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SRX8030789: GSM4445942: H3K27ac; Mus musculus; ChIP-Seq
1 ILLUMINA (Illumina MiSeq) run: 14.8M spots, 1.7G bases, 606.2Mb downloads

Submitted by: NCBI (GEO)
Study: BCL11A promotes myeloid leukemogenesis by abrogating the transcriptional activity of PU.1 [ChIP-seq]
show Abstracthide Abstract
The transcriptional repressor Bcl11a is involved in hematological malignancies, B-cell development and fetal to adult hemoglobin switching, however, the molecular mechanism how Bcl11a promotes development of myeloid leukemia remains largely unknown. We found that Bcl11a cooperates with the pseudokinase Trib1 in AML development. Bcl11a promotes proliferation of Trib1-expressing AML cells both in vitro and in vivo. ChIP-seq analysis showed that Bcl11a is significantly associated on DNA-binding with PU.1 that promotes myeloid differentiation, and Bcl11a represses a number of PU.1 target genes such as Clec5a, Fcgr3 and Csf1r. The repression of PU.1 target genes by Bcl11a is achieved by both sequence-specific DNA binding activity and recruitment of corepressors by Bcl11a, and suppression of corepressor components HDAC1 and LSD1 cancelled the repressive activity. Association of high level of expression of BCL11A and worse prognosis is observed in human AML patients, and blocking of BCL11A expression upregulates PU.1 target expression, inhibits engraftment to bone marrow, and enhances myeloid differentiation of HL-60 cells, suggesting that BCL11A is involved in human myeloid malignancies via the PU.1 transcriptional activity. Overall design: Examination of binding sites of 2 transcription factors and Histone H3K27ac in a single cell line
Sample: H3K27ac
SAMN14488157 • SRS6403147 • All experiments • All runs
Organism: Mus musculus
Library:
Instrument: Illumina MiSeq
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: SINGLE
Construction protocol: Lysates were clarified from sonicated nuclei and immunoprecipitated with each antibodies Libraries were prepared according to Illumina's instructions accompanying the ThruPLEX DNA-seq 6S (12) Kit (R400523). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3' end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on an Illumina instrument following the manufacturer's protocols.
Experiment attributes:
GEO Accession: GSM4445942
Links:
Runs: 1 run, 14.8M spots, 1.7G bases, 606.2Mb
Run# of Spots# of BasesSizePublished
SRR1145305614,790,1511.7G606.2Mb2021-12-23

ID:
10471752

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