Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24761121.fastq.gz | Fastqsanger.gz | |||
| SRR24761122.fastq.gz | Fastqsanger.gz |
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Project description:Actr3 WT (control), Actr3 KO and Actr3-Ift88 double KO mIMCD3 cells were generated using CRISPR/Cas9. Single cells clones (Actr3 Ctrl.-1, Actr3 KO-1, Actr3-Ift88 dKO) were selected and validated by western blotting confirming loss of Actr3 or Ift88 in KO cell lines on protein level. Transcriptome profiling (RNA-Sequencing) and differential gene expression analysis of three independent replicates of starved (ciliated) Actr3 Ctrl.-1, Actr3 KO-1, Actr3-KO Ift88-KO (dKO) and 0.5 µM Ciliobrevin D treated Actr3 KO-1 cells was performed.
2025-10-16 | GSE287677 | GEO
Project description:Proliferative zone chondrocytes were microdissected from control and Ift88-deleted growth plates to determine gene expression profiles regulated by primary cilia. Four total samples were analyzed. Two biological replicates of proliferative zone chondrocytes microdissected from control mice and two biological replicates from Ift88 deleted (Col2aCre;Ift88fl/fl) mice. Control and experimental mice were in the Bl/6 background.
2013-01-02 | E-GEOD-35003 | biostudies-arrayexpress
Project description:Lysosome-enriched fractions from the liver of Cln8 KO mice and WT mice. Included are four datasets: 1. Lysosome-enriched fraction from the liver of Cln8 KO mice, replicate 1 (CLN8_KO_1). 2. Lysosome-enriched fraction from the liver of Cln8 KO mice, replicate 2 (CLN8_KO_2). 3. Lysosome-enriched fraction from the liver of WT mice, replicate 1 (WT_1). 4. Lysosome-enriched fraction from the liver of WT mice, replicate 2 (WT_2).
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Project description:β-cell specific IFT88 knock-out mice recapitulate human diabetes with impaired insulin secretion and altered islet hormone paracrine regulation. To examine the signaling pathways regulating islet cell function, we subjected protein lysates of whole islets from control and IFT88 knockout mice to a commercial signaling-protein array analysis (Full Moon Bio, Inc). Samples were probed against 1358 antibodies with 2 replicates per antibody on 76 x 25 x 1mm glass slides.
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Project description:Proteomics RAW data from Mus musculus liver supporting “Identification of ACBP as a potential target in ciliopathic obesity through multi-omics network analysis”. Liver proteomics in WT and Alms1 KO mice before and after preventive anti-ACBP treatment reveal the impact of ACBP neutralization on lipid-metabolism–related proteins in Alms1 KO mice.
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Project description:β-cell specific IFT88 knock-out mice recapitulate human diabetes with impaired insulin secretion and altered islet hormone paracrine regulation. To examine the signaling pathways regulating islet cell function, we subjected protein lysates of whole islets from control and IFT88 knockout mice to a commercial phospho-antibody array analysis (Full Moon Bio, Inc). Samples were probed against 1318 site-specific and phospho-specific antibodies with 2 replicates per antibody on 76 x 25 x 1mm glass slides.
2019-10-30 | GSE138856 | GEO
Project description:To investigate the role of the transient receptor potential channel vanilloid type 1 (TRPV1) channel in hepatic glucose metabolism, we performed proteomics analysis of the liver of C57Bl/6J (WT) and Trpv1 KO mice (n = 4 per group). Liver from Trpv1 KO mice showed significant proteomics changes consistent with enhanced glycogenolysis, as well as increased gluconeogenesis and inflammatory features.
2022-06-21 | MSV000089696 | MassIVE
Project description:Hyaluronan receptor LYVE-1 is expressed by liver sinusoidal endothelial cells (LSEC), lymphatic endothelial cells and specialized macrophages. Besides binding hyaluronan, LYVE-1 mediates adhesion of leukocytes and cancer cells to endothelial cells. Here, we analyzed the impact of LYVE-1 on physiological liver functions and metastasis. Mice with deficiency of Lyve-1 (Lyve-1 KO) were analyzed using histology, immunofluorescence, RNA sequencing, plasma proteomics and flow cytometry. Liver metastasis was studied by intrasplenic/intravenous injection of melanoma (B16F10luc2, WT31) or colorectal carcinoma (MC38) cell lines. Results: Hepatic architecture, liver size, endothelial differentiation and angiocrine functions were unaltered in Lyve-1 KO mice. Hyaluronan plasma levels were significantly increased in Lyve-1-KO mice; besides, plasma proteomics revealed increased carbonic anhydrase-2 and decreased FXIIIA, potential modulators of metastatis. Furthermore, gene expression analysis of LSEC indicated regulation of immunological pathways. Therefore, liver metastasis of a highly and of a weekly immunogenic tumor, i.e. melanoma and colorectal carcinoma (CRC), was analyzed in Lyve-1 KO mice. Hepatic metastasis of B16F10 luc2 and WT31 melanoma cells, but not MC38 CRC cells, was significantly reduced in Lyve-1 KO mice. While short-term adhesion assays with B16F10 luc2 cells in vivo did not show differences between Lyve-1 KO and wild-type mice, increased numbers of resident hepatic CD4+, CD8+ and regulatory T cells were detected in Lyve-1 KO livers. In addition, iron deposition was detected in F4/80+ liver macrophages known to exert pro-inflammatory effects. Conclusions: LYVE-1 deficiency controlled hepatic metastasis in a tumor cell-specific manner reducing hepatic metastasis of melanoma, but not CRC. Anti-tumorigenic effects are likely due to enhancement of the resident hepatic immune microenvironment.
2023-03-11 | PXD032717 | Pride
Project description:We studied the role of the post-translational modification called O-GlcNAcylation during liver regeneration. Here we generated O-GlcNAc transferase (OGT-KO) and O-GlcNAcase (OGA-KO) hepatocyte-specific knock-out mice. 70% partial hepatectomy (PHX) was performed to induce liver regeneration. We showed that OGA-KO mice had normal liver regeneration whereas OGT-KO mice had a defect in the termination of liver regeneration.
2022-02-25 | GSE188882 | GEO
Project description:Activation of protein kinase C epsilon (PKCε) in the liver has been widely associated with hepatic insulin resistance. PKCε is proposed to inhibit insulin signalling through phosphorylation of the insulin receptor. We have tested this directly by breeding PKCε floxed mice with mice expressing Cre recombinase under the control of the cytomegalovirus, albumin or adiponectin promoters to generate global, liver- and adipose tissue-specific PKCε knockout (KO) mice. Global deletion of PKCε recapitulated the benefits for diet-induced glucose intolerance that we previously described using conventional PKCε KO mice. However, we did not detect PKCε-dependent alterations in hepatic insulin receptor phosphorylation. Furthermore, liver-specific KO mice were not protected against diet-induced glucose intolerance or insulin resistance determined by euglycemic clamp. In contrast, adipose tissue-specific KO mice exhibited improved glucose tolerance and mildly increased hepatic triglyceride storage, but no change in liver insulin sensitivity. Phosphoproteomic analysis of insulin signalling in PKCε KO adipocytes revealed no defect in the canonical INSR/AKT/mTOR pathways. However, PKCε KO resulted in changes in phosphorylation of several proteins associated with the endosome and cell junctions suggesting regulation in secretory pathways and a potential role of PKCε in endocrine function. Indeed, RNA-seq analysis revealed adipose-tissue PKCε-dependent changes in the hepatic expression of several genes linked to glucose homeostasis and hepatic lipid metabolism. The primary effect of PKCε on glucose homeostasis is therefore not exerted directly in the liver as currently assumed. However, PKCε in adipose tissue modulates glucose tolerance and is involved in crosstalk with the liver that affects gene expression and lipid accumulation.
2018-10-04 | PXD010212 | Pride