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ChIP-seq of MOZ (Flag-V5-BIO tagged) in mouse mouse craniofacial development

ABSTRACT: Carboxy-terminally tagged MOZ (Flag-V5-BIO tagged) was detected by ChIP-seq using anti-V5 antibody (Sigma, A7345) to precipitate chromatin associated with MOZ

ORGANISM(S): Mus musculus

PROVIDER: GSE134607 | GEO | 2019/07/23

REPOSITORIES: GEO

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ChIP-seq of MOZ (Flag-V5-BIO tagged) in mouse mouse craniofacial development

Project description:ChIP-seq of MOZ (Flag-V5-BIO tagged) in mouse mouse craniofacial development

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Gene expression analysis of V5 tagged Sox17 expressing ES cells

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Gene expression analysis of V5 tagged Sox17 expressing ES cells

Project description:Analysis of the expression of KH2 embryonic stem cells inducibly expressing V5 tagged Sox17 protein. Results provide information on the endodermal gene expression program activated after Sox17 expression in ES cells. Total RNA extracted from 48 hours doxycycline induced compaired to non-induced Sox17-V5 expressing ES cells

2013-04-23 | E-GEOD-43233 | biostudies-arrayexpress

ChIP-seq for V5 in the mammary tissues of Elf5-V5 mice

Project description:V5 tagged Elf5.

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ChIP-Seq analysis of V5-tagged budding yeast Rif1

Project description:Genomic locations of V5-tagged budding yeast Rif1 (including wilt-type and designer mutants) were analysed by ChIP-Seq. Mutants tested were rif1-7A and rif1-7E, in which Ser/Thr residues in the cluster of SQ/TQ sites were mutated to Ala or Glu, respectively. We also tested tested rif1-∆594, in which the C-terminal 594 amino acids were deleted.

2023-11-19 | E-MTAB-13452 | biostudies-arrayexpress

The genome wide mapping of H3K9 and H3K23 acetylation in Moz+/+ and Moz-/- MOZ-TIF2 AML cells

Project description:Monocytic leukemia Zinc finger protein (MOZ) is a MYST-type acetyltransferase involved in chromosomal translocation in acute myelogenous leukemia (AML) and myelodysplastic syndrome. MOZ is established as essential for hematopoiesis; however, the role of MOZ in AML has not been addressed. We propose that MOZ is critical for AML development induced by MOZ-TIF2 fusions. Moz-deficient hematopoietic stem/progenitor cells (HSPCs) expressing MOZ-TIF2 could form colonies in vitro but could not induce AML in mice. By contrast, Moz was dispensable for colony formation by HOXA9-transduced cells and AML development caused by HOXA9 and MEIS1, suggesting a specific requirement for MOZ in AML induced by MOZ/MLL-fusions. Expression of the of Meis1, but not Hoxa9, was reduced in Moz-deficient MOZ-TIF2 AML cells. AML development induced by MOZ-TIF2 was rescued by introducing Meis1 into Moz-deficient cells carrying MOZ-TIF2. Meis1 deletion impaired MOZ-TIF2-mediated AML development. Active histone modifications were also severely reduced at the Meis1 locus in Moz-deficient MOZ-TIF2 AML cells. These results suggest that endogenous MOZ is critical for MOZ-fusion-induced AML development and maintains active chromatin signatures at target gene loci.

2022-07-24 | GSE208741 | GEO

V5-tagged LIMD1 in HEK293 cells with or without JNK2 activation

Project description:The experiment was conducted to identify JNK phosphorylation sites on human LIM domain containing protein-1 (LIMD1). V5-tagged LIMD1 was co-transfected or not with a constitutively active form of JNK2 and purified. The purified proteins were subjected to SDS-PAGE, protease K digestion and MS/MS analysis. The data were searched against Swissprot using Mascot server v2.3. The fixed modification was set to carbamidomethylation of C, and variable modifications were set to oxidation of M, phosphorylation of ST, phosphorylation of Y. Mass values were set as monoisotopic. Peptide mass tolerance was set to +/-10ppm, and MS/MS tolerance was set to +/-0.8Da.

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Trichormus variabilis V5 strain:V5

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Distribution of MOZ (KAT6A) in the genome and effects of MOZ on gene expression during mouse craniofacial development

Project description:Distribution of MOZ (KAT6A) in the genome and effects of MOZ on gene expression during mouse craniofacial development

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MORF and MOZ acetyltransferases target unmethylated CpG islands through the winged helix domain

Project description:Human acetyltransferases MOZ and MORF are implicated in chromosomal translocations associated with aggressive leukemias. Oncogenic translocations involve the far amino terminus of MOZ/MORF, the function of which remains unclear. Here, we identified and characterized two structured winged helix domains, WH1 and WH2, in MORF and MOZ. WHs bind DNA in a cooperative manner, with WH1 specifically recognizing unmethylated CpG sequences. Structural and genomic analyses show that the DNA binding function of WHs targets MORF/MOZ to gene promoters, stimulating transcription and H3K23 acetylation, and WH1 recruits oncogenic fusions to HOXA genes that trigger leukemogenesis. Cryo-EM, NMR, mass spectrometry and mutagenesis studies provide mechanistic insight into the DNA-binding mechanism, which includes the association of WH1 with the linker DNA and binding of WH2 to the dyad of the nucleosome, with the latter being further modulated by the neighboring domain DPF and autoacetylation of MORF. The discovery of WHs in MORF and MOZ and their DNA binding functions could open a new avenue in developing therapeutics to treat diseases associated with aberrant MOZ/MORF acetyltransferase activities.

2023-03-11 | PXD036192 | Pride

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