Ask about this productRelated genes to: ADAMDEC1 Blocking Peptide
- Gene:
- ADAMDEC1 NIH gene
- Name:
- ADAM like decysin 1
- Previous symbol:
- -
- Synonyms:
- M12.219
- Chromosome:
- 8p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-24
- Date modifiied:
- 2016-10-05
Related products to: ADAMDEC1 Blocking Peptide
Related articles to: ADAMDEC1 Blocking Peptide
- Colorectal cancer (CRC) is one of the most commonly diagnosed and globally spread malignant diseases. Cancer-associated fibroblasts (CAFs) are key architects of the tumor microenvironment, yet their origin, stability, and interconvertibility remain poorly understood. Using transcriptomic profiling of fibroblasts from colorectal cancer (CRC) patients, we identify highly expressed (HEX) markers that define fibroblast subpopulations and uncover mechanisms governing their plasticity. We find that ADH1B marks normal colon-associated fibroblasts (NAFs), which consist of PI16-NAFs and ADAMDEC1-NAFs. ITGA3 delineates the total CAF population, which comprises myofibroblastic CAFs (myCAFs), whose characterizing markers were associated with poor prognosis and proteolytic inflammatory CAFs (piCAFs), characterized by markers not associated with prognosis. An AGT/TGM2-expressing fibroblast subset is present in both healthy and tumor tissues, suggesting alternative trajectories to the classical NAF-to-CAF transition model. While PI16-NAFs, AGT/TGM2-fibroblasts, and myCAFs maintain stable identities in long-term culture, the ADAMDEC1-NAF and piCAF phenotypes are lost in vitro. ITGA3-CAFs demonstrate dynamic plasticity, with TGF-β stably inducing myCAF formation and TNF-α or inhibition of DNA methylation promoting transient piCAF emergence. These findings redefine fibroblast heterogeneity in CRC and reveal a coexisting stable and plastic fibroblast network that may be amenable to modulation and provides a framework for future functional and translational studies. We identified highly expressed markers (HEX markers) to distinguish CAFs, NAFs and corresponding subpopulations in CRC. ADH1B characterized NAFs, which consisted of stable (solid outline) PI16-NAFs and unstable (dashed outline) ADAMDEC1-NAFs. ITGA3 identified CAFs consisting of stable myCAFs associated with poor prognosis and unstable piCAFs not associated with prognosis. AGT/TGM2 fibroblasts did not express ADH1B or ITGA3, were stable in culture and could be detected in both healthy colon and CRC. Treatment of PI16-NAFs with LPS or IFN-γ induced ADAMDEC1-NAFs, TGF-β the formation of myCAFs, while treatment with TNF-α led to the formation of piCAFs. Reduced DNA methylation converted myCAFs and PI16-NAFs into piCAFs. - Source: PubMed
Publication date: 2026/04/28
Demmler RichardAnchang Charles GYong YongsongRamming AndreasRauber SimonSchellerer Vera SSchmid BenjaminHartmann ArndtMerkel SusanneImkeller KatharinaNaschberger ElisabethStürzl Michael - - Source: PubMed
Publication date: 2026/04/22
Lin ShuchenCong HuiLi ZhenZhang LihuaYang XinmiaoFu Jie - Intestinal fibrosis is a severe complication of Crohn's disease (CD). While ADAMDEC1 has been identified as a marker for specific fibroblast subsets, its functional role in fibrogenesis remains unclear. This study aimed to elucidate the pathophysiological significance of ADAMDEC1 in the fibrotic cascade. - Source: PubMed
Publication date: 2026/04/08
Tanabe HiroshiWatanabe DaisukeAgawa MisakiNakamura HirotakaYoshizaki TetsuyaInoue JunUrai ShinBando HironoriKodama Yuzo - Rheumatoid arthritis (RA) is a systemic autoimmune inflammatory disorder. KLRB1 (killer cell lectin like receptor B1), which is intricately linked to immune modulation and inflammatory responses, represents a promising biomarker for the identification of RA. This study mainly explores the relationship between KLRB1 and RA, and identifies biomarkers related to KLRB1 in RA, providing theoretical support for the diagnosis and treatment of RA. - Source: PubMed
Publication date: 2026/04/09
Song JialeLu JunqinZhao HaoyuSong FeiZhou WeiZhou Jian - Esophageal squamous cell carcinoma (ESCA) constitutes a major global health burden, with immune evasion and therapeutic resistance posing significant challenges. This study aims to elucidate the molecular mechanisms underlying ESCA immune escape and resistance to neoadjuvant therapy, focusing on the role of ADAMDEC1 in regulating the tumor microenvironment (TME) and immune evasion. - Source: PubMed
Publication date: 2026/04/07
Cheng JiweiMa HaiboQian XinXing Wenqun