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Regulation and destabilization of HIF-1alpha by ARD1-mediated acetylation.
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.
Regulation and Destabilization of HIF-1α by ARD1-Mediated Acetylation
Primary and Essential Role of the Adaptor Protein APS for Recruitment of Both c-Cbl and Its Associated Protein CAP in Insulin Signaling*
- M. Ahn, K. D. Katsanakis, Farheen Bheda, T. S. Pillay
- Biology, MedicineJournal of Biological Chemistry
- 14 May 2004
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.
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.
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.
- E. Lee, Tae Hyung Kim, Hyung Sik Kim
- Medicine, BiologyThe Journal of toxicological sciences
- 1 August 2010
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*
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
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.
Histone deacetylase inhibitor, apicidin, inhibits human ovarian cancer cell migration via class II histone deacetylase 4 silencing.