Protein Tob1 Protéines (TOB1)

Mouse (Murine) Protein Tob1 (TOB1) interaction partners

1. Immune cell-specific transcriptional profiling highlights distinct molecular pathways controlled by Tob1 upon experimental autoimmune encephalomyelitis.

2. MiR-26a exerts its effect by directly targeting Tob1, the negative regulator of BMP/Smad signaling pathway by binding to the 3'-untranslated region and thus repressing Tob1 protein expression

3. Collectively, our data support a model of CNOT7, TOB1, CNOT1, and RNA-binding proteins collectively exerting post-transcriptional control on a metastasis suppressive transcriptional program to drive tumor cell metastasis

4. Nfatc2 and Tob1 have non-overlapping function in T cell negative regulation and tumorigenesis.

5. Tob1(-/-), Tob2(-/-), and Tob1/2 double knockout (DKO, Tob1(-/-) & Tob2(-/-)) embryonic stem cells (ESCs) grew faster than wild type (WT) ESCs without losing pluripotency.

6. The expression of Tob1 was significantly increased at day 6 during C2C12 differentiation time, suggesting a possible role in skeletal muscle development.

7. Experimental autoimmune encephalomyelitis in Tob1-eficient mice is associated with augmented central nervous system inflammation, increased infiltrating CD4+ and CD8+ T cell counts, and increased myelin-reactive Th1 and Th17 cells

8. Tob1 is a crucial check point molecule that modulates the expression and activity of cell cycle proteins.

9. Phosphorylation of three regulatory serines of Tob by Erk1 and Erk2 is required for Ras-mediated cell proliferation and transformation

10. deficiency prevents ovariectomy-induced bone loss through the superenhancement of osteoblastic activities in bone and that this results in further augmentation in the bone formation rate and the mineral apposition rate after ovariectomy in vivo

11. regulation of nuclear localization of Tob is important for its antiproliferative activity

12. KLF2 and TOB1 activate the mouse Dpp2 promoter.

Human Protein Tob1 (TOB1) interaction partners

1. MiR-590 targets Tob1 that is significantly decreased in patients with multiple sclerosis.

2. The dual-luciferase reporter assay also confirmed that miR-25 harbored the A allele which caused an incapacitation of binding at the TOB1. In conclusion, rs41274221 in miR-25 was a subgroup which may protect the patients from further growth and metastasis of gastric cancer and might serve as a novel biomarker for the disease

3. A novel role for TOB1 in mediating survival of estrogen-independent breast cancers.

4. Reduced TOB1 expression in gastric adenocarcinoma is associated with the extent of differentiation and the TNM stage of gastric cancer.

5. miR-25 promotes GC progression by directly downregulating TOB1 expression, and may be a noninvasive biomarker for the prognosis of GC patients.

6. arsenite-induced oxidative stress inhibits deadenylation of mRNA primarily through downregulation of Tob and Pan3, both of which mediate the recruitment of deadenylases to mRNA

7. Tob is a key factor in the regulation of c-myc gene expression, which is essential for cell growth.

8. TOB1 demonstrated a radioprotective function in the immortalized normal human bronchial epithelial cell line.

9. TOB1 modulates the radiosensitivity of lung cancer cells via the MAPK/ERK signaling pathway.

10. Cdc7 phosphorylates and interacts with Tob to inhibit the Cul4-DDB1(Cdt2)-dependent Tob degradation.

11. study demonstrates that the overexpression of Tob1 inhibits gastric cancer progression by activating Smad4- and inhibiting betacatenin-mediated signaling pathways

12. TOB1 overexpression not only increased the expression of the phosphatase and tensin homolog (PTEN), an important tumor suppressor, but also regulated the downstream effectors in the PI3K/PTEN signaling pathway, including Akt, ERK1/2, etc.

13. The antiproliferative and the mRNA deadenylation/decay-promoting effects of TOB1 and TOB2 proteins are linked.

14. Silencing of HIC1 and TOB1 expression is a common occurrence in gastric cancer and may contribute to the development and progression of the disease.

15. Longer survival was associated with hypomethylation at specific CpG sites (e.g. GREB1, TGIF and TOB1) and hypermethylation in other genes (e.g. TMCO5, PTPRN and GUCY2C).

16. Together, these results indicate that Tob mediates the recruitment of Caf1 to the target of CPEB3 and elicits deadenylation and decay of the mRNA.

17. Tob interactions with Caf1 and a C-terminal domain of PABPC1

18. functions as lateral signal transmitter

19. Antiproliferative proteins of the BTG/Tob family are degraded by the ubiquitin-proteasome system. the C-terminal regions are necessary and sufficient to control the stabilities of BTG1, BTG2, Tob, and Tob2 proteins.

20. identified as a MAPK substrate