anti-Spondin 2 (SPON2) Antibodies

Human Spondin 2 (SPON2) interaction partners

1. High SPON2 expression is associated with hepatocellular carcinoma.

2. Matricellular protein SPON2 acts as an HCC suppressor and utilizes distinct signaling events to perform dual functions in HCC microenvironment

3. spondin-2 might be a novel therapeutic target and prognostic biomarker for squamous cell carcinoma patients

4. Egr-1 regulates mindin expression by directly binding to the mindin promoter; mindin suppresses colon cancer progression by blocking angiogenesis.

5. Spondin-2 overexpression contributes to tumor aggressiveness and prognosis in gastric cancer.

6. SPON2 is a transcriptional target of the metastasis gene MACC1. SPON2 induces cell motility in vitro and CRC metastasis in mice. In patients, SPON2 serves as prognostic indicator for CRC metastasis and survival, and might represent a promising target for therapeutic approaches.

7. Data suggest that spondin-2 could be an independent diagnostic and prognostic biomarker of colon cancer.

8. Mindin protects against vascular hyperplasia by suppression of abnormal VSMC proliferation, migration and phenotypic switching in an AKT-dependent manner.

9. Using tissue microarray by immunohistostaining, we found SPON2 to be over-expressed in prostate cancer (PCa). SPON2 staining was more intense in Gleason score sum 7-8 and in PCa patients with metastasis.

10. mindin serves as a novel mediator that protects against cardiac hypertrophy and the transition to heart failure by blocking AKT/GSK3beta and TGF-beta1-Smad signalling.

11. High Mindin is associated with diabetic nephropathy in type 2 diabetes.

12. Spondin 2, which is regulated by T(3), has an important role in cell invasion, cell migration, and hepatoma tumor progression.

13. The structure of the F-spondin domain of mindin was determined at 1.8-A resolution.

Mouse (Murine) Spondin 2 (SPON2) interaction partners

1. Mindin is a novel modulator of hepatic I/R injury through regulating inflammatory responses, as well as hepatocyte apoptosis and proliferation via inactivation of the Akt signaling pathway.

2. Mindin protects against vascular hyperplasia by suppression of abnormal VSMC proliferation, migration and phenotypic switching in an AKT-dependent manner.

3. Spondin 2 regulates hepatic lipid metabolism and alleviates hepatic steatosis, obesity, inflammation, and insulin resistance via its interaction with PPARalpha.

4. The data of this study demonstrated that mindin is a critical mediator of ischemic brain injury in an experimental stroke model.

5. Data show that mindin, as an intrinsic cardioprotective factor, prevents maladaptive remodelling and the transition to heart failure by blocking AKT/GSK3beta signalling.

6. Mindin expression is upregulated during intestinal inflammation and may induce NF-kappaBp65 promoter activation in a TLR-9 mediated manner.

7. Mindin is a pattern-recognition molecule for microbial pathogens.

8. Mindin-integrin interactions play a key role in regulating Rho GTPase expression in DCs and DC priming of T lymphocytes.

9. mindin plays an essential role in the host innate immune response to influenza virus infection and suggest that mindin may be used as an immune-enhancing agent in influenza infection.

10. mindin participates in integrin-dependent trafficking of eosinophils and can contribute to the severity of allergic airways disease.

11. The structure of the F-spondin domain of mindin was determined at 1.8-A resolution.