ECM1 Antibody (Antigen Affinity Purified)
- Known as:
- ECM1 Antibody (Antigen Affinity Purified)
- Catalog number:
- 10362-RP02
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- ECM1 Antibody (Antigen Affinity Purified)
Ask about this productRelated genes to: ECM1 Antibody (Antigen Affinity Purified)
- Gene:
- ECM1 NIH gene
- Name:
- extracellular matrix protein 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-09-19
- Date modifiied:
- 2016-10-05
Related products to: ECM1 Antibody (Antigen Affinity Purified)
Related articles to: ECM1 Antibody (Antigen Affinity Purified)
- : A pterygium is a fibrovascular ocular surface lesion whose recurrence after surgical excision remains a major clinical challenge, yet its molecular determinants of recurrence remain poorly understood. This study investigated transcriptomic profiles of primary pterygium tissue collected at the time of surgery to identify molecular signatures associated with subsequent recurrence. : Eighty-five patients undergoing primary pterygium surgery were enrolled and followed for a mean of 7.32 years. RNA sequencing was performed on primary pterygium tissues collected at the time of surgery. Samples from four pterygia that developed recurrence and four non-recurrent pterygia were studied, with differential expression analyzed using DESeq2 and pathway enrichment via Reactome and GSEA. : Recurrence occurred in 5.8% of patients (mean time to recurrence was 8.87 months), exclusively in higher-grade (T2-T3) lesions. Transcriptomic analysis identified 1374 differentially expressed genes (1020 upregulated, 354 downregulated), showing separation between pterygia that developed recurrence from non-recurrent samples. Upregulated genes, including ECM1, HOXB5, MARCO, SHISAL1, CWH43, and PSORS1C1, reflected extracellular matrix remodeling and innate immune pathways, whereas downregulated genes, such as LCN10, ZBTB16, and GPR101, were linked to GPCR signaling and neuronal communication. Samples with the earliest recurrence displayed the most pronounced transcriptomic changes. : These findings suggest that extracellular matrix remodeling and innate immunity activation, already present at initial surgery, are associated with subsequent pterygium recurrence and may help in the identification of candidate molecular biomarkers for recurrence risk stratification. - Source: PubMed
Publication date: 2026/09/18
Simunovic Martina ParadzikDegoricija MarinaKorac-Prlic JelenaSimunovic MarkoLesin MladenStanic RobertPuljak LiviaOlujic IvanaMarin Lovric JosipaVucinovic AnaLjubic ZanaBucan KajoTerzić Janoš - Endometrial dysfunction in women with polycystic ovary syndrome (PCOS) significantly contributes to adverse pregnancy outcomes, including recurrent implantation failure and high miscarriage rates. However, the specific roles of individual cell types in this dysfunction, particularly in non-obese and obese PCOS patients, remain unclear. - Source: PubMed
Publication date: 2026/09/03
Wang QiaolingZhi YunqingXie HuiliangLang JingwenYang WanliLiang AjuanZhu XiuxianFu Yonglun - This study aimed to explore the potential of atorvastatin as an adjuvant on endothelial inflammation, vascular function, and the tumor microenvironment in diabetic pancreatic cancer. - Source: PubMed
Li LuHe YongTian PeikaiChen JinxinGong XunLi Xiaowu - Lipoid proteinosis (LP), or Urbach-Wiethe disease, is a rare autosomal recessive disorder caused by pathogenic variants in ECM1. Early-onset hoarseness and moniliform blepharosis are characteristic, but diagnosis may be delayed when early airway findings are nonspecific or the mucocutaneous features are not considered together. - Source: PubMed
Publication date: 2026/08/21
Hu LiyeXu YingmeiZhao Weijia - N-methyladenosine (mA) plays a critical role in osteoarthritis (OA) pathogenesis. This study investigates the role of the mA reader insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) in OA progression. OA models were established in vivo through destabilization of the medial meniscus (DMM) surgery in mice and in vitro by stimulating primary chondrocytes with interleukin-1β (IL-1β). Cartilage destruction was assessed histopathologically. Chondrocyte viability, proliferation, and apoptosis were measured by CCK-8, EdU, and flow cytometry, respectively. Inflammatory cytokine levels, lactate, glucose, and total mA were quantified using commercial kits. Expression levels of IGF2BP3, extracellular matrix protein 1 (ECM1), ECM turnover markers, and glycolysis-related genes were analyzed by RT-qPCR, Western blot, immunohistochemistry, and immunofluorescence. Potential mA modification sites in ECM1 transcripts were predicted using the SRAMP database, and IGF2BP3-mediated, mA-dependent regulation of ECM1 was validated through RNA immunoprecipitation (RIP), MeRIP-qPCR, and actinomycin D decay assays. Results revealed elevated levels of IGF2BP3, ECM1, mA modification, and glycolytic activity in OA cartilage and IL-1β-treated chondrocytes. IGF2BP3 knockdown reversed IL-1β-induced reductions in chondrocyte viability and proliferation, suppressed apoptosis, decreased inflammatory cytokine secretion, attenuated ECM degradation, and reduced glycolytic flux in vitro, while also mitigating cartilage damage and matrix breakdown in vivo. Mechanistically, IGF2BP3 stabilized ECM1 mRNA in an mA-dependent manner, thereby modulating ECM1 expression. Restoration of ECM1 expression abolished the chondroprotective effects of IGF2BP3 knockdown against injury, inflammation, and enhanced glycolysis. In conclusion, IGF2BP3 enhances ECM1 expression via an mA-dependent pathway, thereby promoting glycolysis and exacerbating OA progression. - Source: PubMed
Publication date: 2026/08/19
Yuan Xing-ShiZhang Hao-JieDing Jia-XiangLuo Zheng-LiangChen MinZhang Xiao-QiShang Xi-FuNi ZheWu Ke-Rong