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Transcriptional profiling reveals an upregulation of genes related to Sphingolipid metabolism and Oxidative phosphorilation in HRas and NRas double-KO mice (DKO), which die because of a severe respiratory distress

ABSTRACT: Transcriptional profiling reveals an upregulation of genes related to Sphingolipid metabolism and Oxidative phosphorilation in HRas and NRas double-KO mice (DKO), which die because of a severe respiratory distress

PROVIDER: PRJNA772757 | ENA |

REPOSITORIES: ENA

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Transcriptional profiling reveals an upregulation of genes related to Sphingolipid metabolism and Oxidative phosphorilation in HRas and NRas double-KO mice (DKO), which die because of a severe respiratory distress.

Project description:We used microarrays to investigate gene expression changes in the lungs of Control, Hras-KO, Nras-KO and DKO mice. These DKO animals die at birth because of respiratory distress, caused by an impaired lung maturation.

2019-07-15 | GSE130415 | GEO

2021-10-22 | GSE186161 | GEO

Project description:Transcriptional profiling reveals an upregulation of genes related to Sphingolipid metabolism and Oxidative phosphorilation in HRas and NRas double-KO mice (DKO), which die because of a severe respiratory distress.

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Germline NRAS mutation causes a novel human autoimmune lymphoproliferative syndrome

Project description:The p21 RAS subfamily of small GTPases, including KRAS, HRAS, and NRAS, regulates cell proliferation, cytoskeletal organization and other signaling networks, and is the most frequent target of activating mutations in cancer. Activating germline mutations of KRAS and HRAS cause severe developmental abnormalities leading to Noonan, cardio-facial-cutaneous and Costello syndrome, but activating germline mutations of NRAS have not been reported. Autoimmune lymphoproliferative syndrome (ALPS) is the most common genetic disease of lymphocyte apoptosis and causes autoimmunity as well as excessive lymphocyte accumulation, particularly of CD4-, CD8- ab T cells. Mutations in ALPS typically affect CD95 (Fas/APO-1)-mediated apoptosis, one of the extrinsic death pathways involving tumor necrosis factor receptor (TNFR) superfamily proteins, but certain ALPS individuals have no such mutations. We show here that the salient features of ALPS as well as a predisposition to hematological malignancies can be caused by a heterozygous germline Gly13Asp activating mutation of the NRAS oncogene that does not impair CD95-mediated apoptosis. The increase in active, GTP-bound NRAS augments RAF/MEK/ERK signaling which markedly decreases the pro-apoptotic protein BIM and attenuates intrinsic, nonreceptor-mediated mitochondrial apoptosis. Thus, germline activating mutations in NRAS differ from other p21 Ras oncoproteins by causing selective immune abnormalities without general developmental defects. Our observations on the effects of NRAS activation indicate that RAS-inactivating drugs, such as farnesyl-transferase inhibitors (FTIs) should be examined in human autoimmune and lymphocyte homeostasis disorders. Keywords: NRAS

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Normal mouse skin lacking Hras

2015-03-01 | GSE60769 | GEO

Normal mouse skin lacking Hras

Project description:Oncogenic activating mutations in Ras genes are among the most common drivers of human disease. Treating mouse skin with the chemical carcinogen DMBA induces a characteristic mutation in Hras at codon 61. To understand how skin responds to a constitutive lack of Hras, we generated a cohort of Hras knockout mice. A backcross was generated using male Mus spretus and female FVB/N Hras-/- mice; female F1 hybrids were mated with male FVB/N Hras -/- or Hras -/+ mice to generate a backcross population. This series contains mice that were Hras -/-. Mice were aged to 8 weeks and a tail skin sample was snap frozen.

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Transcription profiling of human peripheral blood mononuclear cells WITH a germline NRAS mutation vs controls reveals NRAScauses a novel human autoimmune lymphoproliferative syndrome (ALPS)

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An integrated global analysis of compartmentalized HRAS signaling - Phosphoproteomics

Project description:Modern omics technologies allow us obtaining global information on different types of biological networks. However, integrating these different types of analyzes into a coherent framework for a comprehensive biological interpretation remains challenging. Here, we present a conceptual framework that integrates protein interaction, phosphoproteomics and transcriptomics data. Applying this method to analyze HRAS signaling from different subcellular compartments shows that spatially-defined networks contribute specific functions to HRAS signaling. Changes in HRAS protein interactions at different sites lead to different kinase activation patterns that differentially regulate gene transcription. HRAS mediated signaling is the strongest from the plasma membrane, but it regulates the largest number of genes from the endoplasmic reticulum. The integrated networks provide a topologically and functionally resolved view of HRAS signaling. They reveal new HRAS functions including the control of cell migration from the endoplasmic reticulum and p53 dependent cell survival when signaling from the Golgi apparatus.

2019-03-08 | PXD012506 | Pride

An integrated global analysis of compartmentalized HRAS signaling - Ras IP

2019-03-08 | PXD012505 | Pride

An integrated global analysis of compartmentalized HRAS signaling

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