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ASCL1 phospho-regulation during lineage restrictions of embryonic stem cells (ATAC-Seq)

ABSTRACT: Here we investigate how ASCL1 levels and phosphorylation modulate its activity during lineage restrictions of embryonic stem cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE267617 | GEO | 2024/11/27

REPOSITORIES: GEO

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ASCL1 phospho-regulation during lineage restrictions of embryonic stem cells (RNA-Seq)

Project description:Here we investigate how ASCL1 levels and phosphorylation modulate its activity during lineage restrictions of embryonic stem cells.

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ASCL1 phospho-regulation during lineage restrictions of embryonic stem cells (ATAC-Seq)

Project description:ASCL1 phospho-regulation during lineage restrictions of embryonic stem cells (ATAC-Seq)

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ASCL1 phospho-regulation during lineage restrictions of embryonic stem cells (RNA-Seq)

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ASCL1 is a lineage oncogene providing therapeutic targets for high-grade neuroendocrine lung cancers

Project description:ChIP-Seq analysis performed on 5 ASCL1(+) cell lines and 2 ASCL1 (-) cell lines in order to understand the transcriptome of ASCL1 as it pertains to high-grade neuroendocrine lung cancers 5 ASCL1(+) lung cancer cell lines and 2 ASCL1(-) lung cancer cell lines were compared using ChIP-Seq analysis

2014-10-01 | E-GEOD-61197 | biostudies-arrayexpress

ASCL1 activates neuronal stem cell-like lineage programing through remodeling of the chromatin landscape in prostate cancer [ATAC-Seq]

Project description:Treatment with androgen receptor pathway inhibitors (ARPIs) in prostate cancer leads to the emergence of resistant tumors characterized by lineage plasticity and divergent differentiation toward neuroendocrine lineage. We found that ARPIs induce a rapid epigenetic alteration mediated by large-scale chromatin remodeling to support activation of stem/neuronal transcriptional programs. We identified motifs for the proneuronal transcription factor ASCL1 to be enriched in hyper-accessible regions. ASCL1 acts as a driver of the lineage plastic, neuronal transcriptional program to support treatment resistance and neuroendocrine phenotype. Targeting ASCL1 switches the neuroendocrine lineage back to the luminal epithelial state. This effect is modulated by disruption of the polycomb repressive complex-2 and change the chromatin architecture in favor of luminal phenotype. Our study provides insights into the epigenetic alterations induced by ARPI governed by ASCL1, provides a proof of principle of targeting ASCL1 to reverse the neuroendocrine phenotype, support luminal conversion and re-addiction to ARPIs.

2022-03-30 | GSE183196 | GEO

Molecular profiles, sources and lineage restrictions of stem cells in an annelid regeneration model

Project description:Regeneration of missing body parts can be observed in diverse animal phyla, but it remains unclear to which extent these capacities rely on shared or divergent principles. Research into this question requires detailed knowledge about the involved molecular and cellular principles in suitable reference models. By combining single-cell RNA sequencing and mosaic transgenesis in the marine annelid Platynereis dumerilii, we map cellular profiles and lineage restrictions during posterior regeneration. Our data reveal cell-type specific injury responses, re-expression of positional identity factors, and the re-emergence of stem cell signatures in multiple cell populations. Epidermis and mesodermal coelomic tissue produce distinct putative posterior stem cells (PSCs) in the emerging blastema. A novel mosaic transgenesis strategy reveals both developmental compartments and lineage restrictions during regenerative growth. Our work supports the notion that posterior regeneration involves dedifferentiation, and reveals molecular and mechanistic parallels between annelid and vertebrate regeneration.

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ChIP NS5 Ascl1-ERT2

Project description:Here we performed a ChIP-seq experiment on a sample of adherent cultures of mouse neural stem cells (NS5 cell line) under normal growth conditions and upon short term activation (30 minutes) of an inducible version of the proneural factor Mash1/Ascl1 (Ascl1-ERT2). This resulted in the generation of a genome-wide map of Ascl1 binding to chromatin.

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ASCL1 is a lineage oncogene providing therapeutic targets for high-grade neuroendocrine lung cancers

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FOXO3 shares common targets with ASCL1 genome-wide and inhibits ASCL1-dependent neurogenesis

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