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Regulation and destabilization of HIF-1alpha by ARD1-mediated acetylation.
TLDR
The role of ARD1 in the acetylation of HIF-1alpha provides a key regulatory mechanism underlying Hif-1 alpha stability, and is critical to proteasomal degradation.
Primary and Essential Role of the Adaptor Protein APS for Recruitment of Both c-Cbl and Its Associated Protein CAP in Insulin Signaling*
TLDR
Results indicate that APS plays a central role in recruiting both CAP and c-Cbl to the insulin receptor after insulin stimulation and is necessary and sufficient for the insulin-stimulated phosphorylation of c- Cbl, whereas SH2-Bα may provide an alternative pathway for the recruitment of CAP.
Jab1 interacts directly with HIF-1alpha and regulates its stability.
TLDR
Jab1 should be considered as a novel regulator of HIF-1alpha stability via direct interaction, and the binding of Hif-1 alpha and p53 tumor suppressor protein was interfered in a Jab1-dependent manner.
Negative regulation of hypoxia inducible factor-1alpha by necdin.
TLDR
It is suggested that necdin can be a novel negative regulator of HIF-1alpha stability via the direct interaction, and has an anti-angiogenic activity in the tube formation assay and CAM assay, which might be due to the downregulation of Hif-1 alpha.
Evaluation of liver and thyroid toxicity in Sprague-Dawley rats after exposure to polybrominated diphenyl ether BDE-209.
TLDR
It is demonstrated that BDE-209 induces hyperthyroidism and hepatotoxicity in male rats, and further research is needed to determine the relationship between target organ toxicity and blood concentrations of Bde-209.
Jab1 Interacts Directly with HIF-1α and Regulates Its Stability*
TLDR
Jab1 should be considered as a novel regulator of HIF-1α stability via direct interaction, as it led to increase the expression of VEGF, a major Hif-1 target gene.
Effect of di(n‐butyl) phthalate on testicular oxidative damage and antioxidant enzymes in hyperthyroid rats
TLDR
It is suggested that hyperthyroidism can cause a change in the expression level of PPAR‐r in testes, and may increase the levels of oxidative damage induced by the metabolic activation of DBP.
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