mProX™ Human CDK4 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 Generated CDK4/6 Inhibitor-Resistant Cell Lines Have Dramatically Increased CDK6 Protein Expression.
Together with a gradual decline in CDK1 expression, there was also a slight stepwise increase in cyclin E levels. All resistant cells retained RB phosphorylation at the CDK4/6 sites Ser807/Ser811, as well as at Thr356.
Ref: Cornell, Liam, et al. "MicroRNA-mediated suppression of the TGF-β pathway confers transmissible and reversible CDK4/6 inhibitor resistance." Cell reports 26.10 (2019): 2667-2680.
Pubmed: 30840889
DOI: 10.1016/j.celrep.2019.02.023
Research Highlights
D-type cyclins, along with cyclin-dependent kinases 4 and 6 (CDK4 and CDK6), are the activating partners that connect the extracellular milieu to the central machinery of the cell cycle. In a number of cancer forms, constitutive activation of cyclin D-CDK4/6 is the primary cause of carcinogenesis.
Fassl, Anne, Yan Geng, and Piotr Sicinski. "CDK4 and CDK6 kinases: From basic science to cancer therapy." Science 375.6577 (2022): eabc1495.
Pubmed:
35025636
DOI:
10.1126/science.abc1495
These studies established the basic idea that CDK4/6 inhibitors could be useful in the treatment of cancer, especially when paired with the suppression of related mitogen-dependent signal transduction pathways.
Sherr, Charles J., David Beach, and Geoffrey I. Shapiro. "Targeting CDK4 and CDK6: from discovery to therapy." Cancer discovery 6.4 (2016): 353-367.
Pubmed:
26658964
DOI:
10.1158/2159-8290.CD-15-0894