Extracellular Matrix Protein 1 (ECM1) ELISA Kits

Human Extracellular Matrix Protein 1 (ECM1) interaction partners

1. Extracellular matrix protein 1 (ECM1) interacted with moesin (MSN) and recruited it adjacent to the membrane in order to promote MSN membrane translocation and phosphorylation, which facilitated invadopodia formation by breast cancer cells.

2. Herein we report ocular manifestations of lipoid proteinosis due to a genetic mutation in ECM1 gene.

3. High ECM1 expression is associated with gastric cancer metastasis.

4. These observations are consistent with a model in which the loss of Dkk-3 in prostate cancer leads to increased secretion of TGFBI and ECM-1, which have tumor-promoting and tumor-protective roles, respectively

5. The results showed a significant upregulation of ECM1 and ITGB3, and a significant downregulation for FBLN5 in pelvic organ prolapse patients.

6. Three patients with homozygous mutations in sixth and seventh exons of the ECM1 gene had a drug-resistant course at the end of long-term follow-up

7. This proteome analysis indicate that ECM1 is a potential novel plasma protein biomarker for the detection of primary ESCC and evaluation of neoplasms progression

8. The TT genotype of ECM1 gene rs3737240 SNP significantly increased susceptibility for Ulcerative Colitis and azathioprine use in Ulcerative Colitis patients in a Turkish population.

9. our work has identified a novel function of ECM1 in inhibiting Th17 cell differentiation in the experimental autoimmune encephalomyelitis model

10. Our results indicate that although mutation in ECM1gene is responsible for lipoid proteinosis, it is likely that this is not the only gene causing this disease and probably other genes may be involved in the pathogenesis of the LP disease.

11. ECM1, which displayed a high expression in hepatocellular carcinoma (HCC) specimens, was closely associated with clinicopathologic data and may promote migration and invasion of HCC cells by inducing epithelia-mesenchymal transition.

12. Cell invasion (matrigel) was reduced only in the Hs578T cells (p < 0.01). Silencing decreased the expression of the prometastatic molecules S100A4 and TGFbetaR2 in both cell lines and CD44 in Hs578T cells. We conclude that ECM1 is a key player in the metastatic process and regulates the actin cytoskeletal architecture of aggressive breast cancer cells at least in part via alterations in S100A4 and Rho A.

13. Overexpression of miR-486-3p inhibited cell growth and metastasis by targeting ECM1.

14. For 1q21 loci, we confirmed gene ECM1 as the most plausible gene from this region to be involved in pathogenesis of inflammatory bowel disease

15. In conclusion, the domain-specific anti-ECM1 MAbs produced in this study should provide a useful tool for investigating ECM1's biological functions, and cellular pathways in which it is involved.

16. Lipoid proteinosis is a rare autosomal recessive disorder caused by mutations in ECM1, encoding extracellular matrix protein 1, a glycoprotein expressed in many organs and which has important protein-protein interactions in tissue homeostasis

17. MMP-2 protein and ECM1 gene are useful preoperative markers for defining malignancy in suspicious thyroid nodules

18. association between beta-catenin and the MUC1 cytoplasmic tail was increased by ECM1

19. Genetic testing of theECM1 gene showed a homozygous nonsense mutation c.1441C > T (p.Arg481X) in exon 10, confirming the diagnosis of lipoid proteinosis.

20. Lipoidproteinosis results from a large homozygous deletion of ECM1 gene in a Chinese family.

Mouse (Murine) Extracellular Matrix Protein 1 (ECM1) interaction partners

1. data identify ECM1 as a soluble protein to promote TFH cell differentiation and antibody production.

2. ECM1 seems to be critical for PTHrP action in chondrogenesis, as blockage of ECM1 nearly abolishes PTHrP regulation of chondrocyte hypertrophy, and overexpression of ECM1 rescues disorganized growth plates of PTHrP-null mice; ECM1 and progranulin chondrogenic growth factor constitute an interaction network.

3. HA accumulation primes the vasculature for atherosclerosis by crosslinking and reorganizing the extracellular matrix (ECM) and by pushing VSMC differentiation towards a less mature phenotype.

4. Retinoid signaling in the stroma activates expression of Ecm1, which in turn down-regulates Ret expression in the ureteric bud cleft, where bifurcation normally occurs and normal branching progresses.

5. regulates TH2 cell egress from lymph nodes during allergic airway inflammation