JAG1 monoclonal antibody (M08), clone 3C10
- Known as:
- JAG1 mab (anti-) (M08), clonality 3C10
- Catalog number:
- H00000182-M08
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- JAG1 monoclonal antibody (M08) clone 3C10
Related genes to: JAG1 monoclonal antibody (M08), clone 3C10
- Gene:
- ANAPC15 NIH gene
- Name:
- anaphase promoting complex subunit 15
- Previous symbol:
- C11orf51
- Synonyms:
- HSPC020, DKFZP564M082, APC15
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-06
- Date modifiied:
- 2015-09-11
- Gene:
- JAG1 NIH gene
- Name:
- jagged canonical Notch ligand 1
- Previous symbol:
- AGS, JAGL1
- Synonyms:
- AHD, AWS, HJ1, CD339
- Chromosome:
- 20p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-22
- Date modifiied:
- 2019-04-23
- Gene:
- KIAA0100 NIH gene
- Name:
- KIAA0100
- Previous symbol:
- -
- Synonyms:
- DKFZp686M0843, MGC111488, BCOX1, CT101, BCOX, FMP27
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-22
- Date modifiied:
- 2019-04-12
- Gene:
- TMEM184B NIH gene
- Name:
- transmembrane protein 184B
- Previous symbol:
- C22orf5
- Synonyms:
- HS5O6A, DKFZP586A1024, FM08
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-29
- Date modifiied:
- 2016-10-05
Related products to: JAG1 monoclonal antibody (M08), clone 3C10
Related articles to: JAG1 monoclonal antibody (M08), clone 3C10
- Epilepsy and glioblastoma (GBM) share pathological features including neuroinflammation, glial activation, and disrupted cellular homeostasis; however, their systems-level molecular organization remains poorly understood. This study investigated context-dependent alterations in Notch signalling, innate immune pathways, and oxidative stress responses across human control, epileptic, and GBM brain tissues. Differential expression, correlation, and co-expression network analyses were performed using qRT-PCR data, complemented by independent GTEx and GEO transcriptomic datasets. NOTCH1 expression was increased in both epilepsy and GBM, whereas NOTCH2 was elevated specifically in GBM. GFAP and IBA1 expression increased in epilepsy, while only IBA1 remained elevated in GBM. KI67 expression was markedly increased in GBM and modestly elevated in epilepsy, while NEUN expression was reduced in GBM. KEAP1, NRF2, JAG1, NLE1, and TLR4 showed no significant differences among groups, whereas TLR3 was selectively upregulated in GBM. Despite limited differential expression of oxidative stress-related transcripts, correlation analyses revealed substantial differences in gene-gene co-expression patterns. Epilepsy showed stronger co-expression relationships among Notch, immune, and glial markers, whereas GBM exhibited greater integration of Notch, oxidative stress, and inflammatory genes. Independent GTEx and GEO datasets broadly reproduced these major disease-associated co-expression patterns. These findings suggest distinct disease-associated co-expression patterns involving Notch signalling and inflammatory, glial, and oxidative stress pathways in epilepsy and GBM that may not be evident from differential expression alone. - Source: PubMed
Publication date: 2026/09/27
Meshkinkhood NoorMohammadEbrahimi SafiehAlipour FatemehNourbaksh FarshidGhadipasha MasoudGharehdaghi JaberMeuth Sven GSpeckmann Erwin-JosefStummer WalterGorji AliGhadiri Maryam Khaleghi - (Ct) infection is a major cause of infertility, primarily through inducing tubal fibrosis. Epithelial-mesenchymal transition (EMT) plays a central role in this fibrotic process. However, the molecular mechanisms by which Ct infection triggers EMT are not fully understood. IFN-γ is a major component of the host immune pressure acting on infected epithelial cells during Ct infection. To mimic this immune environment in vitro and investigate how host signaling responses to Ct infection influence EMT, we maintained Ct-infected HeLa cells under continuous IFN-γ treatment and examined Wnt/β-catenin and Notch signaling. Under this condition, both pathways were activated and exhibited functional crosstalk potentially involving JAG1. Inhibition of either pathway attenuated EMT-associated phenotypes and was associated with reduced infectious progeny production. These findings support a role for Wnt/β-catenin-Notch crosstalk in promoting EMT in Ct-infected cells under continuous IFN-γ treatment. - Source: PubMed
Publication date: 2026/09/17
Yang YeweiFang ChunxiaWu HongrongChen LiliWen YatingLi Zhongyu - Congenital heart disease (CHD) combined with anomalies of the kidney and urinary tract (CAKUT) belongs to severe clinical conditions that represent isolated cases or can be part of complex inherited syndromes. To date, knowledge of the genetic basis of cardio-renal birth defects is very limited. Using chromosomal microarray analysis and exome sequencing, we investigated the spectrum of copy number variations (CNVs) and point genetic variants in a pediatric cohort of 30 patients presenting with combined CHD and CAKUT. Two patients possessed a pathogenic deletion in the 22q11.2 genomic region, well-known as the DiGeorge/velocardiofacial syndrome locus. Four other patients harbored rare copy number gains, which included one of the dosage-sensitive genes: (5q14.1), (2q13), (5p12), and (15q26.2). In six children, novel or previously described causative variants were detected in the genes associated with orphan monogenic disorders such as Kabuki (, Noonan (), Adams-Oliver (), and Alagille () syndromes, as well as - and -related syndromes. Furthermore, potentially disease-contributing variants were identified in the genes that primarily code for cardiac transcription factors, chromatin remodeling proteins, Notch- or signaling molecules, and components of cilia. Notably, two children had loss-of-function variants in , encoding one of the receptors of the SLIT/ROBO signaling pathway. studies on cardiac mesenchymal cells demonstrated a dramatically diminished expression level of ROBO1 in a patient with novel compound heterozygous variants c.541_542del (p.Val181CysfsTer18) and c.657+4A>G and a moderately reduced ROBO1 expression in a patient with a heterozygous stop-gain variant c.2758C>T (p.Arg920Ter), which suggests a haploinsufficiency mechanism. Together, our findings underlined the utility of early cytogenetic screening for the 22q11.2 deletion among children with cardio-renal malformations and confirmed the importance of rare single-nucleotide variants in the genes involved in cardiogenesis and kidney development. In particular, can be regarded as a candidate gene associated with combined heart and kidney structural defects and should be included in appropriate diagnostic gene-sequencing panels. The results support the usefulness of WES and array-based comparative genomic hybridization (array-CGH) analysis for new candidate gene identification, more accurate diagnosis, and family genetic counseling. - Source: PubMed
Publication date: 2026/09/09
Zlotina AnnaZhuk SergeiKozyrev IvanSorokina MargaritaNikitina EkaterinaShagimardanova ElenaMelnik OlesiaVershinina TatianaPetrova NataliaKagantsov IlyaVasichkina ElenaPervunina TatianaKostareva Anna - Alagille syndrome (ALGS) is an autosomal dominant multisystem developmental disorder associated with JAG1 and NOTCH2 mutations. Although vascular involvement is recognized, life-threatening intracranial hemorrhage as the initial presentation is extremely rare. - Source: PubMed
Publication date: 2026/09/11
Wang YuSun YangyangYang ZhenxingChen JinlongWan DingHuang Dejun - To identify key genes associated with keloid through integrative analysis of multiple transcriptomic datasets, and to explore their potential regulatory roles in disease development with experimental validation. - Source: PubMed
Publication date: 2026/09/17
Yang LingyiMo WenshenCao WendiMi LinWu Xiaowei