mProX™ Human RPS6KA4 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 a-LA inhibition of RPS6KA4 and its association with p53 induction.
Inhibition of RPS6KA4 by a-LA and its correlation with p53 activation was examined in HCT116 cells, both p53-WT and p53-deficient variants, via transfection with escalating doses of WT-RPS6KA4 expression vectors. Subsequent to a 24-hour transfection period, cells were subjected to treatment with a-LA (100 mmol/l) and 5-FU (100 mmol/l). The levels of RPS6KA4 and p53 expression were assessed through RT-PCR and western blot assays conducted 48 hours post-treatment.
Ref: Yoo, Tae-Hyoung, et al. "α-Lipoic acid prevents p53 degradation in colon cancer cells by blocking NF-κB induction of RPS6KA4." Anti-Cancer Drugs 24.6 (2013): 555-565.
Pubmed: 23599020
DOI: 10.1097/CAD.0b013e32836181eb
Research Highlights
Wu, Shasha. et al. "Comprehensive analysis of the RSK gene family in acute myeloid leukemia determines a prognostic signature for the prediction of clinical prognosis and treatment responses." Hematology (Amsterdam, Netherlands), 2023.
The prognosis of acute myeloid leukemia (AML) continues to be unfavorable, despite significant advancements in basic and translational research on the genetics and pathopoiesis of AML. Numerous targeted therapies have been developed as a result. Therefore, there is a critical need to further investigate the molecular pathogenesis of AML in order to advance the development of innovative treatment strategies. The knowledge gained from this research may lead to improved outcomes for patients.
Wu, Shasha. et al. "Comprehensive analysis of the RSK gene family in acute myeloid leukemia determines a prognostic signature for the prediction of clinical prognosis and treatment responses." Hematology (Amsterdam, Netherlands), 2023.
Pubmed:
37462338
DOI:
10.1080/16078454.2023.2235833
Qiu, Moqin. et al. "Potentially functional genetic variants in RPS6KA4 and MAP2K5 in the MAPK signaling pathway predict HBV-related hepatocellular carcinoma survival." Molecular carcinogenesis, 2023.
Hepatocellular carcinoma (HCC) represents the third leading cause of cancer-related deaths, marked by a discouraging 5-year survival rate. Aberrant activation of the mitogen-activated protein kinase (MAPK) signaling pathway fuels the growth and metastatic potential of HCC cells. Consequently, the study undertook a two-stage survival analysis of 10,912 single nucleotide polymorphisms (SNPs) across 79 MAPK pathway genes, assessing their impact on the overall survival (OS) of 866 HBV-related HCC patients, with subsequent functional annotation. Within combined datasets, they uncovered two novel SNPs (RPS6KA4 rs600377 T>G and MAP2K5 rs17300363 A>C) as prognostic factors for HBV-related HCC, conveying adjusted allelic hazard ratios of 1.24 (95% confidence interval [CI] = 1.05-1.46, p = 0.010) and 1.48 (1.15-1.91, p = 0.001), respectively. Moreover, these risk genotypes collectively indicated poor survival in a dose-response pattern (Ptrend < 0.001) within the combined dataset. Supplementary functional analysis revealed that RPS6KA4 rs600377 G and MAP2K5 rs17300363 C alleles correlated with heightened mRNA expression levels in corresponding genes in normal tissues, offering fresh insights into the role of genetic variations within MAPK signaling pathway genes in HBV-related HCC survival.
Qiu, Moqin. et al. "Potentially functional genetic variants in RPS6KA4 and MAP2K5 in the MAPK signaling pathway predict HBV-related hepatocellular carcinoma survival." Molecular carcinogenesis, 2023.
Pubmed:
37278562
DOI:
10.1002/mc.23583