Similar Datasets
Project description:Effect of sirt6 deficiency on gene expression in zebrafish at 3 dpf
| PRJNA946304 | ENA
Project description:Gene expression is tightly regulated in Hematopoietic stem cells (HSCs). SIRT6 play a important role in HSCs function. We used microarrays to detail the global programme of gene expression in SIRT6 KO HSC SIRT6 knockout HSC and Wild type HSC were selected for RNA extraction and hybridization on Affymetrix microarrays.
2016-06-01 | E-GEOD-73392 | biostudies-arrayexpress
Project description:Expanding the exercise capacity is an emerging strategy to combat metabolic diseases. Skeletal muscle fiber type determination is critical for the exercise performance, but the regulatory basis is largely unknown. Here, we report that Sirt6 has a role in regulating myofiber configuration toward oxidative type and that Sirt6 activator can be an exercise mimetic. To elucidate molecular mechanisms, we performed RNA-sequencing analysis using WT and skeletal muscle-specific Sirt6 KO mice. Transcriptomic analysis enabled us to discover major signaling nodes altered by Sirt6 deficiency in close association with mitochondrial function and muscle phenotypes.
2022-02-25 | GSE186105 | GEO
Project description:Gene expression is tightly regulated in Hematopoietic stem cells (HSCs). SIRT6 play a important role in HSCs function. We used microarrays to detail the global programme of gene expression in SIRT6 KO HSC
2016-06-01 | GSE73392 | GEO
Project description:To know whether SIRT6-/- monkey sustains embryonic features at transcriptome level, we compare the transcriptional profiles of SIRT6 null monkey to datasets of fetal organs.
2018-07-26 | GSE102830 | GEO
Project description:Podocyte injury is a major determinant in proteinuric kidney disease and identification of potential therapeutic targets for preventing podocyte injury has clinical importance. Here, we show that histone deacetylase Sirt6 protects against podocyte injury through epigenetic regulation of Notch signaling. Sirt6 is downregulated in renal biopsies from patients with podocytopathies and its expression negatively correlates withglomerular filtration rate. Podocyte-specific deletion of Sirt6 exacerbates podocyte injury and proteinuria in two independent mouse models including diabetic nephropathy and adriamycin-induced nephropathy. Sirt6 has pleiotropic protective actions in podocytes including anti-inflammatory and anti-apoptotic effects, is involved in actin cytoskeleton maintenance, and promotes autophagy. Sirt6 also reduces urokinase plasminogen activator receptor expression, which is a key factor for podocyte foot process effacement and proteinuria. Mechanistically, Sirt6 inhibits Notch1 and Notch4 transcription by deacetylating the histone H3K9. We suggest Sirt6 as a potential therapeutic target in proteinuric kidney disease.
2017-06-20 | GSE100185 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE13206: Human shSIRT6 TNF-alpha timecourse GSE13207: Mouse Sirt6-/- TNF-alpha timecourse GSE13208: Mouse Sirt6-/- tissues GSE13209: Mouse Sirt6-/- RelA+/- tissues Refer to individual Series
2010-06-24 | E-GEOD-13272 | biostudies-arrayexpress
Project description:Preadipocytes initiate differentiation into adipocytes through a cascade of events. Mitotic clonal expansion, as one of the earliest event, is essential for adipogenesis. However, the underlying mechanisms that regulate mitotic clonal expansion remain elusive. SIRT6 is a member of the evolutionarily conserved sirtuin family of NAD+ dependent protein deacetylases and plays roles in genomic stability, aging, glucose metabolism and inflammatory response. Here, we show that SIRT6 deficiency in preadipocytes blocked their adipogenesis. Analysis of gene expression during adipogenesis reveals that KIF5C, which belongs to kinesin family, is negatively regulated by SIRT6. Furthermore, we show that KIF5C is a negative factor for adipogenesis through interacting with CK2α’, a catalytic subunit of CK2. This interaction blocks CK2α’ nuclear translocation and CK2 kinase activity, and inhibits mitotic clonal expansion during adipogenesis. Thus, SIRT6 acts as an important factor of adipogenesis through inhibiting KIF5C expression and enhancing CK2 kinase activity.
2018-01-16 | GSE94058 | GEO
Project description:SIRT6, the sixth member of sirtuin family proteins, has been identified as a crucial regulator in multiple molecular pathways related to aging, including genome stability, DNA damage repair, telomere maintenance and inflammation. However, the exact roles of SIRT6 during mammalian oocyte meiosis have not yet fully clarified. Here, we investigated the critical events during porcine oocyte meiotic maturation with the treatment of SIRT6 specific inhibitor SIRT6-IN-1. We found that SIRT6 inhibition resulted in oocyte meiotic failure by displaying the poor expansion of cumulus cells and reduced rate of polar body extrusion. Meanwhile, the compromised spindle assembly, chromosome alignment and actin dynamics were also observed in SIRT6-inhibited oocytes. Moreover, inhibition of SIRT6 led to the defective cytoplasmic maturation by showing the abnormal distribution of cortical granules and their component ovastacin. Notably, we identified that expression of genes related to oocyte meiosis, oxidative phosphorylation and cellular senescence was remarkably altered in SIRT6-inhibited oocytes by transcriptome analysis, and validated that the meiotic defects caused by SIRT6 inhibition resulted from the excessive ROS-induced early apoptosis in oocytes. Taken together, our findings demonstrate that SIRT6 promotes the porcine oocyte meiotic maturation via maintaining the organelle dynamics.
2021-03-16 | GSE161068 | GEO
Project description:Friedreich ataxia (FRDA) is a recessive neurodegenerative disease characterized by progressive ataxia, dyscoordination, and loss of vision. The variable length of the pathogenic GAA triplet repeat expansion in the FXN gene in part explains Inter-individual variability in severity of disease. The GAA repeat expansion leads to epigenetic silencing of FXN; therefore, variability in properties of epigenetic effector proteins could also regulate the severity of FRDA. In an exploratory analysis, DNA from 88 FRDA patients was analyzed to determine if any of 5 non-synonymous SNPs in HDACs/ SIRTs predicted FRDA disease severity. Results suggested the need for a full analysis (569 FRDA patients) at the rs352493 locus in SIRT6 (S46N SNP). Disease features were compared between patients with the common N46 SIRT6 variant and the less common S46 variant. Biochemical properties of SIRT6 were compared between S46 and N46. Linear regression of the exploratory cohort suggested a SNP (rs352493) in SIRT6 predicted neurologic severity. In follow up analysis, the genotype of SIRT6 at the locus rs352493 predicted disease features of FRDA. Patients with the S46 SIRT6 variant performed better on measures of neurological and visual function over time when compared to the more common N46 SIRT6 variant. S46 SIRT6 did not alter expression or enzymatic activity of SIRT6 or FXN however, S46 patients showed whole transcriptome differences compared to N46 patients, indicative of compensatory mechanisms against whole transcriptome changes seen in FRDA.
2022-10-04 | GSE200907 | GEO