Polyclonal Rabbit EFEMP1 Antibody
- Known as:
- Polyclonal Rabbit EFEMP1 Antibody
- Catalog number:
- KA1140
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit EFEMP1 Antibody
Related genes to: Polyclonal Rabbit EFEMP1 Antibody
- Gene:
- EFEMP1 NIH gene
- Name:
- EGF containing fibulin extracellular matrix protein 1
- Previous symbol:
- DHRD, FBNL
- Synonyms:
- S1-5, FBLN3, MTLV
- Chromosome:
- 2p16.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-30
- Date modifiied:
- 2017-10-12
Related products to: Polyclonal Rabbit EFEMP1 Antibody
Related articles to: Polyclonal Rabbit EFEMP1 Antibody
- Truncating mutations in the tumor suppressor , which encodes a component of the cohesin complex, are prevalent across diverse human cancers. Here, we report that acute reconstitution of physiological STAG2 levels in -mutant human glioblastoma multiforme cancer cells triggers a rapid reduction in the size of chromatin loops genome-wide. Despite this global change in chromatin loop size, early transcriptional responses to STAG2 restoration are limited to a small number of genes, most of which are induced by STAG2 reconstitution. Notably, the growth-suppressor EFEMP1 (Fibulin-3), a secreted glycoprotein that functions as an extracellular matrix-associated inhibitor of glioblastoma growth and invasion, was the only gene consistently induced across all experimental models. The most robust and conserved STAG2-induced genes all reside within intense chromatin loops whose anchors and overall intensity did not appear to change in response to STAG2 reconstitution. These findings suggest that inactivating mutations of STAG2 promote neoplastic transformation by alleviating a restriction on chromatin loop size, allowing for an expanded range of chromatin interactions that disrupts the maintenance of a tumor-suppressive transcriptome. - Source: PubMed
Publication date: 2026/05/29
Yang TianyiKim Jung-SikMellows ClaraXu WanyingYa AlvinSadzewicz LisaTallon LukeSarkaria JannJin FulaiWaldman Todd - Despite its strong regenerative capacity, liver aging paradoxically increases susceptibility to fibrosis and metabolic dysfunction-associated steatotic liver disease through dysregulated inflammation, senescence-associated secretory phenotypes, and immune-metabolic crosstalk. To systematically characterize these processes, we integrated longitudinal transcriptomics, single-cell RNA sequencing, and machine-learning approaches. We identified 252 aging-associated genes and developed an Aging Gene Score (AGS) to quantify senescence burden across hepatic cell populations. Single-cell analysis revealed macrophages as key drivers of fibrosis progression, with high-AGS myeloid subsets markedly expanded in cirrhotic livers. Using combined Boruta and LASSO algorithms, we established a five-gene biomarker panel (EFEMP1, LUM, DKK3, GPRC5B, NCAM2) that accurately predicts advanced fibrosis (AUC > 0.77). Furthermore, a network pharmacology framework was applied to screen medicine-food homology (MFH) herbs, identifying Fagopyrum dibotrys (Jinqiaomai) and Astragalus membranaceus (Huangqi) as top candidates. Molecular docking demonstrated strong binding between the bioactive compound MOL000098 and the fibrosis-related target COL3A1. Functional assays showed that Jinqiaomai-containing serum alleviates oxidative stress, improves HepG2 cell viability, reduces ALT and AST levels, and suppresses macrophage lipid accumulation, accompanied by reduced expression of inflammatory and fibrosis-related markers. Collectively, our findings highlight macrophage-centered mechanisms linking liver aging and fibrosis and suggest MFH-derived compounds as promising anti-aging and anti-fibrotic dietary interventions. - Source: PubMed
Publication date: 2026/05/26
Xu YingqiLi MaohaoZhu LunLuo YawenSheng WanluJia PanleiSuo RinaBao Lidao - Metabolic dysfunction-associated steatotic liver disease (MASLD) affects about one-quarter of adults worldwide, and liver fibrosis is its strongest predictor of liver-related morbidity and mortality. Using combined in-silico screening and experimental evaluation, we aimed to identify circulating biomarkers associated with fibrosis progression. Fibulin-3 was identified, and its diagnostic performance was evaluated in biopsy-proven MASLD cohorts. - Source: PubMed
Publication date: 2026/04/20
Laraño Allen AnthonyPalmisano SilviaBonazza DeborahMarina DiscipioMeroni MaricaFracanzani Anna LudovicaCrocè Lory STiribelli ClaudioDongiovanni PaolaRosso NataliaGiraudi Pablo - Triple-negative breast cancer (TNBC) is characterised by high rates of chromosomal instability (CIN) and rewired intercellular communication driven by both soluble factors and extracellular vesicles (EVs). To assess how CIN might affect EV-mediated signalling in TNBC, we studied the EV landscape of TNBC cell lines with induced CIN. We find that CIN leads to increased secretion of EVs and that these EVs promote cell migration of recipient cells. EVs are enriched for extracellular matrix (ECM) proteins, including EFEMP1. Indeed, modulation of EFEMP1 levels in EVs significantly alters migration behaviour of EV-treated cells. We show that EFEMP1 expression is regulated by STAT1, that EVs from STAT1-deficient cells no longer promote migration, and that this can be rescued by overexpression of EFEMP1 in STAT1-null cells. Xenografting TNBC cells with EFEMP1-enriched cells promotes migration in zebrafish embryos, suggesting that EFEMP1 expression is a factor that promotes metastasis. Together, our results identify a CIN-associated EV program in triple-negative breast cancer and highlight EFEMP1 as a potential therapeutic target to impair EV-driven tumour cell migration. - Source: PubMed
Publication date: 2026/04/13
Zheng SiqiTian RuifangSiburian MarsudiHaider Rubio AnnaLiu YuanyuanWardenaar ReneShirzai MarjanKempe LauraDijkstra EmmaWarszawik ElizaSuarez Peredo Rodriguez MariaSjollema KlaasBakker Petra LRijn Patrick vanBorghesan MichaelaParidaen Judith TmlSantaguida StefanoFoijer Floris - To study the clinical, genetic, and phenotypic aspects of Malattia Leventinese (ML)/Doyne honeycomb retinal dystrophy (DHRD) and to differentiate it from age-related macular degeneration (AMD). - Source: PubMed
Shakeel AreebaBhatt DarshanSripriya SarangapaniRatra Dhanashree