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Transcriptome sequencing of K562 cells stably expressing SUMO negative MYB

ABSTRACT: Transcriptome sequencing of K562 cells stably expressing SUMO negative MYB

PROVIDER: PRJNA512467 | ENA |

REPOSITORIES: ENA

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			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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Transcriptome sequencing of K562 cells stably expressing SUMO negative MYB

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

SUMO proteome analysis of K562 cells expressing only TBC1D23-S or -L

Project description:A number of 40000000 TBC1D23 KO K562 cells, or cells expressing only TBC1D23-L or -S were collected for identifying and quantitating endogenous SUMO modifications. Intracellular SUMO Remnant Motif identification was performed using a PTMScan HS Ubiquitin/SUMO remnant kit (Cell Signaling Technologies, #59322) according to the instructions of manufacturers.

2026-01-04 | PXD072614 |

MYB ChIP-Seq of K562 cells

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

MYB ChIP-Seq of K562 cells

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Transcriptional repression of c-Myb and GATA-2 is involved in the effects of C/EBPα in p210 BCR/ABL-expressing cells

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.

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Transcription profiling of human monocytes infected with adenovirus expressing either c-Myb or v-Myb

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.

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Transcriptome analysis of melanoma cells stably expressing BMP6

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Gene expression data from MCF7 cells stably expressing COX7RP

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Expression (Gene) array from AMl12-Zfp125- stably expressing cells

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Bidirectional enhancer RNAs regulate different MYB promoters

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

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