RORC antibody - middle region (ARP33243_P050)
- Known as:
- RORC (anti-) - middle region (ARP33243_P050)
- Catalog number:
- arp33243_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RORC antibody - middle region (ARP33243_P050)
Related genes to: RORC antibody - middle region (ARP33243_P050)
- Gene:
- RORC NIH gene
- Name:
- RAR related orphan receptor C
- Previous symbol:
- -
- Synonyms:
- RZRG, RORG, NR1F3, TOR
- Chromosome:
- 1q21
- Locus Type:
- gene with protein product
- Date approved:
- 1995-04-13
- Date modifiied:
- 2019-04-23
Related products to: RORC antibody - middle region (ARP33243_P050)
Related articles to: RORC antibody - middle region (ARP33243_P050)
- γδ T cells boost inflammatory responses and exacerbate tissue damage after ischemic stroke. However, the origin, dynamics, and tissue adaptation of γδ T cells in the ischemic brain and its border regions remain poorly understood. A systematic integration of large-scale datasets is urgently needed. Here, we investigated the impact of ischemic stroke on the state of meningeal and brain-infiltrating γδ T cells and explored their potential contributions to post-stroke inflammation. - Source: PubMed
Publication date: 2026/04/09
Zha MingmingJander AlinaCai HaodiPiepke MariusDegenhardt KarolineWinter LeoMagnus TimGelderblom Mathias - Memory T helper (Th) cells sustain protective recall responses but can also drive chronic inflammation, necessitating precise regulation of their effector programs. Although Th cells produce acetylcholine (ACh) and express nicotinic acetylcholine receptors (nAChRs), the contribution of nAChRs to human memory Th function across central (Tcm) and effector (Tem) subsets is poorly defined. We examined the effect of nicotine and GTS-21, a compound previously described as targeting α7nAChR, on total memory Th cells and purified Tcm and Tem from healthy participants. Nicotine or GTS-21 diminished IFN-γ, IL-4, and IL-17A secretion, downregulated TBX21, GATA3, and RORC, and reduced NF-κB p65 phosphorylation in total memory Th cells. Disruption of CHRNA7 abolished nicotine-mediated suppression but did not eliminate the inhibitory effects of GTS-21. Within CCR7-defined subsets, nicotine and GTS-21 lowered Th1/Th2/Th17 frequencies in Tcm, but not in Tem. In purified subsets, nicotine suppressed IFN-γ, IL-4, IL-17A, IL-21, BCL6, and CD40L selectively in Tcm, whereas GTS-21 suppressed them in both Tcm and Tem. Collectively, nicotine engages an α7nAChR-dependent checkpoint that preferentially regulates Tcm responses, while GTS-21 exerts broader suppressive effects not fully explained by α7nAChR loss. This cholinergic checkpoint in Tcm may limit Tfh-associated help and pathogenic recall responses in immune-mediated disease. - Source: PubMed
Gholizadeh FatemehHajiaghayi MehriRahbari NiloufarChoi Jennifer SHeidt SamanthaComo AlexiaKazerouni MaryamKargar MelikaPinard-LaRoche AudeShih Steve C CDarlington Peter J - Beyond their well-established roles in type 3 immunity, RORγt innate immune cells are also essential for secondary lymphoid organ (SLO) formation and gut homeostasis. However, the transcriptional mechanisms governing RORγt expression in these cells, including group 3 innate lymphoid cells (ILC3s), lymphoid tissue inducer (LTi) cells, and antigen-presenting cells (APCs), remain largely unresolved. Here, we identified two key cis-regulatory elements within conserved non-coding sequences (CNS)9 and 11 in the Rorc locus, which were sequentially utilized during differentiation. Initially, Runx-binding sites in CNS11 established chromatin accessibility as early as the hematopoietic stem cell (HSC) stage. Disruption of this chromatin priming prevented subsequent transcriptional activation, thereby abolishing the initial induction of RORγt in these cells. At later stages, CNS9 played a critical role, particularly in the development of RORγt⁺ APCs, contributing to colonic peripheral Treg (pTreg) cell induction. This hierarchical transcriptional regulation was essential for SLO formation and postnatal type 3 immunity and for restraining excessive intestinal type 2 immune responses through pTreg cell induction. - Source: PubMed
Publication date: 2026/03/24
Fukui TakumaWatanabe MiyukiKobayashi ReoYamada TaishoNakano KentaTanaka KaoriHarada AkihitoOkamura TadashiSonoda Koh-HeiOhkawa YasuyukiSumiya ErikoShao RuiqiSuyama MikitaTaniuchi IchiroKojo SatoshiSawa Shinichiro - Gastric cancer (GC) represents a malignant neoplasm with high global incidence and mortality rates. The limited efficacy of current clinical treatment regimens underscores the urgent need for novel and more effective therapeutic targets. - Source: PubMed
Publication date: 2026/01/20
Liu XinRen BingbingMa WenyueFu LangLiu ShuhanSun Daqing - T helper 17 (Th17) cells are pivotal in mucosal defense and autoimmune pathology, with their function governed by the transcription factor retinoic acid receptor-related orphan receptor gamma t (RORγt). Although genome-wide association studies link RORC variants to inflammatory diseases, their functional consequences remain poorly understood. We identify a pathogenic RORγt mutation N277D (mouse homolog N275D) that amplifies Th17 pathogenicity through cooperation with hypoxia-inducible factor HIF-1α. This mutation enhances IFN-γ and other Th1-type cytokine production by Th17 cells, exacerbating colitis without disrupting T cell development or homeostasis. Integrated transcriptomic and metabolomic profiling reveals activation of glycolytic and hypoxia-associated pathways, consistent with increased RORγt recruitment by HIF-1α to the Pdk1 locus. Notably, silencing Pdk1 normalizes the excessive IFN-γ production in RORγt Th17 cells. Together, these findings define a regulatory axis linking RORγt and HIF-1α that coordinates transcriptional and metabolic programs in pathogenic Th17 cells, providing a framework for dissecting the functional impact of autoimmune risk variants. - Source: PubMed
Publication date: 2026/03/17
Dong PeixianLiu LiangYu JohnLi NingDavidorf BenjaminShen StevenBouch RonaldZhang JingHo DavidXiao GutianAkbari OmidZhang BingHe Zhiheng