mProX™ Human CDK16 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 CDK16 regulates cell proliferation by phosphorylating PRC1 and modulating spindle formation.
Analysis of spindle formation in CDK16-KD and control MDA-MB-231 cells. Antibodies against pericentrin (red), alpha-tubulin (green), and DAPI (blue) were used to immunostain the cells.
Ref: Li, Xiao, et al. "CDK16 promotes the progression and metastasis of triple-negative breast cancer by phosphorylating PRC1." Journal of Experimental & Clinical Cancer Research 41.1 (2022): 149.
Pubmed: 35449080
DOI: 10.1186/s13046-022-02362-w
Research Highlights
Triple-negative breast cancer (TNBC) is known to exhibit elevated expression of CDK16. There is a correlation between worse outcomes for patients with breast cancer and higher CDK16 expression.
Li, Xiao, et al. "CDK16 promotes the progression and metastasis of triple-negative breast cancer by phosphorylating PRC1." Journal of Experimental & Clinical Cancer Research 41.1 (2022): 149.
Pubmed:
35449080
DOI:
10.1186/s13046-022-02362-w
In human NSCLC tumor tissue, CDK16 is markedly overexpressed. It promotes cell proliferation and, in a p27-dependent way, inhibits apoptosis in NSCLC cells, thereby acting as an oncogene. Moreover, CDK16 uses protein degradation and ubiquitination to negatively regulate p27 production.
Wang, Hongtao, et al. "CDK16 overexpressed in non-small cell lung cancer and regulates cancer cell growth and apoptosis via a p27-dependent mechanism." Biomedicine & Pharmacotherapy 103 (2018): 399-405.
Pubmed:
29674275
DOI:
10.1016/j.biopha.2018.04.080