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CRSP1/TRAP220 Antibody

RRID:AB_577241

Antibody ID

AB_577241

Target Antigen

CRSP1/TRAP220 human, mouse

Proper Citation

(Thermo Fisher Scientific Cat# A300-793A, RRID:AB_577241)

Clonality

polyclonal antibody

Comments

Discontinued; Applications: WB (1:2,000-1:10,000), IP (2-5 µg/mg lysate)

Host Organism

rabbit

Vendor

Thermo Fisher Scientific

Cat Num

A300-793A

Publications that use this research resource

ERK-Induced Activation of TCF Family of SRF Cofactors Initiates a Chromatin Modification Cascade Associated with Transcription.

  • Esnault C
  • Mol. Cell
  • 2017 Mar 16

Literature context:


Abstract:

We investigated the relationship among ERK signaling, histone modifications, and transcription factor activity, focusing on the ERK-regulated ternary complex factor family of SRF partner proteins. In MEFs, activation of ERK by TPA stimulation induced a common pattern of H3K9acS10ph, H4K16ac, H3K27ac, H3K9acK14ac, and H3K4me3 at hundreds of transcription start site (TSS) regions and remote regulatory sites. The magnitude of the increase in histone modification correlated well with changes in transcription. H3K9acS10ph preceded the other modifications. Most induced changes were TCF dependent, but TCF-independent TSSs exhibited the same hierarchy, indicating that it reflects gene activation per se. Studies with TCF Elk-1 mutants showed that TCF-dependent ERK-induced histone modifications required Elk-1 to be phosphorylated and competent to activate transcription. Analysis of direct TCF-SRF target genes and chromatin modifiers confirmed this and showed that H3S10ph required only Elk-1 phosphorylation. Induction of histone modifications following ERK stimulation is thus directed by transcription factor activation and transcription.

LRP8-Reelin-Regulated Neuronal Enhancer Signature Underlying Learning and Memory Formation.

  • Telese F
  • Neuron
  • 2015 May 6

Literature context:


Abstract:

One of the exceptional properties of the brain is its ability to acquire new knowledge through learning and to store that information through memory. The epigenetic mechanisms linking changes in neuronal transcriptional programs to behavioral plasticity remain largely unknown. Here, we identify the epigenetic signature of the neuronal enhancers required for transcriptional regulation of synaptic plasticity genes during memory formation, linking this to Reelin signaling. The binding of Reelin to its receptor, LRP8, triggers activation of this cohort of LRP8-Reelin-regulated neuronal (LRN) enhancers that serve as the ultimate convergence point of a novel synapse-to-nucleus pathway. Reelin simultaneously regulates NMDA-receptor transmission, which reciprocally permits the required γ-secretase-dependent cleavage of LRP8, revealing an unprecedented role for its intracellular domain in the regulation of synaptically generated signals. These results uncover an in vivo enhancer code serving as a critical molecular component of cognition and relevant to psychiatric disorders linked to defects in Reelin signaling.

Funding information:
  • NIGMS NIH HHS - T32 GM008471(United States)