Effect of SIRT7 deletion on gene expression of aged mouse liver
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA854611 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19908534.fastq.gz | Fastqsanger.gz | |||
| SRR19908535.fastq.gz | Fastqsanger.gz | |||
| SRR19908536.fastq.gz | Fastqsanger.gz | |||
| SRR19908537.fastq.gz | Fastqsanger.gz | |||
| SRR19908538.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Male Sirt7 KO mice exhibit an lifespan extension and increased FGF21 expression in liver. To reveal the mechanism of the increase of hepatic FGF21 expression in aged male Sirt7 KO mice, we performed RNA-seq analysis of the liver.
2023-07-01 | GSE207272 | GEO
Project description:SIRT7 is a member of the mammalian sirtuin family of NAD+ dependent deacylases, and interacts with RNA polymerase I and UBF to regulate rDNA transcription. Various studies in mammalian cells and human clinical data have linked SIRT7 to cancer. However studies differ as to whether SIRT7 is oncogenic or tumor suppressive. Here we analyzed SIRT7 knockout mice and found SIRT7 deficiency caused sub-Mendelian birth numbers and a reduction in body size. Moreover, at 18 month of age, roughly 60 % of the SIRT7 knockout mice develop hepatocellular carcinoma (HCC), in many cases leading to suspected metastasis. Several HCC associated genes were up-regulated in livers of mice as young as 6 months of age, particularly targets of the proto-oncogene, c- MYC. Indeed SIRT7 interacts with MYC at endogenous protein levels and also represses MYC activity. Our findings thus show that SIRT7 acts as a tumor suppressor in vivo, and may suggest novel strategies to treat liver cancer. The mRNAs from 3 replicates of mouse Wildtype liver compared to 3 replicates of mouse liver lacking SIRT7
2014-08-20 | E-GEOD-50076 | biostudies-arrayexpress
Project description:SIRT7 is a member of the mammalian sirtuin family of NAD+ dependent deacylases, and interacts with RNA polymerase I and UBF to regulate rDNA transcription. Various studies in mammalian cells and human clinical data have linked SIRT7 to cancer. However studies differ as to whether SIRT7 is oncogenic or tumor suppressive. Here we analyzed SIRT7 knockout mice and found SIRT7 deficiency caused sub-Mendelian birth numbers and a reduction in body size. Moreover, at 18 month of age, roughly 60 % of the SIRT7 knockout mice develop hepatocellular carcinoma (HCC), in many cases leading to suspected metastasis. Several HCC associated genes were up-regulated in livers of mice as young as 6 months of age, particularly targets of the proto-oncogene, c- MYC. Indeed SIRT7 interacts with MYC at endogenous protein levels and also represses MYC activity. Our findings thus show that SIRT7 acts as a tumor suppressor in vivo, and may suggest novel strategies to treat liver cancer.
2014-08-20 | GSE50076 | GEO
Project description:Effect of whole-body deletion of Gclc on the liver
| PRJNA1096112 | ENA
Project description:Sirtuin proteins regulate diverse cellular pathways that influence genomic stability, metabolism, and ageing. SIRT7 is a mammalian sirtuin whose biochemical activity, molecular targets, and physiologic functions have been unclear. Here we show that SIRT7 is an NAD+-dependent, histone H3 acetyl-lysine 18 (H3K18Ac) deacetylase that stabilizes the transformed state of cancer cells. Genome-wide binding studies reveal that SIRT7 binds to promoters of a specific set of gene targets, where it deacetylates H3K18Ac and promotes transcriptional repression. The spectrum of SIRT7 target genes is defined in part by interaction of SIRT7 with the cancer-related ETS transcription factor ELK4, and comprises numerous genes with links to tumour suppression. Notably, selective hypoacetylation of H3K18Ac has recently been linked to oncogenic transformation, and in patients, is associated with aggressive tumour phenotypes and poor prognosis. We find that deacetylation of H3K18Ac by SIRT7 is necessary for maintaining essential features of human cancer cells including anchorage independent growth and escape from contact inhibition. Moreover, SIRT7 is necessary for a global hypoacetylation of H3K18Ac associated with cellular transformation by viral oncoproteins. Finally, SIRT7 depletion markedly reduces the tumourigenicity of human cancer cell xenografts in mice. Together, our work establishes SIRT7 as the first known site-specific H3K18Ac deacetylase and demonstrates a pivotal role for SIRT7 in chromatin regulation, cellular transformation programs, and tumour formation in vivo. SIRT7 ChIP-seq was performed in K562 cell lines under normal conditions. Two replicates were performed for both the SIRT7 ChIP as well as input control.
2012-05-06 | E-GEOD-28149 | biostudies-arrayexpress
Project description:Mycobacterium tuberculosis (Mtb) secretes several virulence determinants that alter phagosome biogenesis, enabling its survival within the cell. Nevertheless, the mechanism underlying this process remains considerably obscure. Here, we have identified a novel regulatory mechanism whereby SIRT7 mediates Rac1 activation in cytoskeletal remodelling during Mtb infection. We found that SIRT7 are significantly decreased during Mtb infection in both mRNA and protein levels. SIRT7 deficiency impairs macrophage phagocytosis and bacteriacidal activity by disrupts actin cytoskeleton dynamics. In the murine TB model, the deficiency of Sirt7 had an adverse effect on the host's response to Mtb since it led to an increase in bacterial burden and inflammation in the lung. Conversely, the overexpression of Sirt7 impeded bacterial growth. Mechanistically, we have shown that SIRT7 limits Mtb infection by directly interacting with and activating RAC1. Therefore, we conclude that SIRT7 is responsible for driving cytoskeletal remodeling through RAC1, thus providing crucial insight into host response during Mtb infection and offering a potential target for tuberculosis treatment.
2023-12-20 | GSE245205 | GEO
Project description:To investigate the functional role of Sirt7 in VSMCs calcification, we knockdowned Sirt7 expression in VSMCs using siRNAs, and performed RNA-seq to identify the downstream genes regulated by Sirt7
2023-12-01 | GSE247550 | GEO
Project description:SIRT7 is an NAD+-dependent protein deacetylase with important roles in ribosome biogenesis and cell proliferation. Previous studies have established that SIRT7 is associated with RNA polymerase I, interacts with pre-rRNA and promotes rRNA synthesis. Here we show that SIRT7 is also associated with snoRNAs that are involved in pre-rRNA processing and rRNA maturation. Knockdown of SIRT7 impairs U3 snoRNA-dependent early cleavage steps that are necessary for generation of 18S rRNA. Mechanistically, SIRT7 deacetylates U3-55k, a core component of the U3 snoRNP complex, and reversible acetylation of U3-55k modulates the association of U3-55k with U3 snoRNA. Deacetylation by SIRT7 enhances U3-55k binding to U3 snoRNA, which is a prerequisite for pre-rRNA processing. Under stress conditions, SIRT7 is released from nucleoli, leading to hyperacetylation of U3-55k and attenuation of prerRNA processing. The results reveal a multifaceted role of SIRT7 in ribosome biogenesis, regulating both transcription and processing of rRNA. CLIP-seq was performed in Flag-SIRT7-293T cells.
2016-01-07 | E-GEOD-76578 | biostudies-arrayexpress