Ask about this productRelated genes to: MAdCAM1 antibody
- Gene:
- MADCAM1 NIH gene
- Name:
- mucosal vascular addressin cell adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- MACAM1
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-11
- Date modifiied:
- 2014-11-19
Related products to: MAdCAM1 antibody
Related articles to: MAdCAM1 antibody
- Given the global issue of the rising incidence of early-onset colorectal cancer (CRC), we tested the hypothesis that tumor vasculature phenotypes might vary with age at CRC diagnosis. - Source: PubMed
Publication date: 2026/03/25
Matsuda KosukeUgai SatokoMiyahara SatoshiYao QianCazaubiel JulesNakazawa NobuhiroHigashioka MayuZhong YuxueChan Andrew TMeyerhardt Jeffrey ANg KimmieSong MingyangVäyrynen Juha PNowak Jonathan AGiannakis MariosUgai TomotakaOgino Shuji - Tissue resident memory CD4+ T cells (TRMs) populate mucosal sites and play a critical role in local immune responses. Gut TRM cells persist for extended periods in the gut mucosa where they rapidly respond to invading pathogens and provide long lasting protection. This study investigates the factors that mediate differentiation of naïve CD4+ T cells into cells presenting a gut TRM phenotype. Naïve CD4+ T cells were cultured under conditions that mimicked mucosal environments. This included signaling through MAdCAM-1 in the presence of Retinoic Acid (RA) and TGF-β. This combination of stimuli primed naïve CD4+ T cells to adopt a TRM phenotype. However, to fully differentiate into TRMs an additional soluble factor provided by memory T cells was required. Our results identified IL-6 as one of the key factors that induces the expression of TRM -associated markers, including CD69, CD103 and CCR5. This unique combination of stimuli promoted TRM differentiation despite low level proliferation. TRM differentiation was mediated through JAK/STAT signaling, and antagonists that target JAK/STAT pathways suppressed MAdCAM-1 mediated TRM cell formation. Our findings revealed that MAdCAM-1 works together with TGF-β, RA and IL-6 in this process. Such information may aid in the design of next generation adjuvants and effective mucosal vaccines. Additionally, each of these factors may be targeted to treat excessive gut inflammation associated with conditions like inflammatory bowel disease. Overall, these findings provide new strategies aimed at modulating immune responses to invading pathogens and identify therapeutic approaches toward regulating gut inflammation. - Source: PubMed
Publication date: 2026/03/16
Kim Han GChan AmandaVimopatranon SinmanusGirard AlexandreJiang AndrewWertz SamuelHwang Il-YoungKehrl John HSchmeisser HanaSeemiller Madelyn MLusso PaoloHuang DaweiWei DanlanGoes Livia RSoares MarceloMartinelli ElenaArthos JamesCicala Claudia - - Source: PubMed
Publication date: 2026/02/25
Li YuananLiu YifanLu BingnanYao YuntaoLyu DonghaoZhang HangbiaoCui XingangPan Xiuwu - Enhanced expression of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) on high endothelial venules facilitates lymphocyte migration to sites of intestinal inflammation in inflammatory bowel disease (IBD). This process may be accompanied by increased shedding of soluble MAdCAM-1 (sMAdCAM-1) from endothelial cells. Hence, circulating sMAdCAM-1 may serve as a biomarker of intestinal inflammation in IBD. - Source: PubMed
Publication date: 2026/02/24
Muschaweck MoritzGutbier ChristianSellge GernotPappa AngelikiWenzl TobiasHamesch KarimWagner NorbertSchippers Angela - Pediatric pouchitis has no established treatment strategy, and management is particularly challenging in recurrent or antibiotic-refractory cases. Tumor necrosis factor alpha (TNF-α) and mucosal vascular addressin cell adhesion molecule 1 (MAdCAM-1) are established and emerging therapeutic targets, respectively, in adult ulcerative colitis (UC) and pouchitis; however, their expression profiles and clinical relevance in pediatric pouchitis remain unclear. Therefore, we evaluated the pathological and clinical significance of TNF-α and MAdCAM-1 in pediatric pouchitis. We performed immunohistochemical analysis of surgically resected ileal tissues and subsequent pouch biopsy specimens obtained from 10 pediatric patients with UC. Paired pouchitis biopsies were collected during both active (high pouchitis disease activity index, PDAI) and improved (low PDAI) phases. TNF-α, MAdCAM-1, and immune cell markers (CD68, CD163, and CD8) in the mucosal stroma were quantitatively assessed using HALO image analysis. Compared with baseline ileal tissues, pouchitis specimens showed increased MAdCAM-1-positive vasculature and infiltration of CD68- and CD163-positive cells. In paired specimens, MAdCAM-1, TNF-α, and CD68 expression was significantly reduced in low-PDAI tissues. MAdCAM-1 and TNF-α expression was positively correlated with inflammatory cell infiltration. This exploratory study provided the first histological evidence that MAdCAM-1 and TNF-α could be upregulated in pediatric pouchitis and associated with disease severity, highlighting the pathological relevance of adult UC therapeutic targets in this setting. - Source: PubMed
Publication date: 2026/02/17
Otake SayakaKhorolgarav EnkhtuvshinYokobori TakehikoGombodorj NavchaaOgushi KenjiroSuzuki NaomiOkami HarukaZadeh Seyed Mostafa MostafaviShiraishi TakuyaOzawa NaoyaDorjkhorloo GendensurenOkada TakuhisaSano AkihikoSakai MakotoSuzuki MakotoKuwano HiroyukiShirabe KenSaeki Hiroshi