anti-Sprouty-Related, EVH1 Domain Containing 2 (SPRED2) Antibodies

Zebrafish Sprouty-Related, EVH1 Domain Containing 2 (SPRED2) interaction partners

1. The present study demonstrates the possible role of Spred-2 signalling in cell proliferative phase during the neural repair in the injured zebrafish brain

Human Sprouty-Related, EVH1 Domain Containing 2 (SPRED2) interaction partners

1. Our findings show that miR-487a, mediated by heat shock factor 1, promotes proliferation and metastasis of Hepatocellular carcinoma (HCC) by PIK3R1 and SPRED2 binding, respectively. Our study provides a rationale for developing miR-487a as a potential prognostic marker or a potential therapeutic target against HCC.

2. data indicate that Spred2 induces tumor cell death in an autophagy-dependent manner.

3. Cosuppression of Sprouty and Sprouty-related negative regulators of FGF signalling in prostate cancer

4. Spred2 was involved in erythroid differentiation of chronic myeloid leukemia cells and participated in imatinib induced erythroid differentiation partly through ERK signaling.

5. Downregulation of SPRED2 mRNA is associated with prostate cancer.

6. Data present that galectin-1, ataxin-3 and sprouty-related EVH1 domain-containing protein 2 (SPRED2) may be associated with the progression and development of Down syndrome.

7. Tyrosines 303/343/353 within the Sprouty-related domain of Spred2 are essential for its interaction with the p85 subunit of phosphatidylinositol 3-kinase.

8. the knockdown of Spred2 markedly enhanced tumor growth in vivo.

9. Sprouty and Spred proteins are negative regulators of the ERK/Elk-1 pathway activation induced not only by growth-factors, but also by reactive lipidic mediators.

10. data in the present study suggests that Spred2 is a regulator of TGF-beta1-induced malignance in transformed keratinocytes

11. NMR assignment of the human Spred2 EVH1 domain

12. Spred-2 was found to be strongly expressed in glandular epithelia and, at the subcellular level, its immunoreactivity was associated with secretory vesicles. It becomes most likely that Spred-2 is involved in the regulation of secretory pathways

13. We show here that Spred-1 and Spred-2 appear to have distinct mechanisms whereby they induce their effects, as the Sprouty domain of Spred-1 is not required to block MAPK (mitogen-activated protein kinase) activation, while that of Spred-2 is required.

14. Loss of Spred-2 inhibits bone growth in transgenic mice by inhibiting chondrocyte differentiation through up-regulation of the MAPK signaling pathway.

15. reduction of Spred expression in hepatocellular carcinoma (HCC) is one of the causes of the acquisition of malignant features. Thus, Spred could be not only a novel prognostic factor but also a new therapeutic target for human HCC

16. These results suggest a role for Spred-2 tyrosine phosphorylation and ubiquitination in controlling Spred-2 expression levels.

17. Linkage analysis of SPRED2 excluded its involvement in Cafe-au-lait spots in a patient with a severe form of Noonan syndrome.

18. findings suggest a critical function for NBR1 in the regulation of receptor trafficking and provide a mechanism for down-regulation of signaling by Spred2 via NBR1.

Mouse (Murine) Sprouty-Related, EVH1 Domain Containing 2 (SPRED2) interaction partners

1. Spred2-/- mice developed severer acute liver injury with increased levels of TNFalpha and IL-1beta in the livers.

2. It is a known inhibitor of ERK1/2 signaling, which influences the severity of lung ischemia reperfusion injury.

3. Spred2 plays an important role in the regulation of colonic epithelial cell proliferation and inflammation by potentially down-regulating the activation of ERK.

4. Cosuppression of Sprouty and Sprouty-related negative regulators of FGF signalling in prostate cancer

5. SPREDs promote self-renewal and inhibit mesodermal differentiation of murine ES cells by selective suppression of the ERK/MAPK signaling pathway in pluripotent cells

6. Spred-2 controls the development of lipopolysaccharide-induced lung inflammation.

7. Spred-2 negatively regulates APAP-hepatotoxicity under the control of Kupffer cells and NK cells.

8. Identification of SPRED2 (sprouty-related protein with EVH1 domain 2) as a negative regulator of the hypothalamic-pituitary-adrenal axis.

9. Data show that both SPRED1 and SPRED2 inhibit the ability of DYRK1A to phosphorylate its substrates.

10. SPRED2 is likely involved in the regulation of dynamic developmental processes.

11. Spred-2 functions as a negative regulator of aorta-gonad-mesonephros hematopoiesis by inhibiting hematopoietic cytokine signaling.

12. These data suggest that Spreds are key regulators of RhoA-mediated cell motility and signal transduction. Furthermore, our study suggests that the induction of Spreds could be a novel strategy for preventing cancer cell metastasis.

13. Spred-1 and Spred-2 were found to be expressed predominantly in brain. It becomes most likely that Spred-2 is involved in the regulation of secretory pathways

14. We show here that Spred-1 and Spred-2 appear to have distinct mechanisms whereby they induce their effects, as the Sprouty domain of Spred-1 is not required to block MAPK (mitogen-activated protein kinase) activation, while that of Spred-2 is required.

15. Spred2 is essential for embryonic lymphangiogenesis by regulating VEGFR3 signaling.

16. findings suggest a critical function for NBR1 in the regulation of receptor trafficking and provide a mechanism for down-regulation of signaling by Spred2 via NBR1.