We used Illumina-HiSeq4000 to sequence 4sU-labelled RNA samples isolated from unchallenged and DNA damaged HeLa Flp-In cells, which revealed the nature of transcriptional response folowing genotoxic stress and the contribution of P-TEFb kinase in DNA damage-induced gene transcription. Overall design: We mock treated or treated HeLa Flp-In cells for 1 or 2 hr with DMSO, 4-NQO, or 4-NQO + flavopiridol (FP) as indicated below. During the last 30 minutes of the treatments, we labeled the RNA or not with the nucleoside analogue 4-thiouridine (500µM 4sU) for 30 minutes.
P-TEFb Activation by RBM7 Shapes a Pro-survival Transcriptional Response to Genotoxic Stress.
Cell line, Subject
View SamplesGene expression analysis to compare control cells and sorted cells
Identification of two major autoantigens negatively regulating endothelial activation in Takayasu arteritis.
Specimen part
View SamplesTarget gene of mineralocorticoid receptor (MR) is comparatively unknown, although distal convoluted tubule (DCT) expresses MR in in vivo.
Genome-wide analysis of murine renal distal convoluted tubular cells for the target genes of mineralocorticoid receptor.
Cell line, Treatment
View SamplesRat mast cell line RBL-2H3 was analyzed to investigate the molecular mechanism of Dectin-1-mediated activation and responses of mast cells.
Dectin-1-mediated signaling leads to characteristic gene expressions and cytokine secretion via spleen tyrosine kinase (Syk) in rat mast cells.
Specimen part, Cell line
View SamplesEffect of Fut8 deletion in MEF
The absence of core fucose up-regulates GnT-III and Wnt target genes: a possible mechanism for an adaptive response in terms of glycan function.
Cell line
View SamplesTo investigate the evolutionary divergence of transcriptional regulation between the mouse subspecies, we performed transcriptome analysis by microarray on testes from the X-chromosome substitution strain, which carries different subspecies-derived X chromosome on the host subspecies genome. Transcription profiling showed that large-scale aberrations in gene expression were occurred on the introgressed X chromosome. This improper expression was restored by introducing chromosome 1 from the same donor strain as the X chromosome, suggesting that the genetic incompatibility between trans-acting regulatory gene(s) on chromosome 1 and X-linked downstream genes might be a cause of the misregulation.
Evolutionarily diverged regulation of X-chromosomal genes as a primal event in mouse reproductive isolation.
Specimen part
View SamplesThe publicly available genome sequence information of two rice strains, japonica cultivar Nipponbare and indica cultivar 93-11, opens a great opportunity for investigation of performances DNA genotyping by high-density oligonucleotide arrays. Here, we compare single feature polymorphism (SFP) detection performances between whole genome hybridization and transcript hybridization using Affymetrix Rice Expression Array and the two rice cultivars.
A simple optimization can improve the performance of single feature polymorphism detection by Affymetrix expression arrays.
Specimen part
View SamplesCancer 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. HEXIM1 responds to nucleotide stress. Knockdown of HEXIM1 rescues neural crest and melanoma nucleotide stress phenotypes in vivo. Mechanistically, under nucleotide stress, HEXIM1 is induced to form an inhibitory complex with P-TEFb, the kinase that initiates transcription elongation, to pause transcription at tumorigenic genes. The resulting alteration in gene expression also causes anti-tumorigenic transcripts to bind to and be stabilized by HEXIM1. HEXIM1 therefore plays an important role in inhibiting cancer cell-specific gene transcription while also facilitating anti-cancer gene expression. Our study reveals a novel role for HEXIM1 in coupling nucleotide metabolism with transcriptional regulation in melanoma. Overall design: RNA-seq analysis of human A375 melanoma cells treated with either DMSO or 25 µM A771726 for 0-72 hrs.
Stress from Nucleotide Depletion Activates the Transcriptional Regulator HEXIM1 to Suppress Melanoma.
No sample metadata fields
View SamplesCancer 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. HEXIM1 responds to nucleotide stress. Knockdown of HEXIM1 rescues neural crest and melanoma nucleotide stress phenotypes in vivo. Mechanistically, under nucleotide stress, HEXIM1 is induced to form an inhibitory complex with P-TEFb, the kinase that initiates transcription elongation, to pause transcription at tumorigenic genes. The resulting alteration in gene expression also causes anti-tumorigenic transcripts to bind to and be stabilized by HEXIM1. HEXIM1 therefore plays an important role in inhibiting cancer cell-specific gene transcription while also facilitating anti-cancer gene expression. Our study reveals a novel role for HEXIM1 in coupling nucleotide metabolism with transcriptional regulation in melanoma. Overall design: RNA-seq analysis of human Tet-On HEXIM1-inducible A375 melanoma cells treated with either DMSO or 1 µg/mL doxycycline in triplicate for 48 hrs.
Stress from Nucleotide Depletion Activates the Transcriptional Regulator HEXIM1 to Suppress Melanoma.
No sample metadata fields
View SamplesTranscriptional profiling of NKAES-derived NK cells after 7 days of culture compared to primary human NK cells and NK cells stimulated by low or high dose IL2 after 7 days of culture.
Expansion of highly cytotoxic human natural killer cells for cancer cell therapy.
Specimen part
View Samples