ADAM19
- Known as:
- ADAM19
- Catalog number:
- 001142A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADAM19
Related genes to: ADAM19
- 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
Related articles to: ADAM19
- 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 - To investigate the mechanism by which the effective-component combination of Bufei Yishen formula III (ECC-BYF III) ameliorates airway epithelial barrier injury in chronic obstructive pulmonary disease (COPD) through miRNA-mRNA regulatory networks. - Source: PubMed
Publication date: 2025/09/04
Liu ChunleiYue ChangyuanXing XiaoxiangHuang LidongWei YanxinZhao PengLi JianshengGuan Qingzhou - The prediction and treatment of spontaneous preterm labor (sPTL) are critical challenges due to obscure etiology and lack of highly specific and sensitive testing methods. Here, we extended the application of noninvasive prenatal testing into the field of sPTL prediction using high-throughput small RNA sequencing to screen the potential biomarkers for sPTL in maternal peripheral blood. We found that hsa-miR-150-5p and hsa-miR-512-3p decreased in the patients affected by sPTL, compared with either term labor or term not labor patients. The change of hsa-miR-150-5p is validated using quantitative PCR with the area under the receiver operating characteristic curve (AUROC) of hsa-miR-150-5p around 0.8272. In the discovery set, hsa-miR-150-5p exhibited an AUROC of approximately 0.8508, which was validated in an independent cohort, accurately classifying preterm samples with an AUROC of 0.8010. Moreover, we showed miR-150-5p inhibited migration and invasion of chorionic cells by directly targeting a disintegrin and metalloproteinase 19 (ADAM19). The significant increase of ADAM19 in chorion from patients affected by sPTL further indicates its inverse correlationship with miR-150-5p. ADAM19 functions as a sheddase of membrane-bound TNF-α to release the TNF-α trimer into the extracellular environment, reciprocally inducing the expression of ADAM19 to form a regenerative cycle and augmenting the migration and invasion of fetal membrane cells. Remarkably, the predictive efficiency of miR-150-5p for premature rupture of membranes (PROMs)-related sPTL sharply rose to 94.21%, indicating its potential as a biomarker for preterm premature rupture of membranes (pPROMs). These findings establish miR-150-5p both as a promising noninvasive biomarker for identifying the risk of sPTL and a key regulator in pathogenesis of pPROM. MiR-150-5p is identified as a potential noninvasive biomarker associated with sPTL and regulates chorionic cell migration, invasion, and adhesion by targeting ADAM19, a member of the ADAM family, contributing to premature rupture of fetal membranes. These findings provide new insights into the molecular mechanisms of sPTL and suggest that targeting the miR-150-5p/ADAM19 axis may offer novel therapeutic strategies. - Source: PubMed
Publication date: 2025/07/14
Wang NingLiu YuanyuanSun KaiyiChen BingyingSui YanyuWang ZheJiang XiangLi LiLi QinFeng JingqiuTao YiGao Lu