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Binding Changes in Chromatin Factors Upon Targeted XPO1 Inhibition in T Cells

ABSTRACT: We assessed the chromatin localization of XPO1 and p300 in response to C646 (10 uM), S109 (1 uM), and SP100030 (1 uM). We used CUT&RUN sequencing as a lower-input (500,000 cells per sample), higher-sensitivity alternative to ChIP-Seq to assess chromatin binding of different factors

ORGANISM(S): Homo sapiens

PROVIDER: GSE244396 | GEO | 2024/05/07

REPOSITORIES: GEO

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Binding Changes in Chromatin Factors Upon Targeted XPO1 Inhibition in T Cells

Project description:We assessed the chromatin localization of XPO1, different histone markers, and transcription factors associated with T cell activation with and without SP100030 treatment We used CUT&RUN sequencing as a lower-input (500,000 cells per sample), higher-sensitivity alternative to ChIP-Seq to assess chromatin binding of different factors

2024-02-01 | GSE228211 | GEO

Gene expression analysis of hepatic stellate cells using Illumina HumanHT-12_V4 beadchip

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NPM1-fusion proteins promote myeloid leukemogenesis through XPO1-dependent HOX activation [Cut & Run]

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XPO1 amplification abrogates the effects of E571K XPO1 mutation in B-cell lymphoma

Project description:XPO1 gene encodes exportin 1 (XPO1) that controls the nuclear export of cargo proteins and RNAs. Almost 25% of primary mediastinal B-cell lymphomas (PMBL) and classical Hodgkin lymphomas (cHL) cases harboured a recurrent XPO1 point mutation (NM_003400, chr2:g61718472C>T) resulting in the E571K modification within the hydrophobic groove of the protein, the site of cargo proteins binding. We investigated the functional impact of XPO1E571K mutation using cell lines having various XPO1 status. We first confirmed that the mutation was present both within the XPO1 mRNA and the corresponding protein. In the U2940 cell line having a wild-type (wt) XPO1 gene, we introduced the E571K mutation using several CRISPR-Cas9 strategies. Using a barcoding method to trace the mutation, we observed that the mutation gave no advantage in vitro. Indeed, the effects of XPO1E571K mutation were hidden by the presence of the XPO1 wt allele. Strikingly, XPO1E571K mutation never occurred as homozygous or hemizygous in our patients�� cohort. We further showed that XPO1E571K mutation modified selinexor binding to XPO1 and in turn, its sensitivity to this drug. We concluded that the balance between the wild-type and the mutated allele of XPO1 is a key element in defining XPO1 functions and oncogenic properties.

2020-10-01 | PXD016916 | Pride

Targeted in situ genome-wide profiling with high efficiency for low cell numbers

Project description:Cleavage Under Targets and Release Using Nuclease (CUT&RUN) is an epigenomic profiling strategy in which antibody-targeted controlled cleavage by micrococcal nuclease releases specific protein-DNA complexes into the supernatant for paired-end DNA sequencing. As only the targeted fragments enter into solution, and the vast majority of DNA is left behind, CUT&RUN has exceptionally low background levels. CUT&RUN outperforms the most widely- used Chromatin Immunoprecipitation (ChIP) protocols in resolution, signal-to-noise, and depth of sequencing required. In contrast to ChIP, CUT&RUN is free of solubility and DNA accessibility artifacts and has been used to profile insoluble chromatin and to detect long-range 3D contacts without cross-linking. Here we present an improved CUT&RUN protocol that does not require isolation of nuclei and provides high-quality data starting with only 100 cells for a histone modification and 1000 cells for a transcription factor. From cells to purified DNA CUT&RUN requires less than a day at the lab bench and requires no special skills.

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Binding Changes in Chromatin Factors Upon Targeted XPO1 Inhibition in T Cells

Project description:Binding Changes in Chromatin Factors Upon Targeted XPO1 Inhibition in T Cells

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Binding Changes in Chromatin Factors Upon Targeted XPO1 Inhibition in T Cells

Project description:Binding Changes in Chromatin Factors Upon Targeted XPO1 Inhibition in T Cells

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P300-mediated adaptive conversion of glioma stem cells to vascular-like cells in response to therapeutic stress promotes tumor recurrence [ATAC_SeqIRC646]

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