NCBI . NLM . NIH . GOV {
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We began analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC3637879/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC3637879/. The analysis below is for the second page.
Title[redir]:
Induction of pathogenic Th17 cells by inducible salt sensing kinase SGK1 - PMC
Description:
Th17 cells are highly proinflammatory cells critical for clearing extracellular pathogens and for induction of multiple autoimmune diseases1. IL-23 plays a critical role in stabilizing and reinforcing the Th17 phenotype by increasing expression of ...
Title[redir]:
Induction of pathogenic Th17 cells by inducible salt sensing kinase SGK1 - PMC
Description:
Th17 cells are highly proinflammatory cells critical for clearing extracellular pathogens and for induction of multiple autoimmune diseases1. IL-23 plays a critical role in stabilizing and reinforcing the Th17 phenotype by increasing expression of ...
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Keywords {π}
cells, fig, sgk, supplementary, doi, ilr, mice, expression, cell, foxo, pubmed, google, scholar, analysis, differentiation, data, pmc, observed, sgkdeficient, kinase, development, genes, eae, article, increase, production, increased, hsd, role, signaling, transcription, reduced, nlm, transcriptional, network, nacl, vivo, methods, showed, free, nature, salt, vitro, induced, activity, sodium, ncbi, search, primary, national,
Topics {βοΈ}
plate bound anti-cd3/cd28 glucocorticoid-inducible protein kinase glucocorticoid-inducible kinase isoforms heat-inactivated mycobacterium tuberculosis establish il-23r-sgk1-foxo1 integrin-mediated cell adhesion endogenous foxo1-rorΞ³t interaction glucocorticoid-inducible kinase sgk1 pmc beta search generated il17fcresgk1fl/fl mice highest-ranking nodes downstream sgk1-deficient mice exhibited immunized cd4cresgk1fl/fl mice normal ifn-Ξ³ production regulating il-23r expression promotes il-23r expression high salt diet enhancing th17-mediated immunity sgk1-deficient bystander cells glucocorticoid-inducible kinase 1 h3k27me3 reveals specificity increased il-23r expression il-23r-dependent stability il-23-restimulated th17 cells protein-protein interactions il-23-il-23r signaling mog35β55/cfa immunized hosts increased salt intake exhibited impaired il-17 regulates na+ intake observed reduced il-23r il-23r signaling pathway nacl-treated cells showed epithelial sodium channels chip-pcr analysis confirmed impaired renal na th17 cell generation primary th17 differentiation methods summary microarrays increasing sodium concentration il17fcresgk1fl/fl mice govern na+ transport cd4cresgk1fl/fl mice il23rgfp reporter mice th17 cell differentiation gene expression responses exogenous sodium chloride forkhead box o1 luciferase reporter constructs including cell cycle
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