anti-S100 Calcium Binding Protein A4 (S100A4) Anticorps

Human S100 Calcium Binding Protein A4 (S100A4) interaction partners

1. this study demonstrates that metastasized cells are less migratory due in part to the post-metastatic downregulation of S100A4 and GRM3. Targeting S100A4 and GRM3 may help prevent bone metastasis.

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

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

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

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

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

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

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

9. 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

10. 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.

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

12. 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.

13. 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.

14. 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.

15. 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

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

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

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

19. 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.

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

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

1. FSP1-expressiing fibroblasts maintain preadipocyte pool via PDGF signaling and regulate adipose homeostasis.

2. Data suggest that S100 calcium binding protein A4 protein (S100A4) is a potential candidate for the treatment of diet-induced obesity and its complications.

3. this study shows that S100A4 protects myeloid-derived suppressor cells from intrinsic apoptosis via TLR4-ERK1/2 signaling

4. The role of renal Smad2 in the development of tubulointerstitial fibrosis and epithelial-to-mesenchymal transition during streptozotocin-induced diabetic nephropathy by using a fibroblast-specific protein 1 (FSP1)-promotor-driven SMAD2 knockout mouse model, is reported.

5. S100A4 is a critical regulator of macrophage cell matrix degradation, whose actions converge on the dynamics and degradative functions of podosome rosettes.

6. S100A4 expression in liver and its association with stem cell-like phenotype of the hepatocellular carcinoma.

7. Studied the role of S100A4 on the proliferation of MB49 bladder cancer stem cells (MSCSs) and MB49 cells. Found S100A4 was significantly up-regulated in MCSCs and led to increased cell proliferation and an increase in NF-kappaB, IKK, IL-2 and TNF; whereas knock-down of S100A4 reversed such effect.

8. 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.

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

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

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

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

13. 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.

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

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

16. 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

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

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

19. 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.

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