Cloned (Comment) | Organism |
---|---|
gene SIRT6, real-time reverse transcription PCR expression analysis | Homo sapiens |
Protein Variants | Comment | Organism |
---|---|---|
H133Y | catalytically inactive SIRT6 mutant, the SIRT6 H133Y mutant without histone deacetylase activity fails to inhibit phosphorylation and nuclear translocation of Smad2 | Homo sapiens |
additional information | overexpression of SIRT6 in HFL1 cells infected with an adenoviral vector encoding SIRT6 or knockdown by an adenoviral vector encoding SIRT6 short hairpin RNA | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q8N6T7 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
lung | fetal | Homo sapiens | - |
myofibroblast | lung, level of SIRT6 in in vitro model of myofibroblast differentiation, overview | Homo sapiens | - |
Synonyms | Comment | Organism |
---|---|---|
NAD-dependent protein deacetylase sirtuin-6 | UniProt | Homo sapiens |
SIRT6 | - |
Homo sapiens |
sirtuin 6 | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
evolution | sirtuin 6 (SIRT6) is a member of the sirtuin family of nicotinamide adenine dinucleotide?dependent protein deacetylases | Homo sapiens |
malfunction | overexpression of SIRT6 significantly suppresses TGF-beta1-induced myofibroblast differentiation in HFL1 cells. Mutant SIRT6 (H133Y) without histone deacetylase activity fails to inhibit phosphorylation and nuclear translocation of Smad2. Overexpression of wild-type SIRT6 but not the H133Y mutant inhibits the expression of NF-kappaB-dependent genes including interleukin (IL)-1beta, IL-6 and matrix metalloproteinase-9 (MMP-9) induced by TGF-beta1, all of which have been demonstrated to promote myofibroblast differentiation. SIRT6 overexpression suppresses TGF-beta1-induced Smad2 activation | Homo sapiens |
physiological function | sirtuin 6 (SIRT6) is involved in stress tolerance, DNA repair, inflammation, cancer, and life span. SIRT6 plays a protective role in fibrosis of different organs. It inhibits epithelial-to-mesenchymal transition during idiopathic pulmonary fibrosis. Also fibroblast-to-myofibroblast differentiation, which is characterized by increased expression of alpha-smooth muscle actin, is known to be involved in the pathogenesis of idiopathic pulmonary fibrosis. Analysis of the role of SIRT6 in the cellular model of fibroblast-to-myofibroblast differentiation induced by TGF-beta1 using human fetal lung fibroblasts (HFL1). Mechanistically, SIRT6 decreases phosphorylation and nuclear translocation of Smad2 under TGF-beta1 stimulation. SIRT6 interacts with the nuclear factor-kappaB (NF-kappaB) subunit p65 and represses TGF-beta1-induced NF-kappaB-dependent transcriptional activity, which is also dependent on its deacetylase activity. SIRT6 interacts with the nuclear factor-kappaB (NFkappaB) subunit p65 and represses TGF-beta1-induced NF-kappaB-dependent transcriptional activity, which is also dependent on its deacetylase activity | Homo sapiens |