JAK1 (phospho-Tyr1022) Antibody
- Known as:
- JAK1 (phosphorilated-Tyr1022) Antibody
- Catalog number:
- abx000235
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- JAK1 (phospho-Tyr1022) Antibody
Related genes to: JAK1 (phospho-Tyr1022) Antibody
- Gene:
- JAK1 NIH gene
- Name:
- Janus kinase 1
- Previous symbol:
- JAK1B
- Synonyms:
- JAK1A, JTK3
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-04-16
- Date modifiied:
- 2016-10-05
Related products to: JAK1 (phospho-Tyr1022) Antibody
Related articles to: JAK1 (phospho-Tyr1022) Antibody
- Upadacitinib is an oral selective JAK1 inhibitor approved for moderate-to-severe Crohn's disease (CD), but real-world prospective multicentre data in advanced therapy-experienced (AT-experienced) patients are limited. The UPGRADE-CD study evaluated its effectiveness and safety. - Source: PubMed
Publication date: 2026/09/10
Barberio BrigidaD'Amico FerdinandoLaterza LucreziaBezzio CristinaDragoni GabrieleViola AnnaTodeschini AlessiaPrincipi MariabeatriceOnali SaraViganò ChiaraCappello MariaMocci GiammarcoViscido AngeloBodini GiorgiaRibaldone Davide GiuseppeMarafini IrenePugliese DanielaMassari AlessandroSaibeni SimonePastorelli LucaMelotti LauraBergna Irene Maria BambinaGravina Antonietta GerardaDesideri FedericoMerli ManuelaBertani LorenzoSpagnuolo RoccoImperatore NicolaFerracane ConcettaQuadarella AlessandroLuna Imma DiTortorella VincenzaMazzuoli SilviaFelice CarlaBalestrieri PaolaBalducci DanieleAratari AnnalisaBuda AndreaDanese SilvioScaldaferri FrancoArmuzzi AlessandroZingone FabianaChahuan JavierSavarino Edoardo V - Optic neuritis (ON) is a neuroinflammatory autoimmune disease harboring autoreactive lymphocytes. Effector memory CD4 T cells (CD4 T) represent a prominently expanded and pro-inflammatory subset within this compartment, yet their pathogenic metabolic programs remain poorly defined. B cell dysfunction also contributes to ON pathogenesis. However, whether T cell-intrinsic metabolic rewiring directly fuels this B cell dysregulation awaits elucidation. Here, through single-cell transcriptomic profiling of peripheral blood mononuclear cells (PBMCs) from ON patients, we conceptualized a pathological circuit linking T cell metabolic reprogramming to aberrant T-B crosstalk. In pathogenic CD4 T, JAK1 upregulation and enhanced STAT3 phosphorylation propagated a metabolic rewiring transcriptional program and secured T cell fitness via MCL1 induction. An inferred cholesterol export signature distinguished this subset and engaged the nuclear sensor RORA on B cells to instruct pro-inflammatory polarization and humoral commitment. In turn, subverted B cells perpetuated exaggerated antigen presentation and cytokine secretion, cementing pathogenic CD4 T differentiation and sustaining a self-amplifying inflammatory loop. Cross-disease profiling extended this axis to allied autoimmune disorders. Selective JAK1 blockade with upadacitinib (UPA) restored immune homeostasis and attenuated experimental autoimmune encephalomyelitis (EAE), phenocopied by MCL1 inhibition. Together, these findings nominate UPA as a targeted therapy for ON and allied autoimmune disorders. - Source: PubMed
Publication date: 2026/09/09
Jiang GengchenJiang QiHan LianPeng YueLiu XingyuYang TongHuang HaoLiu JiayingGao YuanYang HuiZou WenjunLi ZhaohuaiSu Wenru - Qingre Bawei capsules (QRBW), derived from the traditional Mongolian medicine Erhemu-8 (-8), have been clinically used to treat respiratory infections associated with lung heat syndrome, including pneumonia, bronchitis, influenza, and acute lung injury (ALI). However, its specific effects and underlying mechanisms in ALI remain unclear. - Source: PubMed
Publication date: 2026/09/09
Shi HanlingZhang YuyaoYou WanyingYang JianjunWang ChanghongWei Xiaohui - Pemphigus erythematosus (PE) is a rare subtype of pemphigus, and management may be particularly challenging when prolonged systemic corticosteroid exposure is undesirable. We report a 31-year-old woman with PE and concomitant erosive gastritis who received off-label treatment with the selective Janus kinase 1 (JAK1) inhibitor upadacitinib after continued systemic corticosteroid therapy was considered unsuitable. Despite initial treatment with methylprednisolone plus upadacitinib 15 mg daily, the disease progressed rapidly, prompting escalation of upadacitinib to 30 mg daily. New blister formation ceased within 1 week, methylprednisolone was discontinued by week 4, complete clinical resolution was achieved by week 8, and anti-desmoglein 1 antibody levels normalized by week 11. After disease control had been achieved, upadacitinib was reduced to 15 mg daily and discontinued after 8 months, with sustained remission and no treatment-related adverse events during 1 year of follow-up. In the context of limited published experience with JAK inhibitors in pemphigus, this single case provides preliminary evidence that upadacitinib may warrant further investigation as a potential corticosteroid-sparing option for selected patients with PE and treatment-limiting comorbidities. - Source: PubMed
Publication date: 2026/09/04
Lo Hou-ManSong Xin-RanZhang QianSu JingLi Wei-WeiLi Dong-MingWang Wen-Hui - Inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), arises from complex interactions among host susceptibility, microbial dysbiosis, altered metabolite profiles, and dysregulated mucosal immune responses. Interleukin-22 (IL-22), a cytokine that acts primarily on non-hematopoietic cells, contributes to epithelial antimicrobial defense, survival, and tissue repair, but may also amplify inflammation under specific chronic or co-inflammatory conditions. This review evaluates the evidence linking major microbiota-associated metabolites-including short-chain fatty acids (SCFAs), bile acids (BAs), tryptophan (Trp) -derived metabolites, and the trimethylamine (TMA)/trimethylamine N-oxide (TMAO) pathway-to IL-22 production, bioavailability, and function in IBD. Relatively direct mechanistic support is available for SCFA-mediated and Trp-Aryl hydrocarbon receptor (AhR) -dependent regulation of IL-22, whereas bile acid effects appear metabolite-, receptor-, and context-dependent. In contrast, the proposed relationship between TMA/TMAO and IL-22 is currently supported mainly by indirect evidence and should be considered an emerging hypothesis. We further incorporate IL-22-binding protein (IL-22BP) as a determinant of local IL-22 bioavailability and distinguish upstream regulation of IL-22 production from downstream signaling initiated through the epithelial IL-22R1/IL-10R2 receptor complex. Particular attention is given to canonical JAK1/TYK2-STAT3 signaling and its context-dependent interactions with NF-κB, PI3K-AKT-mTOR, and MAPK pathways. We propose that the duration and magnitude of IL-22 exposure, its cellular source, the IL-22/IL-22BP balance, epithelial target-cell state, concurrent inflammatory signals, and disease context collectively determine whether IL-22 promotes mucosal repair or contributes to inflammatory amplification. By separating established mechanisms from associative, extrapolated, and hypothesis-generating evidence, this review provides a more evidence-calibrated framework for investigating the microbiota-metabolite-IL-22 network in UC and CD. - Source: PubMed
Publication date: 2026/08/25
Shi PeixinHe XiyuanZhao LingPan WeisongZhou MingmeiZhang Ting