CDKN3
Sign in to saveAlso known as CDI1, CIP2, KAP, KAP1, cyclin-dependent kinase inhibitor 3, cyclin dependent kinase inhibitor 3, CDLN3
Cyclin-dependent kinase inhibitor 3 is an enzyme that in humans is encoded by the CDKN3 gene.
Gene data
CDKN3- Name
- cyclin dependent kinase inhibitor 3
- Type
- protein-coding
- Position
- 54,396,849–54,420,218 (+)
- Aliases
- CDI1, CIP2, KAP, KAP1
- Ensembl
- ENSG00000100526
- RefSeq RNA
- NM_001130851.2, NM_001330173.2, NM_005192.4
- RefSeq protein
- NP_001124323.1, NP_001317102.1, NP_005183.2
The protein encoded by this gene belongs to the dual specificity protein phosphatase family. It was identified as a cyclin-dependent kinase inhibitor, and has been shown to interact with, and dephosphorylate CDK2 kinase, thus prevent the activation of CDK2 kinase. This gene was reported to be deleted, mutated, or overexpressed in several kinds of cancers. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Aug 2008].
Gene Ontology
Biological process
Molecular function
via MyGene.info
Gene · Ensembl
cyclin dependent kinase inhibitor 3
- Symbol
- CDKN3
- Biotype
- Protein coding
- Organism
- Homo sapiens
- Location
- 14:54,396,849-54,420,221
- Strand
- Forward (+)
- Assembly
- GRCh38
via Ensembl · EMBL-EBI
Wikidata facts
- Image
- Protein CDKN3 PDB 1fpz.png
Show 5 more facts
- HomoloGene ID
- 3805
- exact match
- identifiers.org/ncbigene/1033
- genomic end
- 54886936
- genomic start
- 54863567
- cytogenetic location
- 14q22.2
Sources (4)
via Wikidata · CC0
~1 min read
Article
4 sectionsContents
- Interactions
- References
- Further reading
- External links
Cyclin-dependent kinase inhibitor 3 is an enzyme that in humans is encoded by the CDKN3 gene.
The protein encoded by this gene belongs to the dual specificity protein phosphatase family. It was identified as a cyclin-dependent kinase inhibitor, and has been shown to interact with, and dephosphorylate CDK2 kinase, thus prevent the activation of CDK2 kinase. This gene was reported to be deleted, mutated, or overexpressed in several kinds of cancers.