Ask about this productRelated genes to: Jak1 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 antibody
Related articles to: Jak1 antibody
- Atherosclerosis (AS) progression is closely associated with phenotypic transformation of vascular smooth muscle cells (VSMCs) and activation of the Janus kinase 1/signal transducer and activator of transcription 3 (JAK1/STAT3) signaling pathway. This study aimed to elucidate the active components and underlying mechanisms of the Tiaozhi Tongmai Formula (TZTMF) in ameliorating AS through both in vivo and in vitro experiments. - Source: PubMed
Publication date: 2026/03/27
Zhang LuMaimaiti KaidinuerSun Jia-LiZhang Meng-MengZhang Min-Yu - This study retrospectively analyzed the clinical data of the first reported case in China of myeloproliferative neoplasm (MPN) driven by a homozygous germline SH2B3 mutation, aiming to deepen the understanding of this rare MPN subtype. The patient was a 59-year-old female admitted due to intermittent fatigue and fever for 3 years, which had worsened 4 days prior to admission. Next-generation sequencing revealed a homozygous germline SH2B3 gene mutation (c.1481C>A, p.S494*) with a variant allele frequency (VAF) of 100%. Family analysis confirmed its germline origin, and her children were all heterozygous carriers of the SH2B3 mutation with normal phenotypes. Based on hematological examination and bone marrow pathology, MPN was definitively diagnosed. The main clinical manifestations included fever, night sweats, elevated WBC and PLT, and splenomegaly. As a negative regulator of JAK2, inactivating mutations in the SH2B3 gene lead to weakened negative regulation of the JAK2/STAT signaling pathway by the SH2B3 protein, thereby causing continuous activation of this pathway and inducing the development of MPN. After treatment with the JAK1/JAK2 inhibitor ruxolitinib 20 mg twice daily, the patient's body temperature returned to normal, fatigue and night sweats resolved, and spleen size decreased, demonstrating significant therapeutic efficacy. - Source: PubMed
Zhang WLi RTian JJiang L JBai JGu Y HWang Y YSu YLi Y QXue Y MChen J MWei Y P - Prurigo nodularis (PN) is a chronic pruritic dermatosis with incompletely defined pathogenesis, and molecular data from East Asian populations are limited. We characterized the transcriptomic signatures of non-atopic PN in Korean patients to identify pathways linked to chronic itch and lesion persistence. RNA sequencing was performed on lesional and non-lesional skin from 17 PN patients and normal skin from 11 controls, followed by differential expression, functional enrichment, and correlation analyses. Lesional PN skin showed distinct transcriptional signatures with upregulation of Th22/IL-22-related genes and IL-22-inducible epidermal stress markers (S100A7/A8/A9, SERPINB4, HRNR), along with keratinization genes (KRT6C, KRT16, KRT17). Itch severity correlated strongly (Spearman's ρ>0.7) with IL-22-inducible stress genes, IL4R, profibrotic mediators (WNT5A), JAK-STAT regulators (JAK3, SOCS1/3), neuromodulatory/epidermal-neural genes (TRPV3), and senescence markers (CDKN1A, CXCL8, PLAUR). Non-lesional skin showed intermediate expression patterns, consistent with subclinical inflammation. Despite the modest sample size and single-ethnicity design, these findings indicate that non-atopic PN in Korean patients is characterized by IL-22-driven epidermal stress, fibroblast remodelling, neuroimmune signalling, and senescence programsprogrammes, highlighting therapeutic targets including IL-31RA, IL-4Rα/JAK1, antifibrotic and senescence-directed pathways. - Source: PubMed
Publication date: 2026/05/18
Kim Hei SungKim Yoon-SeobYosipovitch Gil - To explore the molecular mechanisms underlying cystoid macular edema (CME) through protein-protein interaction (PPI) network analysis, identifying key regulatory proteins, functional modules, and enriched biological pathways relevant to its pathogenesis. - Source: PubMed
Shariati Mehrdad Motamed - - Source: PubMed
Publication date: 2026/05/17
Licata GaetanoBalato AnnaFranzese PaolinoSorrentino PasqualeArgenziano GiuseppeGiorgio Caterina Mariarosaria