mProX™ Human TNIK Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 In a dose-dependent manner, the transcription activity of the Tcf-reporter TOPFlash was abolished by the expression of all TNIK kinase mutants.
β-catenin/TCF-driven transcription was abrogated by the expression of TNIK kinase mutants (depicted in the second, third, and fourth panels), while an increase in β-catenin/TCF-driven transcription was specifically induced by the overexpression of WT TNIK (as shown in the last panel) in Ls174T CRCs. TOPFlash activity was denoted by black bars, and FOPFlash activity was represented by green bars at 24 hours post transfection of expression vectors, with error bars indicating standard deviation across three independent experiments. Expression of Flag-tagged WT and mutant TNIK proteins was detected using M2 Flag antisera in the Western blot analysis (bottom panel). Significant differences were observed with *P-value<0.05 and **P-value<0.01.
Ref: Mahmoudi, Tokameh, et al. "The kinase TNIK is an essential activator of Wnt target genes." The EMBO journal 28.21 (2009): 3329-3340.
Pubmed: 19816403
DOI: 10.1038/emboj.2009.285
Research Highlights
C Phung Pham, T. et al. "TNIK is a conserved regulator of glucose and lipid metabolism in obesity." Science advances, 2023.
According to recent research, obesity and type 2 diabetes (T2D) are significant health concerns with unresolved treatment requirements. The Traf2- and NCK-interacting protein kinase (TNIK) has been identified as a gene associated with obesity and T2D, but its specific functions have yet to be determined. Findings indicate that TNIK plays a crucial role in regulating the balance of lipids and glucose in the body, highlighting its potential as a therapeutic target for these conditions.
C Phung Pham, T. et al. "TNIK is a conserved regulator of glucose and lipid metabolism in obesity." Science advances, 2023.
Pubmed:
37556547
DOI:
10.1126/sciadv.adf7119
Hu, Guanghui. et al. "LKB1 loss promotes colorectal cancer cell metastasis through regulating TNIK expression and actin cytoskeleton remodeling." Molecular carcinogenesis, 2023.
The study focused on the role of liver kinase B1 (LKB1), also known as STK11, in colorectal cancer (CRC). LKB1 is a major gene responsible for Peutz-Jeghers syndrome (PJS), which is associated with approximately 5%-6% of CRC cases. Through the use of CRISPR-Cas9, LKB1 knockout (KO) CRC cell lines were generated and their behavior was studied in vitro and in vivo. Results showed that LKB1 deficiency enhanced migration and metastasis of CRC cells, and this was mediated by upregulation of TRAF2 and NCK-interacting protein kinase (TNIK), which was repressed by LKB1's kinase activity. Further experiments revealed that TNIK promoted cytoskeleton remodeling through its interaction with ARHGAP29. These findings suggest that the LKB1-TNIK axis may play a critical role in CRC progression.
Hu, Guanghui. et al. "LKB1 loss promotes colorectal cancer cell metastasis through regulating TNIK expression and actin cytoskeleton remodeling." Molecular carcinogenesis, 2023.
Pubmed:
37449799
DOI:
10.1002/mc.23606