EC Number   |
Protein Variants |
Reference |
|---|
   2.3.1.B41 | H133Y |
a catalytically inactive mutant of SIRT6, the acetylation level of PER2 is significantly increased in SIRT6-KO HEK293 cells compared to wild-type |
755978 |
| 2.3.1.B41 | H133Y |
catalytically inactive SIRT6 mutant, the SIRT6 H133Y mutant without histone deacetylase activity fails to inhibit phosphorylation and nuclear translocation of Smad2 |
757294 |
| 2.3.1.B41 | more |
construction of the interfering adenovirus vector, specific short hairpin RNA (shRNA) for the bovine SIRT6 gene are designed, usage of shRNA-399 for SIRT6 gene silencing |
755904 |
| 2.3.1.B41 | more |
enzyme knockout by SIRT6 siRNA expression. SIRT6 overexpression in hepatocellular carcinoma cells reduces E-cadherin levels |
757530 |
| 2.3.1.B41 | M70R |
further decrease in nicotinamide sensitivity compared to wild-type |
730706 |
| 2.3.1.B41 | more |
generation of brS6KO mice, phenotype, overview. Brains of brS6KO mice are significantly smaller, but otherwise structurally normal. brS6KO mice exhibit increased signs of DNA damage, marked by increased levels of ATM and H2AX phosphorylation, increased H3K56ac, and reduced SNF2H recruitment to chromatin. A significant increase in apoptotic cells in the cortex is observed, as determined by TUNEL staining in young mice (3-4 month old). SIRT6-deficient brains have increased signs of DNA damage and cell death. Behavioral defects of brS6KO mice, overview. SIRT6 deletion markedly decreases non-associative (OF) and associative (CFC) learning. SIRT6KO cells are more sensitive to apoptosis, prevented by GSK3 or ATM inhibition |
756392 |
| 2.3.1.B41 | more |
generation of endothelium-specific SIRT6 knockout mice (Tie2-Cre/SIRT6flox/flox, defined as ecSIRT6-/-). Analysis of the effect of endothelium-specific SIRT6 depletion on hyperlipidemic mice |
756672 |
| 2.3.1.B41 | more |
generation of muscle-specific knockout mice SIRT6M -/- and effects of different diets, phenotypes, detailed overview |
-, 755766 |
| 2.3.1.B41 | more |
generation of SIRT6 knockout human mesenchymal stem cells (hMSCs) by targeted gene editing. For generation of SIRT6-deficient human embryonic stem cells (hESCs), the exon 1 of SIRT6 gene is removed in hESCs by a transcription activator-like effector nuclease. SIRT6-deficient hMSCs exhibit accelerated functional decay, a feature distinct from typical premature cellular senescence. Rather than compromised chromosomal stability, SIRT6-null hMSCs are predominately characterized by dysregulated redox metabolism and increased sensitivity to the oxidative stress. SIRT6 forms a protein complex with both nuclear factor erythroid 2-related factor 2 (NRF2) and RNA polymerase II, which is required for the transactivation of NRF2-regulated antioxidant genes, including heme oxygenase 1 (HO-1). Phenotype, overview |
756407 |
| 2.3.1.B41 | more |
generation of SIRT6 knockout MEF cells which exhibit an increased basal level of mobility compared to that in wild-type cells before damage. But the cells do not show the damage-induced increase in total movement after damage |
758437 |
