Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA116391 | ENA |
REPOSITORIES: ENA
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Project description:The purpose of this study is to identify the differential transcriptome profiles in WT, hepatic Atg5 KO, TSC1 KO, Atg5/TSC1 DKO, Atg5/TSC1/p62 TKO and Atg5/TSC1/Nrf2 TKO mouse livers. Hepatic mRNA from 2-month-old mice from 5 different mouse strains were extracted and performed for Nextseq analysis in quadruplicates.
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Project description:Primary pneumocytes from KRas;Atg5fl/+ and KRas;Atg5fl/fl littermates were cultured for 48 hours and infected with AdCre-GFP to induce expression of the KrasG12D oncogene and concomitant Atg5 deletion. The transcriptional profile of those cells was determined by mRNA sequencing and uncovered differential expression in cellular movement, inflammatory response and oxidative stress response. Comparison of transcriptomes from KRas;Atg5fl/+ and KRas;Atg5fl/fl pneumocytes
2014-01-07 | E-GEOD-48387 | biostudies-arrayexpress
Project description:Identification of interacting partners of the Partner and Localizer of BRCA2 (PALB2), essential regulator of DNA repair by homologous recombination. Interacting partners of PALB2 were purified by GFP pull down from asynchronous HEK293 Flp-In T-REx cells, exogenously expressing Flag-EGFP tagged PALB2 at a similar level than the endogenous PALB2 level. Before GFP pull down, whole cell protein extracts were pre-cleared on IgG agarose beads to decrease binding of non-specific proteins during GFP pull down. GFP pull down were performed using GFP-Trap agarose beads (Chromotek) and washed at low salt concentration (150mM NaCl), to maintain interactions of low affinity binding protein partners. As a negative control, Flag-EGFP interacting proteins were purified, following the same protocol as described for the purification of Flag-EGFP PALB2 interacting proteins. Experiments were performed in triplicate.
2017-07-18 | PXD006391 | Pride
Project description:Huntington's disease (HD) is a dominantly inherited genetic disease caused by mutant huntingtin (htt) protein with expanded polyglutamine tracts. A neuropathological hallmark of HD is the presence of neuronal inclusions of mutant htt. p62 is an important regulatory protein in selective autophagy, a process by which aggregated proteins are degraded, and it is associated with several neurodegenerative disorders including HD. Here we investigated the effect of p62 depletion in three HD model mice: R6/2, HD190QG and HD120QG mice. We found that loss of p62 in these models led to longer lifespans and reduced nuclear inclusions, although cytoplasmic inclusions increased with polyglutamine length. In mouse embryonic fibroblasts (MEFs) with or without p62, mutant htt with a nuclear localization signal (NLS) showed no difference in nuclear inclusion between the two MEF types. In the case of mutant htt without NLS, however, p62 depletion increased cytoplasmic inclusions. Furthermore, to examine the effect of impaired autophagy in HD model mice, we crossed R6/2 mice with Atg5 conditional knockout mice. These mice also showed decreased nuclear inclusions and increased cytoplasmic inclusions, similar to HD mice lacking p62. These data suggest that the genetic ablation of p62 in HD model mice enhances cytoplasmic inclusion formation by interrupting autophagic clearance of polyQ inclusions. This reduces polyQ nuclear influx and paradoxically ameliorates disease phenotypes by decreasing toxic nuclear inclusions. Gene expression profiles were analyzed to examine the effects of p62 depletion in mouse with or without mutant huntingtin exon 1 To examine the effect of p62 depletion on the transcriptome of Huntington's disease model mice, we crossed p62 knockout mice with HD model mice. We extracted total RNA from the striatum of these mice at 8 weeks and used for a microaaray analysis. The samples are HD transgenic mice with p62 knockout (HD_p62KO), HD mice with normal p62 (HD_p62WT), non-HD-transgenic mice with p62 knockout (NT_p62KO), and non-HD-transgenic mice with normal p62 (NT_p62WT).
2014-10-10 | E-GEOD-62210 | biostudies-arrayexpress
Project description:To investigate the role of autophagy on cytotoxic CD8 T cells, we developed a new mouse that expresses an Atg5 gene with loxP sites up- and downstream of the exon 3, Cre-recombinase, T cell receptor specific for the OVA peptide SIINFEKL and the congenic marker Thy1.1. These cells were adoptively transferred into wild type mice followed by influenza-OVA infection and induction of Atg5 knockout at day 5 after infection. Tracking the kinetic of the cells show, that the Atg5 knockout cells do not expand as much as the control cells and they experience complete contraction within few days. No memory population is established. To investigate differences in Atg5 knockout cells versus control cells we sorted the donor cells at the peak of immune response and investigated their gene expression profile via microarray analysis. 10.000 naive CD8 T cells were isolated from the spleens of transgenic mice (untreated) and were adoptively transferred into naive wild type mice. On the next day these mice got intranasally infected with 15 plaque forming units of Influenza strain A/PR8-OVA. At day 5 to 8, Atg5 knockout was induced by intraperitoneal tamoxifen administration. At day 7 and 8, donor cells were sorted from spleens, RNA was isolated and investigated via microarray. Three groups of transgenic cells were compared in two independent experiments: Atg5 knockout cells were compared to two groups of control cells: 1. heterozygously Atg5 loxP expressing cells and 2. homozygously Atg5 loxP expressing cell that lacked the expression of Cre-recombinase.
2015-04-23 | E-GEOD-49254 | biostudies-arrayexpress
Project description:Metastasis is a common cancer hallmark which however, may be acquired by tumor-type specific mechanisms. Here we identify p62/SQSTM1 as a modulator of metastatic genes selectively enriched in melanoma. Loss- and gain-of-function analyses of p62 effectors revealed FERMT2 as an indicator of poor patient prognosis. Analyses in tumor cells, clinical biopsies and genetically-engineered mice (to compare p62 vs. ATG5) demonstrated that known p62 roles in autophagy and stress responses were not essential in melanomas. Instead, a genome-wide transcriptomic/proteomic/interactomic approach demonstrated that p62 controls FERMT2 and yet additional pro-metastatic genes by modulating transcript stability. This function of p62 was exerted by recruiting RNA-binding proteins, here exemplified by IGF2BP1. These data illustrate how genetically altered cancers can coordinately fuel pro-metastatic signatures.
2018-07-05 | GSE99831 | GEO
Project description:Metastasis is a common cancer hallmark which however, may be acquired by tumor-type specific mechanisms. Here we identify p62/SQSTM1 as a modulator of metastatic genes selectively enriched in melanoma. Loss- and gain-of-function analyses of p62 effectors revealed FERMT2 as an indicator of poor patient prognosis. Analyses in tumor cells, clinical biopsies and genetically-engineered mice (to compare p62 vs. ATG5) demonstrated that known p62 roles in autophagy and stress responses were not essential in melanomas. Instead, a genome-wide transcriptomic/proteomic/interactomic approach demonstrated that p62 controls FERMT2 and yet additional pro-metastatic genes by modulating transcript stability. This function of p62 was exerted by recruiting RNA-binding proteins, here exemplified by IGF2BP1. These data illustrate how genetically altered cancers can coordinately fuel pro-metastatic signatures.
2018-07-05 | GSE99830 | GEO
Project description:Metastasis is a common cancer hallmark which however, may be acquired by tumor-type specific mechanisms. Here we identify p62/SQSTM1 as a modulator of metastatic genes selectively enriched in melanoma. Loss- and gain-of-function analyses of p62 effectors revealed FERMT2 as an indicator of poor patient prognosis. Analyses in tumor cells, clinical biopsies and genetically-engineered mice (to compare p62 vs. ATG5) demonstrated that known p62 roles in autophagy and stress responses were not essential in melanomas. Instead, a genome-wide transcriptomic/proteomic/interactomic approach demonstrated that p62 controls FERMT2 and yet additional pro-metastatic genes by modulating transcript stability. This function of p62 was exerted by recruiting RNA-binding proteins, here exemplified by IGF2BP1. These data illustrate how genetically altered cancers can coordinately fuel pro-metastatic signatures.
2018-07-05 | GSE99832 | GEO