Frequently Rearranged in Advanced T-Cell Lymphomas (FRAT1) Kits ELISA

Mouse (Murine) Frequently Rearranged in Advanced T-Cell Lymphomas (FRAT1) interaction partners

1. Gsk3b is exported from the nucleus in a complex with Frat. Loss of PI3K/Akt activity results in dissociation of this complex and retention of Gsk3b in the nucleus.

2. Data show that that Frat synergizes with Diversin in the activation of JNK/AP-1 signaling.

3. FRAT has a role in mediating GSK-3 nuclear export in mouse cells

4. Data suggest that recruitment of Axin and Frat1 to the membrane by LRP5-triggered Wnt3 signaling leads to both Axin degradation and Frat1-mediated inhibition of glycogen synthase kinase-3.

Human Frequently Rearranged in Advanced T-Cell Lymphomas (FRAT1) interaction partners

1. The results of the present study suggest that nuclear FRAT1 activates the Wnt/beta-catenin signaling pathway and confers an increase in prostate cancer cell growth.

2. These data suggest a potential role for targeting FRAT1 in the prevention of hypoxia-induced HCC cancer progression and metastasis mediated by epithelial-to-mesenchymal transition

3. FRAT1 and ABCG2 overexpression is associated with carcinogenesis, progression, and poor prognosis in patients with Pancreatic ductal adenocarcinoma.

4. Positive ROR2 and FRAT1 expression is associated with the progression and poor prognosis of chondrosarcoma.

5. FRAT1 overexpression correlates with pathologic grade, proliferation, invasion and angiogenesis in brain gliomas.

6. The mechanism of inhibiting beta-catenin phosphorylation involves the NDRG1-mediated upregulation of the GSK3beta-binding protein FRAT1.

7. These results highlight the potential role of FRAT1 in tumorigenesis and progression of glioblastoma.

8. The overexpression of Frat1 and beta-catenin was correlated with tumor differentiation, TNM stage, lymph node metastasis, and poor prognosis of NSCLC.

9. Down-regulation of Frat1 expression reduced invasive ability in A549 cell line, further supporting idea that Frat1 may play crucial role in carcinogenesis, tumor invasiveness and dissemination in human lung cancer.

10. Elevated expression of FRAT1 was associated with astrocytomas.

11. Our results suggest that FRAT1 may be an important factor in the tumorigenesis and progression of gliomas, and could be used as a potential molecular marker for pathological diagnosis and a target for biological therapy.

12. CKI epsilon-dependent phosphorylation of Dvl enhances the formation of a complex of Dvl-1 with Frat-1 and this complex leads to the activation of Wnt-3a-induced accumulation of beta-catenin

13. findings support that Wnt/beta-catenin signalling may be aberrantly activated through FRAT1 overexpression in ovarian serous adenocarcinomas

14. PKA phosphorylates FRAT1 in vitro as well as in intact cells and may play a role in regulating the inhibitory activity of FRAT1 toward GSK-3.

15. Aberrant activation of beta-catenin/TCF pathway in esophageal cancer appears to be due to upstream events such as FRAT1 overexpression, and c-Myc may be an important element in oncogenesis of human ESCC induced by FRAT1.