mProX™ Human MAP3K19 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 MAP3K19 facilitated the nuclear translocation of phosphorylated R-Smads, specifically phospho-Smad2 and phospho-Smad3, in response to TGF-β1 stimulation, aiding in their cellular localization.
HeLa cells were subjected to transfection with either nonsense siRNA (at doses of 250 or 500 ng) or MAP3K19 siRNA (at doses of 250 or 500 ng). Subsequently, after an 18-hour incubation, the cells were exposed to TGF-β1 (at a concentration of 1 ng/ml) for a duration of 1 hour. Following this treatment, cell samples were collected, and nuclear extracts were isolated. Western analysis was performed on these nuclear lysates to assess the levels of P-Smad2, P-Smad3, and Smad4, with additional probing for HDAC-1 to confirm uniform protein loading. Densitometry analysis was conducted to compare the ratios of P-Smad2/HDAC-1 and P-Smad3/HDAC-1 levels. Smad4 levels were excluded from densitometry analysis as they remained unaffected. This experimental procedure was repeated three times independently, and a representative instance is presented.
Ref: Boehme, Stefen A., et al. "MAP3K19 is a novel regulator of TGF-β signaling that impacts bleomycin-induced lung injury and pulmonary fibrosis." PloS one 11.5 (2016): e0154874.
Pubmed: 27144281
DOI: 10.1371/journal.pone.0154874
Research Highlights
Tambi, Richa. et al. "Single-Cell Reconstruction and Mutation Enrichment Analysis Identifies Dysregulated Cardiomyocyte and Endothelial Cells in Congenital Heart Disease." Physiological genomics, 2023.
In this study, the prevalence of congenital heart disease (CHD) in neonates was examined. A total of 16,349 variants, including single nucleotide variants (SNVs) and Indels, were collected from 3,166 CHD cases representing 8,308 genes. The researchers utilized ACMG guidelines to exclude 0.1% of benign/likely benign variants, resulting in a dataset consisting of 83% predicted loss of function variants and 17% missense variants. Of note, 17% of the variants were found to be potentially pathogenic based on ACMG criteria.
Tambi, Richa. et al. "Single-Cell Reconstruction and Mutation Enrichment Analysis Identifies Dysregulated Cardiomyocyte and Endothelial Cells in Congenital Heart Disease." Physiological genomics, 2023.
Pubmed:
37811720
DOI:
10.1152/physiolgenomics.00070.2023
Cheng, Zhongshan. et al. "MAP3K19 regulatory variation in populations with African ancestry may increase COVID-19 severity." iScience, 2023.
In order to identify genetic risk variants associated with COVID-19 hospitalization, an integrative analysis of two genome-wide association studies was conducted. This analysis revealed four single nucleotide polymorphisms that were more prevalent in COVID-19-hospitalized patients with non-European ancestry. Of these, the COVID-19 risk SNP rs16831827 exhibited the largest difference in minor allele frequency (MAF) between populations of African and European ancestry. Furthermore, this SNP was found to have a higher MAF in hospitalized COVID-19 patients from cohorts of both mixed and entirely African ancestry (OR = 1.20, 95% CI: 1.10-1.30 and OR = 1.30, 95% CI: 1.02-1.67, respectively). Additionally, rs16831827 is an expression quantitative trait locus for seven genes, most notably TSLP.
Cheng, Zhongshan. et al. "MAP3K19 regulatory variation in populations with African ancestry may increase COVID-19 severity." iScience, 2023.
Pubmed:
37649700
DOI:
10.1016/j.isci.2023.107555