Dataset Information


Histone variant H2A.Z deposition and acetylation directs the canonical Notch signaling response

ABSTRACT: The study deals with the elucidation of potential interaction partners of the intracellular domain of the transmembrane receptor Notch1, termed NICD. The NICD is released from the cytoplasmic tail of the Notch receptor by gamma-secretase treatment and translocated as a transcription factor to the nucleus. Here, virally transduced recombinant NICD constructs (wild-type and deltaEP hyperactive mutant) were employed for AP-MS with the aim of identifying novel NICD interactors in a murine T cell leukemia cell line.


ORGANISM(S): Mus musculus  

TISSUE(S): Tissue Not Applicable To Dataset

DISEASE(S): Acute Leukemia

SUBMITTER: Gerhard Mittler  

LAB HEAD: Gerhard Mittler

PROVIDER: PXD008747 | Pride | 2018-06-25


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A fundamental as yet incompletely understood feature of Notch signal transduction is a transcriptional shift from repression to activation that depends on chromatin regulation mediated by transcription factor RBP-J and associated cofactors. Incorporation of histone variants alter the functional properties of chromatin and are implicated in the regulation of gene expression. Here, we show that depletion of histone variant H2A.Z leads to upregulation of canonical Notch target genes and that the H2  ...[more]

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