mProX™ Human TNFSF8 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Oncology Cell Lines
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Published Data
Fig.1 The assessment of potential target genes associated with apoptosis and mitochondrial biogenesis in PC12 cells was conducted through western blotting analysis, revealing outcomes influenced by the experimental procedure.
The protein expression of ATN1, USP25, and TNFSF8 was silenced using short interfering RNAs (siRNAs), and the effects of protein expression silencing on apoptosis and mitochondrial biogenesis after OGD/R were examined via western blot analysis. A significant reduction in the protein levels of cleaved caspase 3 and Bax, along with the promotion of the expression of mitochondrial biogenesis-related proteins, such as PGC-1α, NRF1, and TFAM, was observed upon the inhibition of TNFSF8.
Ref: Zhang, Qiang, et al. "Neuroprotective Effect of miR-483-5p Against Cardiac Arrest-Induced Mitochondrial Dysfunction Mediated Through the TNFSF8/AMPK/JNK Signaling Pathway." Cellular and Molecular Neurobiology 43.5 (2023): 2179-2202.
Pubmed: 36266523
DOI: 10.1007/s10571-022-01296-3
Research Highlights
Zhang, Yi. et al. "Bioinformatics analysis to screen the key genes in pediatric Chronic Active Epstein-Barr Virus Infection." Cellular and molecular biology (Noisy-le-Grand, France), 2023.
Chronic active Epstein-Barr virus infection (CAEBV) is a serious condition with a poor prognosis and high mortality rate. A research team conducted a bioinformatics analysis to identify key genes associated with CAEBV. They used weighted gene co-expression network analysis (WGCNA) to identify a gene module highly correlated with pediatric CAEBV and investigated the differentially expressed genes (DEGs) between pediatric acute infectious mononucleosis (AIM) and pediatric CAEBV. By using the least absolute shrinkage and selection operator (LASSO) and random forest algorithms, they identified three key genes (TPST1, TNFSF8, and RAB3GAP1) associated with pediatric CAEBV. These genes have a strong diagnostic performance in distinguishing between pediatric CAEBV and AIM. Further analysis showed that these genes are related to inflammatory response and inflammation-related pathways, as well as myeloid cell enrichment and persistent Epstein-Barr virus infection pathway. This study provides new insights into the development of CAEBV and highlights the potential of TPST1, TNFSF8, and RAB3GAP1 as therapeutic targets for this condition.
Zhang, Yi. et al. "Bioinformatics analysis to screen the key genes in pediatric Chronic Active Epstein-Barr Virus Infection." Cellular and molecular biology (Noisy-le-Grand, France), 2023.
Pubmed:
37715397
DOI:
10.14715/cmb/2023.69.7.27
Kiryluk, Krzysztof. et al. "Genome-wide association analyses define pathogenic signaling pathways and prioritize drug targets for IgA nephropathy." Nature genetics, 2023.
IgAN is a progressive kidney disease characterized by the presence of IgA in glomeruli. A genome-wide association study was conducted on 10,146 biopsy-diagnosed IgAN patients and 28,751 controls from 17 international cohorts. Thirty genome-wide significant risk loci were identified, with 16 being new, including TNFSF4/TNFSF18, REL, CD28, PF4V1, LY86, LYN, ANXA3, TNFSF8/TNFSF15, REEP3, ZMIZ1, OVOL1/RELA, ETS1, IGH, IRF8, TNFRSF13B, and FCAR. These loci showed an enrichment of genes that cause abnormal IgA levels in mice. Additionally, a genetic correlation was observed between IgAN and serum IgA levels, and a high polygenic score for IgAN was associated with an earlier onset of kidney failure. Functional analysis of candidate causal genes revealed a convergence of inflammatory signaling pathways and cytokine ligand-receptor pairs, highlighting potential new drug targets. This study provides valuable insights into the genetic basis of IgAN and may aid in the development of targeted treatments for this disease.
Kiryluk, Krzysztof. et al. "Genome-wide association analyses define pathogenic signaling pathways and prioritize drug targets for IgA nephropathy." Nature genetics, 2023.
Pubmed:
37337107
DOI:
10.1038/s41588-023-01422-x