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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression profiles of Ras mutants.

ABSTRACT: Gene expression profiles were collected from HEK-HT cells expressing H-Ras with Ras-activating (G12V), Raf-activating (G12V,T35S), RalGEF-activating (G12V,E37G), or PI3K-activating (G12V,Y40C) mutations. Keywords: Comparison of Ras pathway components. THX=control; 12V=G12V mutation; 35S=G12V,T35S mutation; 37G=G12V,E37G mutation; 40C=G12V,Y40C mutation. 5 replicates of each. Total of 25 samples.

ORGANISM(S): Homo sapiens

SUBMITTER: Jeffrey Chang

PROVIDER: E-GEOD-14934 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A genomic strategy to elucidate modules of oncogenic pathway signaling networks.

Chang Jeffrey T JT Carvalho Carlos C Mori Seiichi S Bild Andrea H AH Gatza Michael L ML Wang Quanli Q Lucas Joseph E JE Potti Anil A Febbo Phillip G PG West Mike M Nevins Joseph R JR

Molecular cell 20090401 1

Recent studies have emphasized the importance of pathway-specific interpretations for understanding the functional relevance of gene alterations in human cancers. Although signaling activities are often conceptualized as linear events, in reality, they reflect the activity of complex functional networks assembled from modules that each respond to input signals. To acquire a deeper understanding of this network structure, we developed an approach to deconstruct pathways into modules represented b ...[more]

PMID: 19362539

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Gene expression profiles of Ras mutants.

Project description:Gene expression profiles were collected from HEK-HT cells expressing H-Ras with Ras-activating (G12V), Raf-activating (G12V,T35S), RalGEF-activating (G12V,E37G), or PI3K-activating (G12V,Y40C) mutations. Keywords: Comparison of Ras pathway components.

2009-02-21 | GSE14934 | GEO

Interrogation of the oncogenic RAS interactomes by BirA* based proximity labeling

Project description:We determined the specific protein interactomes of each RAS isoform (HRAS G12V, NRAS G12V and KRAS G12V) by BirA proximity-dependent biotin identification (BioID) in HEK-HT cells (folder hnk ras). We also determined protein interactomes of KRASG12V (folder: ras1) and HRASG12V (folder: ras2) in PIP5K1A deficient HEK-HT cells.

2018-07-08 | MSV000082583 | MassIVE

Targeted mass spectrometry analyses of somatic mutations in colorectal cancer specimens using differential ion mobility

Project description:Identification of K-Ras and B-Raf mutations in colorectal cancer (CRC) is essential to predict patients' response to anti-EGFR therapy and formulate appropriate therapeutic strategies to improve prognosis and survival. Here, we combined parallel reaction monitoring (PRM) with high-field asymmetric waveform ion mobility (FAIMS) to enhance mass spectrometry sensitivity and improve the identification of low-abundance K-Ras and B-Raf mutations in biological samples without immunoaffinity enrichment. In targeted LC-MS/MS analyses, FAIMS reduced the occurrence of interfering ions and enhanced precursor ion purity, resulting in a three-fold improvement in the detection limit for K-Ras and B-Raf mutated peptides. In addition, ion mobility separation of isomeric peptides using FAIMS facilitated the unambiguous identification of K-Ras G12D and G13D peptides. The application of targeted LC-MS/MS analyses using FAIMS is demonstrated for the detection and quantitation of B-Raf V600E, K-Ras G12D, G13D, and G12V in CRC cell lines and primary specimens.

2023-08-14 | PXD043799 | Pride

Targeted mass spectrometry analyses of somatic mutations in colorectal cancer specimens using differential ion mobility

2023-11-20 | PXD047029 | Pride

Selective and Noncovalent Targeting of RAS Mutants for Inhibition and Degradation

Project description:Activating mutants of RAS are commonly found in many human cancers, but to date selective targeting of RAS in the clinic has been limited to KRAS(G12C) through covalent inhibitors. Here, we have developed a monobody, termed 12VC1, that recognizes the active state of both KRAS(G12V) and KRAS(G12C) up to 400-times more tightly than wild-type KRAS. Affinity purification were performed on PATU8902 and H358 cell lines that contain KRAS(G12V) and KRAS(G12C), respectively, but not from growth factor stimulated HEK293T cells containing only wild-type RAS. The mass spectrometric data was acquired in data dependent mode to show the clear enrichment of KRAS in the 2 cell lines that carry the mutated RAS. In addition, a targeted analysis was performed for the peptide carrying the G12V mutation as well as the wild type KRAS peptide to further verify enrichment of only the KRAS mutant.

2020-12-07 | MSV000086569 | MassIVE

Autophagy mediates the mitotic senescence transition

Project description:ER:RAS-G12V expressing IMR90 cells were given 100nM 4-OHT and assessed for transcriptional profiling at various time points. IMR90 cells expressing a 4-hydroxytamoxifen (4-OHT) inducible estrogen receptor (ER)-coupled RAS-G12V (ER:RAS-G12V) were given 100nM 4-OHT for these eight time points (0, 2, 8, 24hrs, 2, 4, 6 and 8days) then analysed for transcriptional profiling using the illumina expression array platform (human-6 v2 Expression BeadChips). There were three biological replicates (batch A, B and D) for each of the time points.

2014-07-31 | E-GEOD-59522 | biostudies-arrayexpress

HMLER cells expressing either FOXC2 or a vector control

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2013-02-15 | E-GEOD-44335 | biostudies-arrayexpress

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

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. Experiment Overall Design: Describes the discovery of a new gene underlying a novel type of autoimmune lymphoproliferative syndrome, and characterizes the mechanisms involved in the pathogenesis of the disease.

2008-04-04 | E-GEOD-7345 | biostudies-arrayexpress

Gene expression profiling of B9 cells in response to two classes of BRAF inhibitors

Project description:Selective RAF inhibitors including vemurafenib (PLX4032) have demonstrated clinical efficacy in mutant BRAF driven metastatic melanoma. The clinical effectiveness of RAF inhibitors depends on near complete abolition of the MAPK pathway output in tumors harboring BRAF mutations. However these compounds paradoxically activate the MAPK pathway in cells bearing oncogenic RAS or elevated upstream receptor signaling. This paradox can promote cellular proliferation and can manifest clinically with progression of secondary malignancies such as cutaneous squamous cell carcinomas (cuSCC). We have identified next generation RAF inhibitors (“paradox breakers”, e.g. PLX7904) that inhibit mutant BRAF cells without activating the MAPK pathway in cells bearing upstream activation. In murine cuSCC B9 cells that express the same HRAS mutation prevalent in squamous tumors from patients treated with RAF inhibitors, the first-generation RAF PLX4032 stimulated in vitro and in vivo growth; by contrast the paradox breaker PLX7904 had no effect. Here we compared the gene expression changes in B9 cells treated overnight with PLX4032 and PLX7904.

2015-10-01 | GSE71109 | GEO

SA, elf18 treatment of WT and tbf1 mutant

Project description:Identification of TBF1-dependent and SA, elf18-responsive genes in Arabidopsis 24 samples total, 2 treatments with corresponding mock, wild type samples served as control, 3 biological replicates

2012-01-17 | E-GEOD-34047 | biostudies-arrayexpress

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