C57BL/6NCya-Cdkn2aem1/Cya
Common Name:
Cdkn2a-KO
Product ID:
S-KO-01468
Background:
C57BL/6NCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Cdkn2a-KO
Strain ID
KOCMP-12578-Cdkn2a-B6N-VA
Gene Name
Product ID
S-KO-01468
Gene Alias
ARF-INK4a; Arf; INK4a-ARF; Ink4a/Arf; MTS1; Pctr1; p16; p16(INK4a); p16INK4a; p19<ARF>; p19ARF
Background
C57BL/6NCya
NCBI ID
Modification
Conventional knockout
Chromosome
4
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6NCya-Cdkn2aem1/Cya mice (Catalog S-KO-01468) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000107131
NCBI RefSeq
NM_009877
Target Region
Exon 2
Size of Effective Region
~0.3 kb
Detailed Document
Overview of Gene Research
Cdkn2a, also known as cyclin-dependent kinase inhibitor 2A, is a crucial tumor suppressor gene. It encodes p16 and p14, which are involved in regulating the cell cycle. p16 inhibits cyclin-dependent kinases CDK4/6, preventing cell-cycle progression from G1 to S phase, thus playing a vital role in tumor suppression. This gene is associated with pathways controlling cell growth and proliferation, and its function is of great biological importance in maintaining normal cellular homeostasis [1,2].
Loss of Cdkn2a is a frequent event driving melanoma progression. Pharmacological inhibition of the p16 targets CDK4/6 is a potential therapeutic strategy for melanoma patients with Cdkn2a loss [1]. Additionally, Cdkn2a is the most common homozygously deleted gene in all human cancers. Tumors often codelete the nearby gene MTAP, creating a dependency on PRMT5, and an MTA-cooperative PRMT5 methyltransferase inhibitor MRTX1719 selectively kills Cdkn2a/MTAP-codeleted cancers [2]. In familial melanoma, germline mutations in Cdkn2a are common, and carriers may have a worse overall and melanoma-specific survival, with a higher incidence of melanoma and a higher risk of a second melanoma [3].
In conclusion, Cdkn2a is an essential tumor suppressor gene regulating the cell cycle. Model-based research, especially studies related to its loss-of-function, has revealed its significant role in melanoma and other cancers. Understanding Cdkn2a function through these models provides potential therapeutic directions for treating cancers where Cdkn2a is mutated or deleted.
References:
1. Kreuger, Inger Z M, Slieker, Roderick C, van Groningen, Tim, van Doorn, Remco. 2022. Therapeutic Strategies for Targeting CDKN2A Loss in Melanoma. In The Journal of investigative dermatology, 143, 18-25.e1. doi:10.1016/j.jid.2022.07.016. https://pubmed.ncbi.nlm.nih.gov/36123181/
2. Mulvaney, Kathleen M. . Early Clinical Success of MTA-Cooperative PRMT5 Inhibitors for the Treatment of CDKN2A/MTAP-Deleted Cancers. In Cancer discovery, 13, 2310-2312. doi:10.1158/2159-8290.CD-23-0951. https://pubmed.ncbi.nlm.nih.gov/37909092/
3. Taibo, Ana, Paradela, Sabela, Suanzes-Hernández, Jorge, Amado-Bouza, Javier, Fonseca, Eduardo. 2023. Prognosis of CDKN2A germline mutation in patients with familial melanoma: a systematic review and meta-analysis. In Melanoma research, 34, 9-15. doi:10.1097/CMR.0000000000000920. https://pubmed.ncbi.nlm.nih.gov/37924530/
Quality Control Standard
Sperm Test
Pre-cryopreservation: Measurement of sperm concentration, determination of sperm viability.
Post-cryopreservation: A vial of cryopreserved sperms is selected for in-vitro fertilization from each batch.
Environmental Standards:SPF
Available Region:Global
Source:Cyagen