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Results 1 - 10 of 26 > >>
EC Number
General Information
Commentary
Reference
malfunction
enzyme inactivation in cells leads to histone H3-Lys18 hyperacetylation and aberrant accumulation of pericentric transcripts
malfunction
enzyme knockout is associated with derepression of Oct4, Sox2 and Nanog, which in turn causes an upregulation of Tet enzymes and elevated production of 5-hydroxymethylcytosine
malfunction
inhibiting SIRT6 activity enhances anti-multiple myeloma activity of doxorubicin in vivo
malfunction
knock-down of SIRT6 does not sensitize bladder cancer cell lines to DNA damaging drugs
malfunction
SIRT6 deficiency causes major retinal transmission defects concomitant to changes in expression of glycolytic genes and glutamate receptors, as well as elevated levels of apoptosis in inner retina cells
malfunction
SIRT6 depletion in cardiac fibroblasts results in increased cell proliferation and extracellular matrix deposition as well as significantly higher expression of alpha-smooth muscle actin, the classical marker of myofibroblast differentiation, and increased formation of focal adhesions. Notably, SIRT6 depletion further exacerbates angiotensin II–induced myofibroblast differentiation
malfunction
SIRT6 loss suppresses proliferation and epidermal hyperplasia in mouse skin. Skin-specific deletion of SIRT6 in the mouse inhibits skin tumorigenesis
metabolism
cells overexpressing Sirt6 have a lower proliferation rate with a lower percentage of cells in mitosis, roles for Sirt6 in the nucleolus and in the mitotic phase of the cell cycle
metabolism
SIRT6 acts as a tumor suppressor in human glioma. SIRT6 binds to poly(C)-binding protein 2 (PCBP2) promoter region and deacetylates H3K9ac, resulting in transcription regression
metabolism
SIRT6 may play a role in synaptic function and neuronal maturation and it may be implicated in the regulation of neuronal survival
Results 1 - 10 of 26 > >>