Similar studies for GEO DataSets (Select 200068053) - GEO DataSets

Select item 2000680531.

Nucleotide stress induction of HEXIM1 suppresses melanoma by modulating cancer cell-specific gene transcription

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other

Platforms:: GPL18573 GPL16791
38 Samples

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Series

Accession:: GSE68053

ID:: 200068053

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Select item 2000680522.

Nucleotide stress induction of HEXIM1 suppresses melanoma by modulating cancer cell-specific gene transcription [ChIP-Seq]

(Submitter supplied) Cancer metabolism has been actively studied to gain insights into tumorigenic survival mechanisms and susceptibilities. In melanoma, we identify HEXIM1, a transcription elongation regulator, as a novel melanoma suppressor that participates in nucleotide stress regulation. HEXIM1 expression is low in melanoma. Its overexpression suppresses melanoma while its inactivation accelerates tumor onset in vivo. more...

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL16791
8 Samples

Download data: BEDGRAPH

Series

Accession:: GSE68052

ID:: 200068052

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Select item 2000680473.

Nucleotide stress induction of HEXIM1 suppresses melanoma by modulating cancer cell-specific gene transcription [reChIP-seq]

(Submitter supplied) Cancer metabolism has been actively studied to gain insights into tumorigenic survival mechanisms and susceptibilities. In melanoma, we identify HEXIM1, a transcription elongation regulator, as a novel melanoma suppressor that participates in nucleotide stress regulation. HEXIM1 expression is low in melanoma. Its overexpression suppresses melanoma while its inactivation accelerates tumor onset in vivo. more...

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL16791
4 Samples

Download data: BEDGRAPH

Series

Accession:: GSE68047

ID:: 200068047

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Select item 2000680454.

Nucleotide stress induction of HEXIM1 suppresses melanoma by modulating cancer cell-specific gene transcription [FAST-iCLIP]

(Submitter supplied) Cancer metabolism has been actively studied to gain insights into tumorigenic survival mechanisms and susceptibilities. In melanoma, we identify HEXIM1, a transcription elongation regulator, as a novel melanoma suppressor that participates in nucleotide stress regulation. HEXIM1 expression is low in melanoma. Its overexpression suppresses melanoma while its inactivation accelerates tumor onset in vivo. more...

Organism:: Homo sapiens

Type:: Other

Platform:: GPL18573
4 Samples

Download data: BW

Series

Accession:: GSE68045

ID:: 200068045

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Select item 2000680445.

Nucleotide stress induction of HEXIM1 suppresses melanoma by modulating cancer cell-specific gene transcription [ChIP-Seq2]

(Submitter supplied) Cancer metabolism has been actively studied to gain insights into tumorigenic survival mechanisms and susceptibilities. In melanoma, we identify HEXIM1, a transcription elongation regulator, as a novel melanoma suppressor that participates in nucleotide stress regulation. HEXIM1 expression is low in melanoma. Its overexpression suppresses melanoma while its inactivation accelerates tumor onset in vivo. more...

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL16791
4 Samples

Download data: BEDGRAPH

Series

Accession:: GSE68044

ID:: 200068044

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Select item 2000680406.

Nucleotide stress induction of HEXIM1 suppresses melanoma by modulating cancer cell-specific gene transcription [RNA-Seq2]

(Submitter supplied) Cancer metabolism has been actively studied to gain insights into tumorigenic survival mechanisms and susceptibilities. In melanoma, we identify HEXIM1, a transcription elongation regulator, as a novel melanoma suppressor that participates in nucleotide stress regulation. HEXIM1 expression is low in melanoma. Its overexpression suppresses melanoma while its inactivation accelerates tumor onset in vivo. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL16791
6 Samples

Download data: XLSX

Series

Accession:: GSE68040

ID:: 200068040

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 2000680397.

Nucleotide stress induction of HEXIM1 suppresses melanoma by modulating cancer cell-specific gene transcription [RNA-Seq1]

(Submitter supplied) Cancer metabolism has been actively studied to gain insights into tumorigenic survival mechanisms and susceptibilities. In melanoma, we identify HEXIM1, a transcription elongation regulator, as a novel melanoma suppressor that participates in nucleotide stress regulation. HEXIM1 expression is low in melanoma. Its overexpression suppresses melanoma while its inactivation accelerates tumor onset in vivo. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL16791
12 Samples

Download data: XLSX

Series

Accession:: GSE68039

ID:: 200068039

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Select item 2000530088.

Genome-wide map of RNA polymerase II, NELF, and DSIF in HeLa cells

(Submitter supplied) Most metazoan promoters have RNA polymerase II (Pol II) paused slightly downstream of the transcription start site by NELF and DSIF. This pausing keeps these promoters available for rapid induction by P-TEFb, whose activity causes NELF to dissociate and Pol II and DSIF to elongate on the gene. ChIP-Seq data was generated for Pol II, NELF, and DSIF in HeLa cells and used to look at pausing downstream of unannotated promoters.

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL11154
3 Samples

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Series

Accession:: GSE53008

ID:: 200053008

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Select item 2001280809.

RNA helicase DDX21 mediates nucleotide stress responses (ChIP-Seq)

(Submitter supplied) The RNA helicase DDX21 acts as trancriptional sensor for nucleotide lowering

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL16791
9 Samples

Download data: NARROWPEAK

Series

Accession:: GSE128080

ID:: 200128080

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Select item 20012852410.

Activation of P-TEFb by cAMP-PKA signaling in autosomal dominant polycystic kidney disease

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:: GPL13112 GPL23479
14 Samples

Download data: BEDGRAPH, TXT

Series

Accession:: GSE128524

ID:: 200128524

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Select item 20012852211.

Activation of P-TEFb by cAMP-PKA signaling in autosomal dominant polycystic kidney disease (RNA-Seq)

(Submitter supplied) We showed that pharmacological inhibition of P-TEFb attenuated cyst development in ADPKD mouse models. Genome-wide analyses demonstrated that P-TEFb inhibition abrogated transcriptional pause release and suppressed a pathologic gene expression program during cystogenesis. This work revealed a mechanism by which aberrant activation of P-TEFb-mediated transcription elongation promotes cystogenesis in ADPKD.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL23479
8 Samples

Download data: TXT

Series

Accession:: GSE128522

ID:: 200128522

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Select item 20012852112.

Activation of P-TEFb by cAMP-PKA signaling in autosomal dominant polycystic kidney disease (ChIP-Seq)

(Submitter supplied) We showed that pharmacological inhibition of P-TEFb attenuated cyst development in ADPKD mouse models. Genome-wide analyses demonstrated that P-TEFb inhibition abrogated transcriptional pause release and suppressed a pathologic gene expression program during cystogenesis. This work revealed a mechanism by which aberrant activation of P-TEFb-mediated transcription elongation promotes cystogenesis in ADPKD.

Organism:: Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL13112
6 Samples

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Series

Accession:: GSE128521

ID:: 200128521

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Select item 20004102313.

Transcriptional profiling of hypoxic cells and identification of HEXIM1-dependent genes.

(Submitter supplied) To identify primary response genes (PRGs) that were differently expressed within 1 hr of hypoxia exposure, we performed global transcriptional profiling using the Agilent Technologies SurePrint G3 Human GE Microarray . To identify Hexim1-dependent genes, we compare profiles of hypoxia PRGs in cells transfected with control or Hexim1 targeting double-strand siRNA

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL14550
5 Samples

Download data: TXT

Series

Accession:: GSE41023

ID:: 200041023

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20002452914.

Expression analysis of transgenic embryos carrying the mitf-BRAFV600E allele in the presence or absence of p53 function

(Submitter supplied) Investigation of expression differences between melanomas harvested from MiniCoopR-GFP versus MiniCoopR-SETDB1 transgenic zebrafish The embryos described in this study are further analyzed in a manuscript submitted for publication by White, et al.

Organism:: Danio rerio

Type:: Expression profiling by array

Platform:: GPL1319
12 Samples

Download data: CEL

Series

Accession:: GSE24529

ID:: 200024529

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Select item 20002452815.

Expression analysis of zebrafish melanoma and skin from the mitf-BRAFV600E;p53-/- line

(Submitter supplied) Investigation of expression differences between skin and melanomas from a transgenic BRAFV600E zebrafish model of melanoma The embryos described in this study are further analyzed in a manuscript submitted for publication by White, et al.

Organism:: Danio rerio

Type:: Expression profiling by array

Platform:: GPL1319
15 Samples

Download data: CEL

Series

Accession:: GSE24528

ID:: 200024528

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Select item 20002452716.

Expression analysis of 24hpf zebrafish embryos treated with Leflunomide 6.5uM

(Submitter supplied) Identification of genes differentially regulated after treatment of zebrafish embryos from 50% epiboly to 24hpf with 6.5uM leflunomide

Organism:: Danio rerio

Type:: Expression profiling by array

Platform:: GPL1319
6 Samples

Download data: CEL

Series

Accession:: GSE24527

ID:: 200024527

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Select item 20002452617.

A375 melanoma cells treated with leflunomide 25uM

(Submitter supplied) Human A375 melanoma cells were treated with leflunomide 25uM for 3 days, then RNA harvested

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL6884
6 Samples

Download data: TXT

Series

Accession:: GSE24526

ID:: 200024526

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Select item 20013690018.

MITF-low melanoma subtype models in zebrafish reveal transcriptional sub-clusters and MITF-independent residual disease

(Submitter supplied) The MITF-low melanoma transcriptional signature is predictive of poor outcome for patients but little is known about its biological signature. We used genetic models of zebrafish with low expression of mitfa (MITF-low) to study this biological subtype. Using genetic inhibition of MITF activity we discover minimal residual disease at the site of regression. We performed single cell RNA-seq (Smart-seq2) to characterise cells at the site of residual disease, and put in relation with primary tumours and recurring disease.

Organism:: Danio rerio

Type:: Expression profiling by high throughput sequencing

Platform:: GPL18413
332 Samples

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Series

Accession:: GSE136900

ID:: 200136900

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Select item 20013003719.

MITF-low zebrafish melanomas reveal cells with no MITF activity at the site of residual disease

(Submitter supplied) The MITF-low melanoma transcriptional signature is predictive of poor outcome for patients but little is known about its biological signature. We used genetic models of zebrafish with low expression of mitfa (MITF-low) to study this biological subtype. We performed whole bulk RNA-seq to classify zebrafish MITF-low melanoma that cluster mainly by their directionality of growth and assess their resemblance to patients’ MITF-low subgroups. more...