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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Analysis of gene expression with the Hmga2 allelic series.

ABSTRACT: In this study, we introduced a series of expression constructs into a mouse lung cancer cell line (482N1): (1) a control short hairpin RNA (shluc) plus the empty expression vector (empty); (2) an shRNA targeting Hmga2 (shHmga2) plus empty; (3) shHmga2 plus an expression vector for the full-length Hmga2 cDNA with the shRNA site mutated (shHmga2 wt); (4) shHmga2 plus the full-length shRNA-mutated Hmga2 with let-7 sites in the 3' UTR mutated (shHmga2 m7); (5) shHmga2 plus the full-length shRNA-mutated Hmga2 with the start codon mutated (shHmga2 ATG wt); and (6) shHmga2 plus the full-length shRNA-mutated Hmga2 with the start codon and let-7 sites mutated (shHmga2 ATG m7). Cells were plated in triplicate, RNA was prepared using RNA-Bee as per manufacturers' instructions and RNA-seq studies were performed using standard methods. For further details on library construction and next-generation sequencing, please contact the contributor.

ORGANISM(S): Mus musculus

SUBMITTER: Julian Downward

PROVIDER: E-GEOD-50932 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Analysis of gene expression with the Hmga2 allelic series.

Project description:In this study, we introduced a series of expression constructs into a mouse lung cancer cell line (482N1): (1) a control short hairpin RNA (shluc) plus the empty expression vector (empty); (2) an shRNA targeting Hmga2 (shHmga2) plus empty; (3) shHmga2 plus an expression vector for the full-length Hmga2 cDNA with the shRNA site mutated (shHmga2 wt); (4) shHmga2 plus the full-length shRNA-mutated Hmga2 with let-7 sites in the 3' UTR mutated (shHmga2 m7); (5) shHmga2 plus the full-length shRNA-mutated Hmga2 with the start codon mutated (shHmga2 ATG wt); and (6) shHmga2 plus the full-length shRNA-mutated Hmga2 with the start codon and let-7 sites mutated (shHmga2 ATG m7).

2013-09-18 | GSE50932 | GEO

Developmental stage-specific interplay between GATA1 and IGF signaling in fetal hematopoiesis and leukemogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE16676: Rescue of murine Gata1s mutant M7 leukemic cells by full-length Gata1 GSE16677: Gene expression profiling of Down Syndrome (DS)-AMKL and non-DS AMKL samples GSE16679: Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia GSE16682: Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors GSE16684: Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors depends on IGF signaling Refer to individual Series

2010-08-01 | E-GEOD-16655 | biostudies-arrayexpress

High mobility group protein-mediated transcription requires DNA damage marker γ-H2AX

Project description:The eukaryotic genome is organized into chromatins, the physiological template for DNA-dependent processes including replication, recombination, repair, and transcription. Chromatin-mediated transcription regulation involves DNA methylation, chromatin remodeling, and histone modifications. However, chromatin also contains non-histone chromatin-associated proteins, of which the high-mobility group (HMG) proteins are the most abundant. Although it is known that HMG proteins induce structural changes of chromatin, the processes underlying transcription regulation by HMG proteins are poorly understood. Here we decipher the molecular mechanism of transcription regulation mediated by the HMG AT-hook 2 protein (HMGA2). We combined proteomic, ChIP-seq, and transcriptome data to show that HMGA2-induced transcription requires phosphorylation of the histone variant H2AX at S139 (H2AXS139ph; γ-H2AX) mediated by the protein kinase ataxia telangiectasia mutated (ATM). Furthermore, we demonstrate the biological relevance of this mechanism within the context of TGFβ1 signaling. The interplay between HMGA2, ATM, and H2AX is a novel mechanism of transcription initiation. Our results link H2AXS139ph to transcription, assigning a new function for this DNA damage marker. Controlled chromatin opening during transcription may involve intermediates with DNA breaks that may require mechanisms that ensure the integrity of the genome.

2020-12-15 | PXD016586 | Pride

Streptomyces sp. M7 LC-MS - Streptomyces sp. M7 has demonstrated ability to remove lindane from culture media and soils

Project description:Streptomyces sp. M7 has demonstrated ability to remove lindane from culture media and soils. In this study, we used MS-based label-free quantitative proteomic to understand lindane degradation and its metabolic context in Streptomyces sp. M7. We identified the proteins involved in the up-stream degradation pathway. Our results demonstrated that mineralization of lindane is feasible since proteins from an unusual down-stream degradation pathway were also identified. Degradative steps were supported by an active catabolism that supplied energy and reducing equivalents in the form of NADPH. This is the first study in which degradation steps of an organochlorine compound and metabolic context are elucidate in a biotechnological genus as Streptomyces. These results serve as basement to study other degradative actinobacteria and to improve the degradation processes of Streptomyces sp. M7.

2018-08-10 | PXD010607 | Pride

Transcription profiling by array of MDA-MB-231 cells with HMGA2 knock-down

Project description:We have reported that the nuclear protein high mobility group A2 (HMGA2), is required for the induction of EMT by TGF-beta (Thuault et al. J. Cell Biol. 2006). HMGA2 regulates a cohort of transcriptional regulators of the EMT process, such as Snail1 and Twist1 (Thuault et al. J. Biol. Chem. 2008, E-Jean Tan et al. J. Biol. Chem. 2012). Since HMGA2 is a chromatin-associated protein, we expect that it should regulate many genes in addition to the EMT-related factors. The aim of our study is to decipher novel molecular mechanisms that explain how EMT links to the process of tumor-initiating cell self-renewal via the chromatin factor HMGA2. In this experiment, we stably transfected human breast cancer MDA-MB-231 cells with shRNA against HMGA2 and investigated effects of the knock-down on global gene expression using Affymetrix arrays, in order to identify novel downstream players involved in this network. In parallel experiments we also analyzed the phenotypic effects of the HMGA2 knock-down on MDA-MB-231 cell proliferation, survival and inavasiveness.

2012-02-13 | E-MEXP-3547 | biostudies-arrayexpress

High Mobility Group protein mediated transcription requires DNA damage marker Î³-H2AX

Project description:The eukaryotic genome is organized into chromatin, which constitutes the physiological template for DNA-dependent processes including replication, recombination, repair and transcription. Chromatin mediated transcription regulation involves histone modifications, chromatin remodeling and DNA methylation. However, the precise biological function of non-histone chromatin-associated proteins is still unclear. The high mobility group proteins are the most abundant non-histone chromatin-associated proteins. Here we combined proteomic, ChIP-seq and transcriptome data to decipher the mechanism of transcriptional regulation mediated by the high mobility group AT-hook protein 2 (HMGA2). We showed that HMGA2-induced transcription requires H2AX phosphorylation at S139 (H2AXS139ph; Î³-H2AX), mediated by the kinase ataxia telangiectasia mutated (ATM). Furthermore, we demonstrated the relevance of this mechanism within the biological context of TGFB1-signaling. Our results link H2AXS139ph, a marker for DNA damage, to transcription, which is a new function for this histone modification. The interplay between HMGA2, ATM and H2AX is a novel mechanism of transcription initiation. Chip-seq data of HMGA2, H2AXS139ph and ATM obtained from Mouse embryonic Fibroblast cells in wt and Ko of Hmga2

2015-11-04 | E-GEOD-63861 | biostudies-arrayexpress

Proteomics of the Bee brain and in olfactory memory

Project description:Previous work has shown that a series of honey bee brain proteins were probably linked to the proboscis extension reflex (PER) , a model studying insect behaviour. Herein, it was the aim of the study to generate a “synaptic proteome” and to investigate which proteins were paralleling olfactory conditioning. To address this information, we applied a non-sophisticated olfactory conditioning model using the proboscis extension reflex (PER) in the honeybee (Apis mellifera). Foraging honeybees were used in the study and three groups were formed, animals on water control, sucrose (PER) and olfactory conditioned (PER-conditioned) using 2-octanone. A synaptosomal preparation of honey bee brain for quantitative proteomics using stable isotope labelling (TMT 10plex) was performed. In addition a synaptosomal brain proteome was generated. Protein levels that were modified during olfactory conditioning were associated with “SNARE interactions in vesicular transport” (BET1 and VAMP7), ABC transporters, and fatty acid degradation pathways.. A honey bee synaptosomal proteome dataset including neurotransmitter receptors and transporters was generated.

2019-05-27 | PXD011217 | Pride

NELF-dependent transcription activation

Project description:Jurkat T-cells were latently infected with a defective HIV provirus carrying a GFP reporer gene. The cells were superinfected with a lentiviral vector expressing shRNA to NELF-E. The impact of NELF-depletion on RNAP II distribution on cellular genes and the HIV provirus was measured by ChIP-Seq. Data sets contained between 45 and 56 million mapped reads Four samples were compared: Control shRNA, NELF-E shRNA, Control shRNA plus TNF-a, NELF-E shRNA plus TNF-a.

2014-03-26 | E-GEOD-47481 | biostudies-arrayexpress

Homo sapiens

Project description:MicroRNA expression array of 1833 cells: control vs. HMGA2 shRNA

| PRJNA187198 | ENA

Transcription factor HMGA2 controls the K-RAS mediated transformation-specific genetic program

Project description:A genome-wide survey of transcriptional targets responding to chronic KRAS/MAPK (mitogen-activated protein kinase) pathway activation in rat ovarian surface epithelial cells (ROSE 199) has identified multiple differentially expressed transcriptional regulators including the architectural transcription factor high mobility group AT hook 2 (HMGA2). To elucidate the role of HMGA2 in the transcriptional network affected by oncogenic signaling, we used an integrated approach combining RNAi-mediated silencing, microarray-based expression profiling, computational prediction of transcription factor binding sites in target gene promoters and phenotypic analysis. Knocking-down HMGA2 resulted in the reversion of epithelial-mesenchymal transition, loss of anchorage independence and in a substantial restoration of the gene expression pattern characteristic of non-transformed ROSE cells. Computational prediction of transcription factor binding sites in the promoters of HMGA2-regulated genes and expression profiling revealed a preferential role of activator complex-1 (AP-1) components Fra-1 and JunB in target gene regulation. Forced expression of HMGA2 did not transform normal ovarian epithelial cells, suggesting that HMGA2 up-regulation is not sufficient for inducing the transformed phenotype, but mediates cancer-specific phenotypic traits in cells expressing mutated KRAS and, hence, oncogene addiction.

2010-03-01 | GSE14658 | GEO

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