Lambert_SAINT2086_BioID_BRD3_mutants_P82_VS5
Ontology highlight
ABSTRACT:
INSTRUMENT(S): TripleTOF 5600
ORGANISM(S): Homo Sapiens (ncbitaxon:9606)
SUBMITTER: 
Anne-Claude Gingras
PROVIDER: MSV000081001 | MassIVE | Tue Apr 25 14:37:00 BST 2017
REPOSITORIES: MassIVE
Similar Datasets
Project description:This submission contains the mass spectrometry files for the manuscript by Lambert, Picaud et al. that describes the characterization of interactome changes induced by JQ1 on the BET proteins. More precisely, files used in the SAINT express task 2841 are in this dataset. The AP-MS experiments using 3xFLAG tagged BET proteins lacking their ET domain acquired on TripleTOF 5600 mass spectrometers are found here. See the README file within "Materials and Methods" and the accompanying files for a complete description of MS data generated.
2017-04-24 | MSV000080988 | MassIVE
Project description:This submission contains the mass spectrometry files for the manuscript by Lambert, Picaud et al. that describes the characterization of interactome changes induced by JQ1 on the BET proteins. More precisely, files used in the SAINT express task 2307 are in this dataset. The AP-MS experiments involving a JQ1 time-course for 3xFLAG tagged BET proteins acquired on TripleTOF 5600 spectrometers are found here; please note that the SWATH/DIA files were used for quantification (MSPLIT-DIA) while the DDA files were used for library construction. See the README file within "Materials and Methods" and the accompanying files for a complete description of MS data generated.
2017-04-25 | MSV000081006 | MassIVE
Project description:This submission contains the mass spectrometry files for the manuscript by Lambert, Picaud et al. that describes the characterization of interactome changes induced by JQ1 on the BET proteins. More precisely, files used in the SAINT express task 2096 are in this dataset. The pulldown experiments using recombinant BRD4 domains acquired on a Velos Orbitrap Elite mass spectrometer are found here. See the README file within "Materials and Methods" and the accompanying files for a complete description of MS data generated.
2017-04-24 | MSV000080986 | MassIVE
Project description:This submission contains the mass spectrometry files for the manuscript by Lambert, Picaud et al. that describes the functional characterization of the human acetyl lysine machinery. More precisely, files used in the SAINT express task 2437 are in this dataset. The AP-MS experiments using 3xFLAG tagged BRD9 fragments acquired on TripleTOF 5600 mass spectrometers are found here. See the README file within "Materials and Methods" and the accompanying files for a complete description of MS data generated.
2017-04-24 | MSV000080981 | MassIVE
Project description:This submission contains the mass spectrometry files for the manuscript by Lambert, Picaud et al. that describes the characterization of interactome changes induced by JQ1 on the BET proteins. This submission contains 16 files associated with endogenous IP-MS analysis of BRD2, BRD3 and BRD4 (IgG was used as a negative control) from K562 cells treated with (+)-JQ1 or DMSO for 1 h; biological duplicate analyses were performed. Sample were analysed on a TripleTOF 5600 spectrometer; please note that the SWATH/DIA files were used for quantification (MSPLIT-DIA) while the DDA files were used for library construction. See the README file within "Materials and Methods" and the accompanying files for a complete description of MS data generated.
2018-08-28 | MSV000082859 | MassIVE
Project description:This submission contains the mass spectrometry files for the manuscript by Lambert, Picaud et al. that describes the characterization of interactome changes induced by JQ1 on the BET proteins. This submission contains 16 files associated with endogenous IP-MS analysis of BRD2, BRD3 and BRD4 (IgG was used as a negative control) from Flp-In T-REx HEK293 cells treated with (+)-JQ1 or DMSO for 1 h; biological duplicate analyses were performed. Sample were analysed on a TripleTOF 5600 spectrometer; please note that the SWATH/DIA files were used for quantification (MSPLIT-DIA) while the DDA files were used for library construction. See the README file within "Materials and Methods" and the accompanying files for a complete description of MS data generated.
2018-08-28 | MSV000082857 | MassIVE
Project description:One critical task in pluripotent reprogramming is to erase the somatic transcriptional program of starting cells. No strategy or theory exists for achieving erasure of somatic gene expression memory. Here, we present a proof-of-principle strategy in which reprogramming to pluripotency is facilitated by small molecules that erase somatic cell transcription memory. We show that mild chemical targeting of the acetyllysine-binding pockets of the BET bromodomains, the transcriptional bookmarking domains, robustly enhances reprogramming. Furthermore, we show that chemical targeting of the transcriptional bookmarking BET bromodomains dramatically downregulates specific somatic gene expression programs in both naïve and reprogramming fibroblasts. Chemical blocking of the BET bromodomains also resulted in loss of fibroblast morphology early in reprograming. In this study, we experimentally demonstrate a concept for cell fate conversion: facilitating the conversion by chemically targeting the transcriptional bookmarking BET bromodomains responsible for transcriptional memory. human BJ cells were treated with JQ1 at 50 nM for 48 hours. Differential expression was compared with DMSO treatment. The same treatments and comparsion were conducted for reprogramming BJ cells, which were transduced with OCT4, SOX2, and KLF4. JQ1iPSC5 is a iPSC (induced pluripotent stem cell) line generated in this study using small molecules JQ1.
2016-08-22 | E-GEOD-75364 | biostudies-arrayexpress
Project description:Background: The present study investigated a role of proteins from BET family (epigenetic readers) in schizophrenia-like abnormalities in MAM-E17 model of schizophrenia. Methods: An inhibitor of BET proteins, JQ1, was given during adolescence in postnatal days (P) 23-P30, and behavioral response (sensorimotor gating, recognition memory) and prefrontal cortex (mPFC) function (long-term potentiation (LTP), molecular and proteomic studies) were performed in adult males and females. Results: Deficits in sensorimotor gating and recognition memory were observed only in MAM-treated males. However, adolescent JQ1 treatment affected control, but MAM-treated groups in both sexes. Electrophysiological study showed an LTP impairment only in male MAM-treated animals, and JQ1 did not have any effect on LTP in the mPFC. In contrast, MAM did not affect immediate early gene expression (markers of neuronal and synaptic activity), but JQ1 altered them in both sexes. Proteomic study revealed alterations in MAM-treated groups only in males, while JQ1 affected both sexes. Conclusions: Prenatal MAM administration induced schizophrenia-like abnormalities only in males. In contrast, adolescent JQ1 treatment affected both sexes and induced behavioral changes in control groups, altered a markers of neuronal and synaptic activity and proteomic landscape in the mPFC of both groups (VEH- and MAM-treated). Thus, adolescent inhibition of BET family might change neuroplasticity in the mPFC.
2021-09-07 | PXD027050 | Pride
Project description:Two human acute lymphoblastic leukemia cell lines were treated with a BET bromodomain inhibitor that blocks BET association with chromatin. These cell lines, MHH-CALL4 and MUTZ-5, each carry translocation of the CRLF2 gene into the IgH locus, and their growth was found to be susceptible to BET inhibition. Gene expression changes were analyzed in each cell line versus vehicle control. Cell were treated for 8 hours with either DMSO or 500nM of the BET bromodomain inhbitor JQ1. Three samples for each treatment were taken and analyzed for each cell line. CEL files were analyzed at both the core and extended gene level by RMA with the Affymetrix Expression Console software.
2012-08-09 | E-GEOD-39995 | biostudies-arrayexpress
Project description:Targeting BET bromodomain proteins utilizing small molecules in an emerging anti-cancer strategy with clinical evaluation of at least six inhibitors now underway. While MYC downregulation was initially proposed as a key mechanistic property of BET inhibitors, recent evidence suggests that additional anti-tumor activities are important. Using the Eμ-Myc model of B-cell lymphoma we demonstrate that BET inhibition with JQ1 is a potent inducer of p53-independent apoptosis that occurs in the absence of effects on Myc gene expression. JQ1 skews the expression of pro-apoptotic (Bim) and anti-apoptotic (BCL-2/BCL-xL) BCL-2 family members to directly engage the mitochondrial apoptotic pathway. Consistent with this, Bim knockout or Bcl-2 overexpression inhibited apoptosis induction by JQ1. We identified lymphomas that were either intrinsically resistant to JQ1-mediated death or acquired resistance following in vivo exposure. Strikingly, in both instances BCL-2 was strongly upregulated and was concomitant with activation of RAS pathways. Eμ-Myc lymphomas engineered to express activated Nras upregulated BCL-2 and acquired a JQ1-resistance phenotype. These studies provide important information on mechanisms apoptosis induction and resistance to BET-inhibition, while providing further rationale for the translation of BET inhibitors in aggressive B-cell lymphomas.
2016-09-18 | GSE87050 | GEO