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Gene Information

Gene symbol: RORC

Gene name: RAR-related orphan receptor C

HGNC ID: 10260

Synonyms: RZRG, RORG, NR1F3, TOR

Related Genes

# Gene Symbol Number of hits
1 GATA3 1 hits
2 IFNG 1 hits
3 IL17A 1 hits
4 RORA 1 hits
5 TBX21 1 hits

Related Sentences

# PMID Sentence
1 22048764 We isolated in vivo-differentiated human Th1 and Th17 cells, as well as intermediate Th1/17 cells, and identified distinct epigenetic signatures at cytokine (IFNG and IL17A) and transcription factor (TBX21, RORC, and RORA) loci.
2 22048764 We also examined the phenotypic and epigenetic stability of human Th17 cells exposed to Th1-polarizing conditions and found that although they could upregulate TBX21 and IFN-γ, this occurred without loss of IL-17 or RORC expression, and resulted in cells with a Th1/17 phenotype.
3 22048764 We isolated in vivo-differentiated human Th1 and Th17 cells, as well as intermediate Th1/17 cells, and identified distinct epigenetic signatures at cytokine (IFNG and IL17A) and transcription factor (TBX21, RORC, and RORA) loci.
4 22048764 We also examined the phenotypic and epigenetic stability of human Th17 cells exposed to Th1-polarizing conditions and found that although they could upregulate TBX21 and IFN-γ, this occurred without loss of IL-17 or RORC expression, and resulted in cells with a Th1/17 phenotype.
5 23668260 The infected mice displayed a significant up-regulation in the expression of chemokines (Cxcl1, Cxcl2 and Ccl2), numerous pro-inflammatory cytokines (Ifng, Il1b, Il6, and Il17f), as well as Il22 and a number of anti-microbial peptides (Defa1, Defa28, Defb1, Slpi and Reg3g) at the site(s) of infection.
6 23668260 However, CD4 T cells of the untreated and C. difficile-infected mice expressed similar levels of CD69 and CD25.
7 23668260 Neither tissue had up-regulated levels of Tbx21, Gata3 or Rorc.
8 23668260 They also displayed significantly higher phosphorylation of AKT and signal transducer and activator of transcription 3 (STAT3), an indication of pro-survival signalling.
9 23668260 These data underscore the local, innate, pro-inflammatory nature of the response to C. difficile and highlight eIF2α phosphorylation and the interleukin-22-pSTAT3-RegIIIγ axis as two of the pathways that could be used to contain and counteract the damage inflicted on the intestinal epithelium.