S100 Calcium Binding Protein A4 (S100A4) ELISA Kits

Human S100 Calcium Binding Protein A4 (S100A4) interaction partners

1. ERRgamma may exert oncogenic activity mainly associated with aggressiveness of EC by activating S100A4 transcription.

2. S100A4 expression is induced by the TGF-beta pathway,.

3. This meta-analysis showed that overexpression of S100A4 seems to be associated with tumor progression and poor prognosis of PC patients.

4. clusterin promotes growth and invasion in renal cell carcinoma cells in vitro and in vivo through upregulation of S100A4

5. miR-3189-3p mimics enhanced the effects of the S100A4 siRNA on the inhibition of gastric cancer cell proliferation and migration by targeting CFL2.

6. Urine S100A4 shows the most promise as an lupus nephritis (LN) activity biomarker.

7. S100A4 is up-regulated in cervical adenocarcinomas and squamous cell carcinomas.

8. Network analysis of overlapping genes revealed the effects on tubulins (Tubb2a, Tubb3, Tubb4b), Nfe2l2, S100a4, Cd44, and Nfkb2, all of which are linked to TBI-relevant outcomes, including epileptogenesis and tissue repair

9. Authors first provide experimental evidence suggesting that FAM107B was downregulated by S100A4 in gastric cancer MGC803 cells. And FAM107B at least partially mediates the biological effect of S100A4 in the cells.

10. MiR-187 could interact with S100A4 3'-UTR.

11. Both the calcium-binding ability and the C-terminal region of S100A4 are important for cancer initiatin cells to sustain their stemness properties and malignancy in head and neck cancers.

12. Studied the role and expression of MIR296 in the metastasis and epithelial-mesenchymal transition of colorectal cancer. Found MIR296 inhibited migration and invasion of tumor cells, as well as suppressed S100A4 abundance in tumor cells.

13. S100A4-expression was associated with poor outcome in early-stage breast cancer, but the low percentage of positive tumors and the modest survival differences imply that the clinical utility in selection of patients for adjuvant treatment is limited.

14. The relative expression of S100A4 mRNA was higher when mod-SHEM was used, although significant differences were detected only when the expression levels were compared with those found in LPCs incubated with IOBA-FBS

15. High S100A4 expression is associated with Mesenchymal Transition in Glioblastoma.

16. our findings demonstrate that S100A4 is post-transcriptionally regulated by tumor suppressor microRNAs

17. findings indicate that Idiopathic pulmonary fibrosis mesenchymal progenitor cells are intrinsically fibrogenic and that S100A4 confers mesenchymal progenitor cells with fibrogenicity.

18. S100a4 is expressed in a limited number of stromal cells throughout the colon. S100A4 was mainly localised in the colorectal tumour-associated stroma, it was also detectable in a limited number of epithelial tumour cells.

19. our results suggest the existence of evolutionarily conserved pathways used by S100A4 to promote metastatic dissemination

20. miR-187-3p inhibits the migration/metastasis and epithelial mesenchymal transition in hepatocellular carcinoma by targeting S100A4 expression.

Mouse (Murine) S100 Calcium Binding Protein A4 (S100A4) interaction partners

1. S100A4 knockout alone inhibits ATC cells (rich endogenous S100A4) survival and invasion, regardless of the BRAFV600E status, and potentiates the effect of vemurafenib on tumor regression in vitro and in vivo.

2. Knockdown of S100A4 significantly reduced cardiac fibrosis and beta-catenin levels.

3. The Smad3 and Bmal1 regulate p21 and S100A4 expression in myocardial stromal fibroblasts through TNF-alpha.

4. High S100A4 expression is associated with Mesenchymal Transition in Glioblastoma.

5. findings indicate that Idiopathic pulmonary fibrosis mesenchymal progenitor cells are intrinsically fibrogenic and that S100A4 confers mesenchymal progenitor cells with fibrogenicity.

6. Data provide the first report on the in vivo role of S100a4 in intestinal tumourigenesis and describe a new role for S100a4 in the aetiology of desmoids formation.

7. S100A4 expression protects cardiac myocytes against myocardial ischemia and is required for stabilization of cardiac function after MI.

8. These findings provide further evidence on extracellular S100A4 as paracrine mediator of prometastatic endothelial dysfunction involving its interaction with RAGE.

9. this study has demonstrated a crucial role for retinoic acid in promoting IL-22 production and tempering dendritic cell function through downregulating S100A4 protein during viral hepatitis

10. Extracellular S100A4 is important for the regulation of bone formation by activating the NF-kappaB signaling pathway in osteoblasts.

11. Interaction of extracellular S100A4 with RAGE prompts prometastatic activation of melanoma cells.

12. Our results indicated that RNV was ameliorated by Ad-S100A4-RNAi transfer in a mouse model of OIR through mediation of the anti-apoptotic effect of Bcl-2 by reducing the expression of CREB.

13. The thymic CD45-FSP1+ cells are a subpopulation of fibroblasts, which is crucial for the maintenance and regeneration of thymic epithelial cells.

14. Enhanced S100A4 expression was observed in remodeled intrapulmonary arteries of mice with smoke-induced emphysema.

15. Downregulation of AKT3 increases migration and metastasis in triple negative breast cancer cells by upregulating S100A4.

16. S100A4 promotes liver fibrosis by activating HSCs, which may represent a potential target for anti-fibrotic therapies.

17. The S100A4 blocking antibody (6B12) reduces tumor growth and metastasis in a model of spontaneous breast cancer.

18. Functional studies of human TH2 cells as well as mouse models of allergy showed that deletion of one of the genes, S100A4, resulted in decreased signs of allergy.

19. S100A4 in endothelial cells is involved in tube formation, and suggest its potential as a molecular target for inhibiting tumor angiogenesis

20. S100A4 is overexpressed in an experimental head and neck squamous cell carcinoma, and its inhibition reduces tumor burden.