Ask about this productRelated genes to: ADAM12 antibody
- Gene:
- ADAM12 NIH gene
- Name:
- ADAM metallopeptidase domain 12
- Previous symbol:
- -
- Synonyms:
- MCMPMltna, MLTN
- Chromosome:
- 10q26.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-01
- Date modifiied:
- 2016-10-05
Related products to: ADAM12 antibody
Related articles to: ADAM12 antibody
- To evaluate the expression of hypoxia-inducible factor 1 alpha (HIF-1α), NOTCH-1, ADAM-12, and heparin-binding epidermal growth factor (HB-EGF) in adenoid cystic carcinoma (ACC), mucoepidermoid carcinoma (MEC), and normal salivary glands (SG), exploring hypoxia-related stromal and parenchymal adaptations with potential implications for tumor stratification and therapeutic targeting. - Source: PubMed
Publication date: 2026/04/13
Tavares Thayna Silva do Carmode Mendonça Raíssa PinheiroBranco Dimitra CasteloKataoka Maria Sueli da SiilvaJúnior Sérgio de Melo AlvesPinheiro João de Jesus Viana - Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with poor prognosis and limited therapeutic options. A disintegrin and metalloproteinase 12 (ADAM12) is aberrantly expressed in multiple cancers and has been implicated in tumor progression. However, its biological role and underlying mechanism in HCC remain unclear. - Source: PubMed
Publication date: 2026/05/06
Wu ShengdongZhu YongfeiXia YanWu ShengjunLu Caide - The placenta is essential for fetal development, yet its molecular evolution across mammals remains elusive. Here, we present a comprehensive single-cell transcriptomic atlas of ~300,000 cells from ten species representing the four primary placental types: discoid, cotyledonary, diffuse, and zonary. Our cross-species analysis identifies trophoblast lineages as the primary drivers of placental diversification. By reconstructing differentiation trajectories, we elucidate the regulatory networks shaping trophoblast development across diverse architectures. We propose that the unique gene expression profile of human trophoblasts underlies the susceptibility to preeclampsia and miscarriage. Functional experiments demonstrate that TGIF1 acts as a key upstream regulator of extravillous trophoblast growth and migration. TGIF1 and its targets, including ADAM12, WNT3A, and ZNF831, are associated with preeclampsia and pregnancy loss. Collectively, this high-resolution framework provides fundamental insights into the molecular evolution of the placenta and its contribution to reproductive success and diseases. - Source: PubMed
Publication date: 2026/05/09
Tan GuanghuiZhang AoCao XueshaYang JingyuCui YoujieWang FeiShi TaoLi HengkuanWang HaopingShan HuiquanRen JilongZhou YaqiWang MenghanLuo FunongGuo XiHuo WuqiangLiu YingranNiyazbekova ZhannurWang XihongXiao ZhenyuZheng YiJiang Yu - Muscle fibrosis is a key pathological feature of Duchenne muscular dystrophy (DMD) and is closely associated with disease progression. Fibroadipogenic progenitors (FAPs) are major contributors to fibrosis, yet the precise mechanisms remain unclear. To investigate FAP dynamics and lineage specification, we generated dual-reporter mice (PRURD2) by crossing D2.B10-Dmdmdx/J (D2-mdx) mice with FAP and brown/beige adipose tissue (BAT) reporter lines. Corresponding control mice (PRURDBA) were established on the DBA/2J background. At 12 months, heart, diaphragm, and tibialis anterior (TA) muscles were collected for histological analysis. FAPs were isolated via FACS and subjected to single-cell RNA sequencing. PRURD2 mice exhibited increased fibrosis across all muscles compared to controls ( < 0.01) and a significant rise in PDGFRα-GFP + FAPs ( < 0.05). UMAP clustering identified 11 distinct FAP subpopulations, with the fibrosis-associated CD55 cluster enriched in PRURD2 mice. Pseudotime analysis showed lineage progression from progenitor clusters toward the fibrogenic CD55 cluster. CellChat analysis indicated increased interactions in PRURD2 mice involving fibrosis-related pathways like COLLAGEN, TGF-β, WNT, NOTCH, and ANGPTL. Additionally, fibrosis-related signaling pathways such as THY1, TWEAK, EPHA, EPHB, and SEMA6 showed increased interactions among FAP clusters in PRURD2 mice. Differential gene expression analysis revealed top upregulated genes including , , and . PRURD2 mice develop severe fibrosis in skeletal and cardiac muscle, driven by FAP-induced signaling pathways and genes. This model is valuable for understanding muscle fibrosis in DMD and developing anti-fibrotic therapies. - Source: PubMed
Publication date: 2026/04/24
Fusagawa HiroyoriLau JustinSharma SankalpLiu MengyaoSamimi YusefFranchet-Schaer GabrielFang AshleyFusagawa MinamiKim HubertFeeley Brian TLiu Xuhui - A disintegrin and metalloproteinase 12 (ADAM12) is known to be involved in chondrocyte proliferation and is upregulated in the synovial tissue of osteoarthritis (OA). However, the underlying mechanisms of ADAM12 on rheumatoid arthritis (RA) synovial cell proliferation remain unknown. Here, we investigated the role of ADAM12 in the proliferation of RA synovial fibroblasts (RASFs). The expression and localization of ADAM12 in RA synovial tissues were examined by immunohistochemistry and compared with OA and healthy control (HC) synovial tissues. The effect of inflammatory cytokines (TNF-α, TGF-β1, and PDGF-BB) on ADAM12 expression in RASFs from RA patients was examined by real-time RT-PCR. The effect of ADAM12 knock-down by ADAM12 siRNA and ADAM12 overexpression on cell proliferation of RASFs were examined by WST-1 assay. ADAM12 was identified predominantly in RA synovial tissue rather than OA and HC synovial tissues. Stimulation with TGF-β1 upregulated the expression of ADAM12 and cell proliferation of RASFs. ADAM12 siRNA suppressed TGF-β1-induced cell proliferation of RASFs, while ADAM12 overexpression promoted the cell proliferation of RASFs. These findings demonstrate that ADAM12 may have a key role in TGF-β1-induced cell proliferation of synovial fibroblasts in patients with RA. - Source: PubMed
Lin DetingHorita MasahiroWatanabe MasahitoHasei JoeOhtsuki TakashiOtsuka NoriakiIchikawa ChinatsuShimizu NoriyukiNaniwa ShuichiOzaki ToshifumiNishida Keiichiro