Transcriptome sequencing of K562 cells stably expressing SUMO negative MYB
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA512467 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8382980_1.fastq.gz | Fastqsanger.gz | |||
| SRR8382980_2.fastq.gz | Fastqsanger.gz | |||
| SRR8382981_1.fastq.gz | Fastqsanger.gz | |||
| SRR8382981_2.fastq.gz | Fastqsanger.gz | |||
| SRR8382976_1.fastq.gz | Fastqsanger.gz |
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Project description:We expanded our previously reported transcriptome profiling of K-562 cells (GSE85187) by analyzing the global transcriptional change upon rescue of endogenous MYB knock down (KD) with SUMO-conjugation deficient mutant of MYB (2KR-MYB) and SUMO-binding deficient mutant of MYB (ANAA-MYB) in comparison with K-562 cells treated with siGENOME non-targeting siRNA (GSE85187) , endogenous MYB KD treated with si2992 (GSE85187), rescue of endogenous MYB KD with wild-type MYB (GSE85187) and rescue of endogenous MYB KD with D152V mutant of MYB (GSE85187).
2023-07-17 | GSE124542 | GEO
Project description:We analyzed genome-wide chromatin binding of the transcription factor c-Myb using ChIP-Seq. K-562 cell lines stably expressing N-termianl 3xTY tagged Myb (pEFneo-3xTY-Myb) and control cell lines expressing the tag (pEFneo-3xTY) were used.
2021-04-28 | GSE124541 | GEO
Project description:MYB is a pivotal oncogenic driver in leukemia and is overexpressed through various mechanisms. Transcriptional regulation of MYB is complex with an alternative MYB promoter (TSS2) located in intron 1. Here, we identified two bidirectional enhancer RNAs transcribed from the -34 kb enhancer of MYB. These two eRNAs both upregulate MYB transcription, and promote proliferation and migration in leukemia cells. To further elucidate how eRNAs regulate MYB expression, we analyzed MYB differential exon usage in RNASeq data with the DEXSeq package after overexpression of eRNAs in K562 cells. We found that bidirectional enhancer RNAs regulate different MYB promoters. Transcription initiating from TSS2 produces N-terminally truncated MYB protein lacking the first 20 amino acids. To analyze the genes and pathways affected by both MYB isoforms, RNA-seq was performed after MYB or N-terminally truncated MYB was overexpressed in K562 cells. We found that N-terminally truncated MYB exhibits different activity in K562 cells, where it not only activates different primary targets, but also different downstream pathways altogether.
2024-08-01 | GSE263511 | GEO
Project description:Effect of c-Myb knockdown in K562 on global gene expression after knockdown using siRNA oligo si323 or si2992.
2012-01-01 | E-MTAB-807 | biostudies-arrayexpress
Project description:Levels of C/EBPα are low in myeloid blast crisis (BC) of chronic myelogenous leukemia (CML) and its expression in p210BCR/ABL-expressing hematopoietic cells induces granulocytic differentiation, inhibits proliferation and suppresses leukemogenesis. To assess the mechanisms involved in these effects, C/EBPα targets were identified by microarray analyses. Upon C/EBPα activation, expression of c-Myb and GATA-2 was repressed in 32D-BCR/ABL, K562 and CML-BC primary cells but only c-Myb levels decreased slightly in CD34+ normal progenitors. The role of these two genes for the biological effects of C/EBPα was assessed by perturbing their expression in K562 cells. Expression of c-Myb blocked the proliferation inhibition and differentiation-inducing effects of C/EBPα while c-Myb siRNA treatment enhanced C/EBPα-mediated proliferation inhibition and induced changes in gene expression indicative of monocytic differentiation. GATA-2 expression suppressed the proliferation inhibitory effect of C/EBPα but blocked in part the effect on differentiation; GATA-2 siRNA treatment had no effects on C/EBPα induction of differentiation but inhibited proliferation of K562 cells, alone or upon C/EBPα activation. In summary, the effects of C/EBPα in p210BCR/ABL -expressing cells depend, in part, on transcriptional repression of c-Myb and GATA-2. Since perturbation of c-Myb and GATA-2 expression has non identical consequences for proliferation and differentiation of K562 cells, the effects of C/EBPα appear to involve different transcription-regulated targets.
2008-06-13 | GSE11766 | GEO
Project description:Earlier we have shown important roles of MYB in pancreatic tumor pathobiology. To better understand the role of MYB in the tumor microenvironment and identify MYB-associated secreted biomarker proteins, we conducted mass spectrometry analysis of the secretome from MYB-modulated and control pancreatic cancer cell lines. We also performed in silico analyses to determine MYB-associated biofunctions, gene networks and altered biological pathways. We further investigated the secreted proteins for their potential biomarker properties.
2021-09-08 | PXD015126 | Pride
Project description:Most E2F-binding sites repress transcription through the recruitment of Retinoblasoma (RB) family members until the end of the G1 cell-cycle phase. Although the MYB promoter contains an E2F-binding site, its transcription is activated shortly after the exit from quiescence, before RB family members inactivation, by unknown mechanisms. We had previously uncovered a nuclear factor distinct from E2F, Myb-sp, whose DNA-binding site overlapped the E2F element and had hypothesized that this factor might overcome the transcriptional repression of MYB by E2F-RB family members. We have purified Myb-sp and discovered that Myc-associated zinc finger proteins (MAZ) are major components. We show that various MAZ isoforms are present in Myb-sp and activate transcription via the MYB-E2F element. Moreover, while forced RB or p130 expression repressed the activity of a luciferase reporter driven by the MYB-E2F element, co-expression of MAZ proteins not only reverted repression, but also activated transcription. Finally, we show that MAZ binds the MYB promoter in vivo, that its binding site is critical for MYB transactivation, and that MAZ knockdown inhibits MYB expression during the exit from quiescence. Together, these data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression.
2017-10-04 | PXD006857 | Pride
Project description:K562 cells, a myeloid leukemia cells line, were engineered to express a tamoxifen inducible dominant negative Myb (MERT). K562-MERT cells were cultured for 3 days in the absence and presence of 1 uM tamoxifen. The RNA was then extracted from the untreated and tamoxifen treated K562-MERT cells and submitted to Incyte Genomics for poly(A) RNA selection, probe preparation, hybridization of the labeled cDNA to the micorarray chip (Incyte Genomics) and data analysis.
2004-06-30 | E-MEXP-91 | biostudies-arrayexpress
Project description:The transcriptional activities of c-Myb and its oncogenic variant v-Myb were compared by expressing them in primary human monocytes using recombinant adenovirus vectors. All the samples were compared to cells infected with a control adenovirus expressing only GFP. The results showed that v-Myb, which differs from c-Myb only by N- and C-terminal deletions and eleven amino acid substitutions, has a qualitatively different transcriptional activity. Experiment Overall Design: 2 replicates of each type were analyzed. Replicates were performed independently, more than a week apart.
2007-12-12 | E-GEOD-2816 | biostudies-arrayexpress