Rat TGFb1 ELISA
- Known as:
- Rat TGFb1 Enzyme-linked immunosorbent assay test
- Catalog number:
- kt-30309
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Rat TGFb1 ELISA
Related genes to: Rat TGFb1 ELISA
- Gene:
- TGFB1 NIH gene
- Name:
- transforming growth factor beta 1
- Previous symbol:
- TGFB, DPD1
- Synonyms:
- CED, TGFbeta
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-16
Related products to: Rat TGFb1 ELISA
Related articles to: Rat TGFb1 ELISA
- Estrogen receptor-positive breast cancer progression involves extensive cellular remodeling, yet the contribution of RNA-binding proteins to this process remains incompletely defined. Here, we constructed a single-cell transcriptomic atlas of 198,286 cells from 39 samples spanning normal tissue, primary tumors, and metastatic lesions. We identified stage-specific transcriptional and post-transcriptional reprogramming across different cell types. Several RBPs, including , , and , were progressively upregulated during malignant progression and associated with cytoskeletal remodeling, extracellular matrix interactions, and stress adaptation. Cell-cell communication analyses revealed metastasis-associated signaling programs involving TIMP1-MMP1 and TGFB1-COL7A1/MMP1, which were spatially enriched at tumor margins and invasive fronts. Functional perturbation experiments in ER breast cancer cells showed that TGF-β stimulation enhanced invasive behavior, whereas knockdown of MMP1 or COL7A1 attenuated epithelial-mesenchymal transition (EMT) marker expression and invasion. Together, our study delineates RBP-associated regulatory programs linking cellular state transitions to invasive signaling in ER breast cancer. - Source: PubMed
Publication date: 2026/05/28
Dong MingjieLi XinyuYang SongyuLi ShujuanLiu ZhengzhengPeng ChuoLi RongyaoLiang WeixinLi XiaBai Jing - Usher syndrome (USH) is an autosomal recessive disorder characterized by hearing loss, retinitis pigmentosa, and variable vestibular dysfunction. USH2A is one of the causative genes of USH. This study is aimed at exploring the mechanism of hearing loss induced by USH2A gene knockout. - Source: PubMed
Publication date: 2026/05/28
Chen ChiXu BaichengDang JiongTan HuanBian PanpanWang YanliGuo Yufen - This study investigated the impact of a high-carbohydrate diet (HC: 25% carbohydrate) on skin wound healing in turbot versus a control diet (CC: 16% carbohydrate). Following 10 weeks of triple replicates of fish (n = 40), standardized 8 mm skin wounds were created and healing assessed macroscopically and molecularly at baseline, 1, 3, and 7 days post-wounding (dpw). While growth performance remained unaffected, HC-fed fish exhibited persistent hyperglycemia and hyperinsulinemia, indicative of systemic insulin resistance. Macroscopic analysis showed significantly impaired wound contraction in the HC group at 3 and 7 dpw compared to CC controls. Histological assessment revealed defective re-epithelialization characterized by aberrant keratinocyte migration, suppressed provisional matrix formation, ill-defined epidermal stratification, and persistent goblet cell aggregation in HC fish. Molecular analyses demonstrated HC-mediated suppression of re-epithelialization markers (suppressed MMP9, EGF, FGF2, and KRT2 gene expression; reduced MMP9 protein distribution), dysregulated inflammation (reduced MPO and NAG activity; lower IL1B, IL6, IL8, TGFB1, and TNF expression; elevated IL10 expression), and impaired tissue form ation and remodelling (downregulated FN1, VEGF, CCN1, LAMB2, and COL1A mRNA; reduced collagen deposition; attenuated CD31-based angiogenesis). Importantly, HC feeding promoted skin AGEs accumulation, which was accompanied by reduced MTOR phosphorylation, decreased HIF1A protein levels, and blunted post-wounding induction of glycolytic genes, including PFK, HK2, and PK. Collectively, these findings indicate that HC feeding compromises multiple phases of skin wound healing in turbot and suggest that AGE-associated suppression of MTOR-HIF1A-mediated glycolytic adaptation is an important metabolic mechanism associated with delayed healing. - Source: PubMed
Publication date: 2026/06/03
Chen ZhichuLi YuantingFang YuanyuanHuang DongÁngeles Esteban MariaChen XinhuaZhang Yanjiao - To define CSC genetic architecture and identify implicated ocular tissues, cell types, genes, and circulating proteins. - Source: PubMed
Publication date: 2026/05/22
Chen LiyinKim Soo HyunTruong BuuRämö Joel TGorman Bryan Rvan Dijk Elon H CBrinks JoostNikopensius TiitChoi Seung HoanKajanne RistoMehtonen JuhaKaarniranta KaiSobrin LuciaKurki MitjaYzer Suzanne Wu Wen-ChihTurunen Joni ASegrè Ayellet JMercader Josep MariaHuerta AliciaDaly Mark JPalotie AarnoEllinor Patrick TBoon Camiel JfIyengar Sudha KPeachey Neal SNatarajan PradeepRossin Elizabeth J - WNT2B is canonically characterized as a secreted WNT-family ligand, which is transported to the extracellular space via the endoplasmic reticulum (ER)-Golgi pathway and binds to cell surface FZDs (frizzled class receptors) to trigger downstream signaling cascades. Here, we identify a previously unrecognized non-secretory intracellular function of WNT2B in impairing endosomal trafficking to inhibit macroautophagy/autophagy, as well as a non-canonical LC3B-II-dependent autophagic secretion mechanism for WNT2B. Specifically, the non-secretory intracellular pool of WNT2B via its conserved middle domain (MD) binds to the spectrin repeat domain (SRD) of WASHC5, competitively displacing WASHC1 and thereby disrupting WASH complex assembly and inhibiting WASHC1-mediated actin polymerization on early endosomes. This disruption impairs endosomal cargo trafficking, including the core autophagy protein ATG9A, leading to defective autophagy initiation and subsequent accumulation of pro-inflammatory and pro-fibrotic factors in fibroblasts. We validated this mechanism in vivo using a TNBS-induced mouse model of chronic colitis. Fibroblast-specific deletion restores autophagy, reduces pro-inflammatory cytokine secretion, and ameliorates intestinal fibrosis. Consistently, in Crohn disease (CD) patient tissues, elevated WNT2B in fibrotic regions negatively correlates with autophagy activity, and positively correlates with pro-fibrotic phenotypes, and clinical disease severity. Moreover, we identify a novel LC3B-II-dependent autophagic secretion pathway for WNT2B, which is distinct from the conventional ER-to-Golgi-dependent protein secretion. Collectively, our study delineates a novel non-canonical WNT2B-WASH complex-ATG9A regulatory axis through which WNT2B impairs endosomal trafficking and disrupts autophagy, ultimately amplifying inflammation and fibrosis. This study suggests that WNT2B may serve as a promising therapeutic target for CD and autophagy-associated fibrotic disorders.: 3-MA: 3-methyladenine; AAV: adeno-associated virus; ACTA2: actin alpha 2, smooth muscle; ARPC2: actin related protein 2/3 complex subunit 2; ATG: autophagy related; CCN3: cellular communication network factor 3; CD: Crohn disease; CK666: 2-fluoro-N-[2-(2-methyl-1H-indol-3-yl)ethyl]benzamide; COL1A1: collagen type I alpha 1 chain; Co-IP: co-immunoprecipitation; CTNNB1: catenin beta 1; DBcAMP: dibutyryl cyclic adenosine monophosphate; DPT: dermatopontin; EEA1: early endosome antigen 1; EGFR: epidermal growth factor receptor; ELISA: enzyme-linked immunosorbent assay; ER: endoplasmic reticulum; ESCRT: endosomal sorting complexes required for transport; EV: extracellular vesicle; FRAP: fluorescence recovery after photobleaching; FL: full length; FZD: frizzled class receptor; GST: glutathione S-transferase; HIF: human intestinal fibroblast; HMGB1: high mobility group box 1; IKBKB: inhibitor of nuclear factor kappa B kinase subunit beta; IL6: interleukin 6; LDELS: LC3-dependent EV loading and secretion; LPS: lipopolysaccharide; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MD: middle domain; MEFs: mouse embryonic fibroblasts; MTOR: mechanistic target of rapamycin kinase; MVB: multivesicular body; NFKB: nuclear factor kappa B; NFKBIA: NFKB inhibitor alpha; PDCD6IP: programmed cell death 6 interacting protein; PLA: proximity ligation assay; RELA/p65: RELA proto-oncogene, NF-kB subunit; SAFB: scaffold attachment factor B; SES-CD: Simple Endoscopic Score for Crohn disease; SIM: super-resolution structured illumination microscopy; SMAD3: SMAD family member 3; SQSTM1/p62: sequestosome 1; SRD: spectrin repeat domain; TEM: transmission electron microscopy; TFRC: transferrin receptor; TGFB1: transforming growth factor beta 1; TGOLN2: trans-golgi network protein 2; TNBS: 2,4,6-trinitrobenzenesulfonic acid; TNF: tumor necrosis factor; VCA: Verprolin homology, Central and Acidic; WASHC: WASH complex subunit; WLS: Wnt ligand secretion mediator; WCL: whole cell lysates; WNT: Wnt family member; WT, wild type. - Source: PubMed
Publication date: 2026/06/03
Liu DanqiongCheng YanlingHuang ChuxiangXie KangJie JiananZhang QingqingLan LinChen PeiyuXie JingWang HongliRen LuLi HuiwenGeng LanlanGong SitangZhu YunCheng Yang