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Gene expression in ABHD5-knockdown RAW264.7 cells

ABSTRACT: RAW cells or ABHD5-KD RAW cells were subjected to microarray assays. Each group contain 3 samples.

ORGANISM(S): Mus musculus

PROVIDER: GSE80066 | GEO | 2016/05/12

SECONDARY ACCESSION(S): PRJNA317736

REPOSITORIES: GEO

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Gene expression in ABHD5-knockdown RAW264.7 cells

Project description:RAW cells or ABHD5-KD RAW cells were subjected to microarray assays. Each group contain 3 samples. To explore the regulatory role of ABHD5 in metabolic pathways, RAW cells or ABHD5-KD RAW cells were subjected to microarray assays.

2016-05-12 | E-GEOD-80066 | biostudies-arrayexpress

Gene expression in ABHD5-KD RAW cells or RAW cell-primed CT-26 cells

Project description:RAW cells,ABHD5-KD RAW cells or those macrophage-primed CT-26 cells were subjected to microarray assays.Each group contain 3 samples.

2019-08-11 | GSE135673 | GEO

Expression profile of the 22Rv1 cells overexpressing ABHD5

Project description:ABHD5 is a crucial metabolic regulator of cancer cells. The goal of this study is to identify the regulation of gene expression by ABHD5 in prostate cancer cells using RNA-seq.

2020-11-19 | GSE151957 | GEO

Next-generation sequencing of RNA samples from the mice heart of Control, ABHD5-KO and ABHD5-KO transduced with AAV9 expressing HDAC4-NT (AAV9-NT)

Project description:The purpose of this experiment is to investigate the consequences of ABHD5 deletion in the heart and to evaluate HDAC4-NT gene transfer using AAV9 in ABHD5-KO.

2019-08-10 | GSE135662 | GEO

ABHD5 inhibits YAP-induced c-Met overexpression and colon cancer cell stemness via suppressing YAP methylation

Project description:Cancer stemness represents a major source of development and progression of colorectal cancer (CRC). c-Met critically contributes to CRC stemness, but how c-Met is activated in CRC remains elusive. We previously identified the lipolytic factor ABHD5 as an important tumour suppressor gene in CRC. Here, we show that loss of ABHD5 promotes c-Met activation to sustain CRC stemness in a non-canonical manner. Mechanistically, we demonstrate that ABHD5 interacts in the cytoplasm with the core subunit of the SET1A methyltransferase complex, DPY30, thereby inhibiting the nuclear translocation of DPY30 and activity of SET1A. In the absence of ABHD5, DPY30 translocates to the nucleus and supports SET1A-mediated methylation of YAP and histone H3, which sequesters YAP in the nucleus and increases chromatin accessibility to synergistically promote YAP-induced transcription of c-Met, thus promoting the stemness of CRC cells. This study reveals a novel role of ABHD5 in regulating histone/non-histone methylation and CRC stemness. We used microarrays to detail the gene expression of HCT116 colon cancer cell and ABHD5 knockdown HCT116 cell.

2021-11-24 | GSE185056 | GEO

Gene expression in ABHD5-KD RAW cells or RAW cell-primed CT-26 cells

Project description:Gene expression in ABHD5-KD RAW cells or RAW cell-primed CT-26 cells

| PRJNA559621 | ENA

Expression profile of the 22Rv1 cells overexpressing ABHD5

Project description:Expression profile of the 22Rv1 cells overexpressing ABHD5

| PRJNA637888 | ENA

Host pathogen interaction between Staphylococcus aureus ATCC25923 and murine RAW264.7 macrophage-like cells

Project description:Macrophages infected with S. aureus were subjected to gene expression profiling to undertake a complete understanding of the interaction induced gene expression changes in both, S.aureus and the RAW macrophages.

2010-08-11 | GSE23538 | GEO

Exosomal-miRNA sequencing of optineurin gene knockdown BV2 cells and wild type BV2 cells

Project description:To compare the miRNA profiles in exosomes derived from optineurin gene knockdown (Optn-KD)BV2s cells and wild type (WT) BV2 cells, BV2 cells were divided into two groups, Optn-KD group or WT group. We treated the Optn-KD group with Optn siRNA for 24 hours. Then, MiRNA profiles for each group were examined by Illumina HiSeq4000. We found differentiated miRNA profiles in the two groups. Compared with WT BV2 cell-derived exosomes, 4 miRNAs (miR-125b-5p, miR-351-5p, miR-505-5p, miR-novel-chr8_37700) were up-regulated and 2 miRNAs (miR-574-5p, miR-99b-5p) were down-regulated in Optn-KD BV2 cell-derived exosomes. This study provides a framework for characterizing the exosomal-miRNAs in Optn-KD BV2 cells.

2021-03-19 | GSE169175 | GEO

Genome-wide maps of gV sPLA2 binding sites in Raw 264.7 cells

Project description:We have searched genome-wide binding sites of mouse group V secretory phospholipase A2 (gV sPLA2) in Raw 264.7 cells. Since we previously had technical problems in immunoblotting analysis and immunoprecipitation of the gV sPLA2 protein due in part to unavailability of a specific antibody against mouse gV sPLA2 and other issues, we used a monoclonal antibody against the Myc-tag to analyze gV sPLA2 knockdown (KD) RAW 264.7 cells with re-constitutive expression of Myc-tagged gV sPLA2 or Myc-tagged gV sPLA2-H48Q, lacking catalytic activity, as well as gV sPLA2 KD RAW 264.7 cells transfected with empty vector. Among the significant peaks, the region corresponding to -375 ~ +6 from the transcriptional start site of the Pgk1 (phosphoglycerate kinase 1) gene was the strongest binding peak in the nucleus of both gV sPLA2 KD cells expressing Myc-tagged gV sPLA2 and gV sPLA2 KD cells expressing Myc-tagged gV sPLA2-H48Q. Meanwhile, the Pgk1 gene was not identified as a significant peak in the nucleus of gV sPLA2 KD cells transfected with empty vector.

2021-03-26 | GSE156528 | GEO

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