mProX™ Human MAP3K10 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Alex Miller (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Alex Miller (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Published Data
Fig.1 MAP3K10 promoted the proliferation of pancreatic cancer cell lines in vitro.
Enhanced cell proliferation in PANC-1 cells was observed with EdU (5-ethynyl-20-deoxyuridine) assays upon MAP3K10 overexpression, whereas a reduction in cell proliferation of BxPC-3 cells was induced by MAP3K10 knockdown.
Ref: An, Yong, et al. "MAP3K10 promotes the proliferation and decreases the sensitivity of pancreatic cancer cells to gemcitabine by upregulating Gli-1 and Gli-2." Cancer letters 329.2 (2013): 228-235.
Pubmed: 23178452
DOI: 10.1016/j.canlet.2012.11.005
Research Highlights
Kartchner, David. et al. "Literature-Based Discovery to Elucidate the Biological Links between Resistant Hypertension and COVID-19." Biology, 2023.
Multiple studies have reported new or exacerbated persistent or resistant hypertension in patients previously infected with COVID-19. The authors utilized literature-based discovery to identify and prioritize multi-scalar explanatory biology that relates resistant hypertension to COVID-19. Using SemNet 2.0, they performed cross-domain text mining of over 33 million PubMed articles within a comprehensive knowledge graph. Through unsupervised rank aggregation, they determined the most relevant concepts utilizing the normalized HeteSim score. After conducting a series of simulations, the authors found that concepts directly related to COVID-19 and resistant hypertension, or connected via one of three renin-angiotensin-aldosterone system hub nodes, were the top-ranking factors. These included various genes, hormones, enzymes, and proteins. The identified concepts were mapped to six physiological themes: altered endocrine function, inflammation or cytokine storm, lipid metabolism and atherosclerosis, sympathetic input to blood pressure regulation, altered entry of COVID-19 virus, and unknown.
Kartchner, David. et al. "Literature-Based Discovery to Elucidate the Biological Links between Resistant Hypertension and COVID-19." Biology, 2023.
Pubmed:
37759668
DOI:
10.3390/biology12091269
Li, Menghua. et al. "Murine cytomegalovirus employs the mixed lineage kinases family to regulate the spiral ganglion neuron cell death and hearing loss." Neuroscience letters, 2023.
Recent studies have shown that sensorineural hearing loss (SNHL) caused by cytomegalovirus (CMV) is a global epidemic. The degree of spiral ganglion neuron (SGN) loss has been found to be linked to hearing loss following CMV infection. The aim of this study was to gain a better understanding of the mechanisms behind CMV-induced SGN death and to identify potential intervention strategies. The findings revealed that both apoptosis and pyroptosis contribute to CMV-induced SGN death, which is mediated by the activation of the p53/JNK and NLRP3/caspase-1 signaling pathways, respectively. It was also demonstrated that the mixed lineage kinase family (MLK1/2/3), known as host restriction factors against viral infection, also serve as upstream regulators of these signaling pathways. Additionally, the MLKs inhibitor URMC-099 was found to have a protective effect against CMV-induced SGN death and hearing loss. These results suggest that targeting the MLK signaling pathway may be a promising approach for preventing both apoptosis and pyroptosis during CMV infection and for treating hearing loss.
Li, Menghua. et al. "Murine cytomegalovirus employs the mixed lineage kinases family to regulate the spiral ganglion neuron cell death and hearing loss." Neuroscience letters, 2023.
Pubmed:
36455693
DOI:
10.1016/j.neulet.2022.136990