Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1004540 | ENA |
REPOSITORIES: ENA
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Project description:Autophagy deficiency caused by conditional knockout of Atg7 results in severe hepatitis accompanied by abundant accumulation of p62. p62 stablizes Nrf2 by disrupting the association between Keap1 and Nrf2. To understand the pathogenesis of hepatitis under the autophagy deficiency, we examined gene expression profiles of livers from Atg7-null, Nrf2-null and Atg7-Nrf2 double mutant mice. Eight week old Atg7F/F:Mx1-Cre mice and Atg7F/F:Mx1-Cre:Nrf2-/- together with control mice were injected with pIpC. At 4 weeks after pIpC injection, total RNAs were purified from each mouse liver.
2010-10-14 | E-GEOD-20415 | biostudies-arrayexpress
Project description:iTRAQ proteomics was performed for Liver samples from WT and Atg7 liver specific KO mice
2023-07-20 | PXD043936 |
Project description:Autophagy deficiency caused by conditional knockout of Atg7 results in severe hepatitis accompanied by abundant accumulation of p62. p62 stablizes Nrf2 by disrupting the association between Keap1 and Nrf2. To understand the pathogenesis of hepatitis under the autophagy deficiency, we examined gene expression profiles of livers from Atg7-null, Nrf2-null and Atg7-Nrf2 double mutant mice.
2010-10-15 | GSE20415 | GEO
Project description:We investigated the Prkar1a+/- mice when bred with Prkaca+/- genetic backgrounds. Prkar1a+/-Prkaca+/- mice not only continued to develop bone lesions but also demonstrated a significant increase in both the number and the severity of the lesions, as well as a reduction in the age of first appearance of any bone abnormality. Histological analysis of bone from Prkar1a+/-Prkaca+/- mice showed that lesions had similarity to tumors from humans with CNC and some resemblance (but also differences) from humans and mice with fibrous dysplasia (FD). Prkar1a+/- and Prkar1a+/-Prkaca+/- mouse lesions always involved a particular sub-population of cells that could be identified as belonging to the osteoblastic lineage, that were initially located on the endosteal surface of the periosteum and nearby trabecular bone proximal to the growth plate of the long bones and vertebrae, and resembled bone stromal cells (BSCs). The bone lesions expressed high level of mesenchymal proteins like n-cadherin, vimentin, snail1, twist1, mmp2 and mmp9 when compared to WT bone. On top of this, bone lesions from Prkar1a+/-Prkaca+/- mice also showed an increased expression of keratin related genes, which are involved in hair follicle and epithelial differentiation, when compared to lesions from Prkar1a+/- mice. Total RNA obtained from bone lesions from Prkar1a+/- and Prkar1a+/-Prkaca+/- mice were compared to those obtained from WT and Prkaca+/- mice.
2010-03-21 | E-GEOD-20984 | biostudies-arrayexpress
Project description:Transcriptome analysis of NesCre:Atg7 conditional knockout mice. Autophagy plays an important role in regulating protein metabolism and tissue homeostasis. Recent studies have reported that neural stem cell-specific Atg7 knockout mice (NesCre:Atg7f/f cKO mice) exhibit neonatal lethal due to severe neurodegeneration. However, the precise mechanisms of how neuronal fate is regulated by the autophagic pathway have not been elucidated. Here, we performed microarray experiments to analyze the changes in gene expression patterns in NesCre:Atg7 cKO mice. As a result, we could find a lot of candidate genes changed by Atg7 deficiency.
2022-10-07 | GSE214939 | GEO
Project description:We investigated the Prkar1a+/- mice when bred with Prkaca+/- genetic backgrounds. Prkar1a+/-Prkaca+/- mice not only continued to develop bone lesions but also demonstrated a significant increase in both the number and the severity of the lesions, as well as a reduction in the age of first appearance of any bone abnormality. Histological analysis of bone from Prkar1a+/-Prkaca+/- mice showed that lesions had similarity to tumors from humans with CNC and some resemblance (but also differences) from humans and mice with fibrous dysplasia (FD). Prkar1a+/- and Prkar1a+/-Prkaca+/- mouse lesions always involved a particular sub-population of cells that could be identified as belonging to the osteoblastic lineage, that were initially located on the endosteal surface of the periosteum and nearby trabecular bone proximal to the growth plate of the long bones and vertebrae, and resembled bone stromal cells (BSCs). The bone lesions expressed high level of mesenchymal proteins like n-cadherin, vimentin, snail1, twist1, mmp2 and mmp9 when compared to WT bone. On top of this, bone lesions from Prkar1a+/-Prkaca+/- mice also showed an increased expression of keratin related genes, which are involved in hair follicle and epithelial differentiation, when compared to lesions from Prkar1a+/- mice.
2010-03-21 | GSE20984 | GEO
Project description:[original title] Prkar1a haploinsufficiency in mice leads to an overall increase in tumors caused by other genetic defects or chemical induction We investigated the Prkar1a+/- mice when bred within the Rb1+/- or Trp53+/- genetic backgrounds, or treated with a 2-step skin carcinogenesis protocol. Prkar1a+/-Trp53+/- mice developed more bone sarcomas than Trp53+/- mice (p<0.05) and Prkar1a+/-Rb1+/- mice grew more and larger pituitary and thyroid tumors than Rb1+/- mice. All mice with double heterozygosity had significantly reduced life-spans compared with their single-heterozygous counterparts. Finally, Prkar1a+/- mice developed more papillomas than wild-type animals when treated with a 2-step skin carcinogenesis protocol. A whole-genome transcriptome profiling of tumors produced by all three models identified Wnt signaling as the main pathway activated by abnormal cAMP signaling in these tissues, along with (expected) cell cycle gene abnormalities, all confirmed by qRT-PCR array and immunohistochemical analyses.
2009-12-24 | GSE19576 | GEO
Project description:To know the crosstalk between Hippo and AKT pathways in the liver metabolism, we generated liver-specific Pten (AKT signaling), Sav1 (Hippo signaling) and double-knockout mice and analysed the liver mRNA expression globally from 4groups (WT, Pten KO, Sav1 KO and Pten;Sav1 dKO).
2018-10-08 | GSE94797 | GEO