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Literature summary for 2.3.1.B41 extracted from

  • Zhang, Q.; Tu, W.; Tian, K.; Han, L.; Wang, Q.; Chen, P.; Zhou, X.
    Sirtuin 6 inhibits myofibroblast differentiation via inactivating transforming growth factor-beta1/Smad2 and nuclear factor-kappaB signaling pathways in human fetal lung fibroblasts (2019), J. Cell. Biochem., 120, 93-104 .
    View publication on PubMed

Cloned(Commentary)

Cloned (Comment) Organism
gene SIRT6, real-time reverse transcription PCR expression analysis Homo sapiens

Protein Variants

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

Organism UniProt Comment Textmining
Homo sapiens Q8N6T7
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Source Tissue

Source Tissue Comment Organism Textmining
lung fetal Homo sapiens
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myofibroblast lung, level of SIRT6 in in vitro model of myofibroblast differentiation, overview Homo sapiens
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Synonyms

Synonyms Comment Organism
NAD-dependent protein deacetylase sirtuin-6 UniProt Homo sapiens
SIRT6
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Homo sapiens
sirtuin 6
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Homo sapiens

General Information

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