mProX™ Human CLK4 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 CDC-like kinase 4 (CLK4) phosphorylates microphthalmia-associated transcription factor (MITF) at Y360.
WT-Flag-CLK4 or the kinase-deficient mutant Flag-CLK4-K189R were transfected into KYSE510 cell lines. Next, anti-phosphor-ser/thr and anti-tyrosine 4G10 antibodies were used to investigate the immunoprecipitated MITF, respectively.
Ref: Shen, Yaxing, et al. "Methionine oxidation of CLK4 promotes the metabolic switch and redox homeostasis in esophageal carcinoma via inhibiting MITF selective autophagy." Clinical and Translational Medicine 12.1 (2022): e719.
Pubmed: 35092699
DOI: 10.1002/ctm2.719
Research Highlights
These findings imply that CLK4 is essential for the invasion and growth of MES-TNBC, particularly during TGF-β-induced processes. Furthermore, CLK4 is described in this work as a unique therapeutic target in breast cancer.
Kang, Eunji, et al. "Targeting CLK4 inhibits the metastasis and progression of breast cancer by inactivating TGF-β pathway." Cancer Gene Therapy 29.8-9 (2022): 1168-1180.
Pubmed:
35046528
DOI:
10.1038/s41417-021-00419-0
These findings offer potential therapeutic targets for the treatment of ESCC by highlighting the possible function of CLK4 in altering redox state and nucleotide metabolism.
Shen, Yaxing, et al. "Methionine oxidation of CLK4 promotes the metabolic switch and redox homeostasis in esophageal carcinoma via inhibiting MITF selective autophagy." Clinical and Translational Medicine 12.1 (2022): e719.
Pubmed:
35092699
DOI:
10.1002/ctm2.719