By Juliette Adjo Aka, Go-Woon Kim (auth.), Tso-Pang Yao, Edward Seto (eds.)
The booklet highlights paintings from many alternative labs that taught us irregular HDACs in all probability give a contribution to the improvement or development of many human ailments together with immune dysfunctions, middle illness, melanoma, reminiscence impairment, getting older, and metabolic disorders.
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Additional resources for Histone Deacetylases: the Biology and Clinical Implication
Example text
In addition, HDAC1 and HDAC3 have been shown to interact with the ODDD domain of HIF-1a, providing a direct mechanism of regulation of HIF-1a stability and transcriptional activity by HDACs (Kim et al. 2007). HIF-1a functions are furthermore affected by the activities of individual class II HDACs. HDAC4 and HDAC6 associate with HIF-1a, thereby increasing its stability and transcriptional activity in a VHL-independent manner (Qian et al. 2006). HDAC7, another member of the class II HDAC family, was shown to translocate from cytoplasm to the nucleus to form a complex with HIF-1a and p300, which potentiates the transcriptional activity of HIF-1a (Kato et al.
2001). In addition, HDAC1 and HDAC3 have been shown to interact with the ODDD domain of HIF-1a, providing a direct mechanism of regulation of HIF-1a stability and transcriptional activity by HDACs (Kim et al. 2007). HIF-1a functions are furthermore affected by the activities of individual class II HDACs. HDAC4 and HDAC6 associate with HIF-1a, thereby increasing its stability and transcriptional activity in a VHL-independent manner (Qian et al. 2006). HDAC7, another member of the class II HDAC family, was shown to translocate from cytoplasm to the nucleus to form a complex with HIF-1a and p300, which potentiates the transcriptional activity of HIF-1a (Kato et al.
Conversely, SIRT1 was shown to play a crucial role in tumor suppression and DNA repair as SIRT1-deficient mice exhibit genome instability, impaired DNA damage response, and an increased rate of tumorigenesis (Wang et al. 2008). 4 Metastasis The ability to metastasize and spread is certainly the most deadly hallmark of cancer cells. Several metastasis repressors such as RECK (reversion-inducingcysteine-rich protein with Kazal motifs), Kangai 1, RhoB (Ras homologue gene family member B), and TIMP-1 (tissue inhibitor of metallo-proteinases-1) are induced in their expression in response to HDAC inhibitors suggesting a promoting role of HDACs for tumor metastasis (Ma et al.