Ask about this productRelated genes to: ADAM19 antibody
- Gene:
- ADAM19 NIH gene
- Name:
- ADAM metallopeptidase domain 19
- Previous symbol:
- -
- Synonyms:
- MLTNB
- Chromosome:
- 5q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-01
- Date modifiied:
- 2014-11-19
Related products to: ADAM19 antibody
Related articles to: ADAM19 antibody
- Type 1 diabetes mellitus (T1DM) is a chronic metabolic disorder characterized by the autoimmune destruction of insulin-producing β-cells in the pancreas, leading to absolute insulin deficiency and persistent hyperglycemia. The immune system plays a pivotal role in the development of T1DM, with dendritic cells (DCs) acting as crucial modulators of immune responses. Despite this, the specific role of ADAM19 within the T1DM immune microenvironment remains poorly understood, particularly its expression in DCs and potential effects on pancreatic β-cell function. Further research is needed to explore these aspects in peripheral blood mononuclear cells (PBMCs) and pancreatic tissues. - Source: PubMed
Publication date: 2026/06/05
Chen LijunYan ChangjianHuang ChunlingLin WanrongXu JinliangLin YingxuanLin HongliJiang ZhengrongZhuang YongHuang Huibin - Peritoneal fibrosis, driven by M2 macrophage polarization, limits the long-term application of peritoneal dialysis (PD). Although ADAM19 is known to mediate fibrosis in other organs, its specific role in PD-associated peritoneal fibrosis remains unclear. PD patients were enrolled in a single center and divided into three groups depending on the PD time. Demographic and clinical data were collected. We detected the expressions of ADAM19, Notch1, Fibrosis-associated protein, chemokines and inflammatory factors in the peritoneum dialysis effluent by real-time PCR and western-blot assays. Macrophages were identified through flow cytometry. Then we analysis the relationship between ADAM19 and clinical data in PD patients. Furthermore, we established mouse models for peritoneal fibrosis to verify the biological function of ADAM19 in regulating macrophage polarization. In the long-term group, the fibrotic proteins (Fibronectin, α-SMA) and inflammatory factors (IL-6, IL-10) and chemokines (CCL5, CCL2, CXCL16) were higher than short-term group and more macrophages polarized towards M2. ADAM19 expression was linearly correlated with dialysis time and Kt/v. The AUROC of ADAM19 was 0.738 to identify the predictive value for peritoneal dialysis adequacy. The cut-off of ADAM19 RNA level was 7.84. In logistic regression models, higher ADAM19 (≥ 7.84) was also independently associated with lower Kt/v (< 1.67). Additionally, the results revealed a moderate increment of M1 macrophage (CD86+) and enormous rise of M2 macrophage (CD206+) with high-glucose dialysis fluid in mice model. Furthermore, the 8-week G4.25% group showed significant growth of M2 macrophage compared to the 4-week G4.25% group, indicating that prolonged dialysis duration has a more pronounced effect on promoting M2 polarization of macrophages via ADAM19/Notch1 signaling pathway. Through stimulating chemokines and inflammatory factors, ADAM19 regulated macrophage polarization and was correlated to the progression of peritoneal fibrosis. ADAM19 is expected to be a novel indicator for detecting peritoneal ultrafiltration function in PD patients. - Source: PubMed
Publication date: 2026/05/02
Xu KunyueYu JinHe MinhuiJiang XueYuan Yuan - Whole genome sequence (WGS) data in multi-ancestry samples supports discovery of low-frequency or population-specific genetic variants associated with chronic obstructive pulmonary disease (COPD) and lung function. - Source: PubMed
Publication date: 2026/01/15
Kim WonjiHu XiaoweiKim KangjinChun SungOrchard PeterQiao DandiRuczinski IngoSaferali AabidaAguet FrancoisAntonacci-Fulton LucindaBalte Pallavi PBartz Traci MAnamika Wardatul JannatZhou XiaoboDuan JunYiBrody Jennifer ACade Brian EDaviglus Martha LDoddapaneni HarshavadranDugan-Perez ShannonDutcher Susan KFrazar Christian DGabriel Stacey BGharib Sina AGupta NamrataHobbs Brian DKasela SilvaLoehr Laura RMetcalf Ginger AMuzny Donna MOelsner Elizabeth CRasmussen-Torvik Laura JSitlani Colleen MSmith JoshuaSofer TamarXu HanfeiYu BingZhang DavidZiniti JohnBarr R GrahamCarson April PFornage MyriamHou LifangKalhan RaviKaplan RobertLappalainen TuuliLondon Stephanie JMorrison Alanna CO'Connor George TPsaty Bruce MRaffield Laura MRedline SusanRich Stephen SRotter Jerome ISilverman Edwin KManichaikul AniCho Michael H - Post-infarct atrial remodelling creates a substrate for atrial fibrillation (AF), yet no cardiac-specific, non-invasive therapy targets this process. Low-intensity pulsed ultrasound (LIPUS) limits ventricular remodelling in preclinical models, but its impact on atrial remodelling and AF after myocardial infarction (MI) is unknown. - Source: PubMed
Yang HongjieHu YugangKong BinShen CaijieShuai Wei - Glaucoma remains the leading cause of irreversible blindness worldwide, with elevated intraocular pressure (IOP) being the only modifiable risk factor in primary open-angle glaucoma (POAG). Despite adequate IOP control, many patients continue to progress to irreversible optic neuropathy, emphasising the need for alternate treatments. Transforming growth factor-beta (TGF-β) promotes extracellular matrix (ECM) production and fibrosis at the optic nerve head (ONH) in glaucoma. A disintegrin and metalloprotease-12 and metalloprotease-19 (ADAM12 and ADAM19) are implicated in fibrosis. Recent studies have explored miRNA-based manipulation of the TGF-β signalling pathway as a potential therapeutic strategy in fibrosis. This study investigates whether miR-29b modulation affects ADAM12, ADAM19, and ECM gene expression in human lamina cribrosa (LC) cells. Primary human normal lamina cribrosa (NLC) and glaucoma LC (GLC) cells were treated with TGF-β1 and transfected with either a miR-29b mimic or control. Gene expression levels of ADAM12, ADAM19, miR-29b, and several ECM genes were quantified using real-time RT-qPCR, and protein expression levels by Western blotting. ADAM12 and ADAM19 expression was elevated in untreated GLC cells, and treatment with TGF-β1 in both NLC and GLC cells increased ADAM12 and ADAM19 expression. The expression of miR-29b was significantly reduced in both GLC- and TGF-β1-treated NLC and GLC cells. Transfection with miR-29b resulted in a marked reduction in ADAM12 and ADAM19 mRNA expression in TGF-β1-treated NLC and GLC cells. Additionally, miR-29b transfection reduced ECM gene expression in both NLC and GLC under TGF-β1 stimulation. Our results demonstrate that miR-29b plays a crucial role in fibrotic remodelling at the LC by antagonising the effects of TGF-β1 on ADAM and ECM gene expression, representing a novel therapeutic target in glaucoma. - Source: PubMed
Publication date: 2025/09/22
Smyth AoifeCallaghan BreedgeIrnaten MustaphaAndrews DarrellWilloughby Colin EO'Brien Colm