_in protein phosphorylation	IBA Inferred from Biological aspect of Ancestor more info
involved_in regulation of G2/M transition of mitotic cell cycle	IBA Inferred from Biological aspect of Ancestor more info
involved_in regulation of gene expression	IBA Inferred from Biological aspect of Ancestor more info
involved_in response to organic substance	IBA Inferred from Biological aspect of Ancestor more info
involved_in signal transduction	IBA Inferred from Biological aspect of Ancestor more info

Component	Evidence Code	Pubs
part_of cyclin-dependent protein kinase holoenzyme complex	IBA Inferred from Biological aspect of Ancestor more info
part_of cyclin-dependent protein kinase holoenzyme complex	ISO Inferred from Sequence Orthology more info
is_active_in cytoplasm	IBA Inferred from Biological aspect of Ancestor more info
is_active_in nucleus	IBA Inferred from Biological aspect of Ancestor more info

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.