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CycT1/Pol II IP-MS DDA dataset

ABSTRACT: DDA MS dataset for Cyclin T1 or RNA Polymerase II co-immunoprecipitants prepared from human DLD-1 cells treated with or without heat shock (42C, 2 h).

INSTRUMENT(S): Orbitrap Exploris 240

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Ali Shilatifard

PROVIDER: MSV000096361 | MassIVE | Fri Nov 08 16:56:00 GMT 2024

SECONDARY ACCESSION(S): PXD057688

REPOSITORIES: MassIVE

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Publications

TurboCas: A method for locus-specific labeling of genomic regions and isolating their associated protein interactome.

Cenik Bercin K BK Aoi Yuki Y Iwanaszko Marta M Howard Benjamin C BC Morgan Marc A MA Andersen Grant D GD Bartom Elizabeth T ET Shilatifard Ali A

Molecular cell 20241201 24

Regulation of gene expression during development and stress response requires the concerted action of transcription factors and chromatin-binding proteins. Because this process is cell-type specific and varies with cellular conditions, mapping of chromatin factors at individual regulatory loci is crucial for understanding cis-regulatory control. Previous methods only characterize static protein binding. We present "TurboCas," a method combining a proximity-labeling (PL) enzyme, miniTurbo, with C ...[more]

PMID: 39706164

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RNA Pol II IP-MS and GFP-CUL3 IP-MS by DIA

Project description:DIA MS dataset for RNA Polymerase II (Pol II) or GFP-CUL3 co-immunoprecipitants prepared from human DLD-1 SPT5-AID cells treated with +/- NVP-2 +/- auxin (for Pol II IP) or +/- auxin (GFP IP).

2024-11-26 | MSV000096543 | MassIVE

PRO-IP-seq: Pol II CTD code at nt-resolution in human K562 cells

Project description:Active sites of transcription were labelled with biotinylated nucleotide during a run-on reacation, where after an immunoprecipitation with antibodies that target Pol II CTD was conducted. This PRO-IP-seq protocol was conducted in human K562 erythroleukemia cells. The K562 cells were either untreated (NHS) or treated with 30 minutes of heat shock at 42°C (HS).

2023-02-24 | GSE200269 | GEO

NELF regulates a promoter-proximal step distinct from RNA Pol II pause-release

Project description:RNA polymerase II (Pol II) is generally paused at promoter-proximal regions in most metazoans, and based on in vitro studies, this function has been attributed to the negative elongation factor (NELF). Here, we show that upon rapid depletion of NELF, Pol II fails to be released into gene bodies, stopping instead around the +1 nucleosomal dyad-associated region. The transition to the 2nd pause region is independent of positive transcription elongation factor P-TEFb. During the heat shock response, Pol II is rapidly released from pausing at heat shock induced genes, while most genes are paused and transcriptionally downregulated during the heat shock response. We find that both aspects of the heat shock response remain intact upon NELF loss. We find that NELF depletion results in global loss of cap-binding complex from chromatin without global reduction of nascent transcript 5’ cap stability. Thus, our studies implicate NELF functioning in early elongation complexes distinct from Pol II pause-release.

2020-03-09 | GSE144786 | GEO

ChIP-seq of HSF-1 and Pol II in C. elegans larval development and heat shock

Project description:To understand the function and regulation of the C. elegans heat shock factor (HSF-1) in larval development, we have used ChIP-seq to analyze the occupancy of HSF1 and RNA Pol II in L2 larvae and young adult (YA) animals grown at 20°C or upon heat shock at 34°C for 30 min. In addition, we have used RNA-seq to analyze the transcriptomes of wild type (N2), hsf-1(ok600) mutants and hsf-1(ok600); rmSi1[hsf-1::gfp] L2 larvae grown at 20°C and characterized the gene expression change by heat shock in wild type (N2) animals at L2 stage.

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Drosophila HSF chromatin IP -cDNA array

Project description:Chromatin immunopurifications from heat shocked drosophila embryos with anti-Heat shock factor sera compared with immunopurification with pre-immune sera. Hybridisations to cDNA arrays. Keywords: repeat sample

2005-05-30 | GSE2398 | GEO

Genome-wide occupancy of RNA polymerase II before and after heat shock in mouse cells

Project description:The goal of this study was to understand changes that occur in RNA polymerase II occupancy upon heat shock using ChIP-seq in mouse cells.

2015-12-30 | GSE66513 | GEO

Analysis of genome wide changes in RNA polymerase II occupancy in murine cells during heat shock and recovery

Project description:The goal of this study was to reveal changes in genome-bound RNA polymerase II in response to heat shock, and monitor the recovery of bound RNA polymerase II as cells return to homeostasis.

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CTDG in non-activated MM6 cells

Project description:Cyclin T1-dependent genes in LPS-activated MM6 cells. HIV-1 is dependent upon cellular co-factors to mediate its replication cycle in CD4+ T cells and macrophages, the two major cell types infected by the virus in vivo. One critical co-factor is Cyclin T1, a subunit of a general RNA polymerase II elongation factor known as P-TEFb. Cyclin T1 is targeted directly by the viral Tat protein to activate proviral transcription. Cyclin T1 is up-regulated when resting CD4+ T cells are activated and during macrophage differentiation or activation, conditions that are also necessary for high levels of HIV-1 replication. Because Cyclin T1 is a subunit of a transcription factor, the up-regulation of Cyclin T1 in these cells results in the induction of cellular genes, some of which might be HIV-1 co-factors. Using shRNA depletions of Cyclin T1 and transcriptional profiling, we identified 54 cellular mRNAs that are Cyclin T1-dependent for their induction in activated CD4+ T cells and during macrophage differentiation and activation. The promoters for these Cyclin T1-dependent genes (CTDGs) are over-represented in two transcription factor binding sites, SREBP1 and ARP1. Notably, 10 of these CTDGs have been reported to be involved in HIV-1 replication, a significant over-representation of such genes when compared to randomly generated lists of 54 genes (p value < 0.00021). SiRNA depletions of two CTDGs identified here, CDK11 and Casein kinase1gamma1, suggest that these genes are also involved in HIV-1 replication. It is therefore likely that the 54 CTDGs identified here include novel HIV-1 co-factors. The presence of CTDGs in the protein space that was available for HIV-1 to sample during its evolution and acquisition of Tat function may provide an explanation for why CTDGs are enriched in viral co-factors. Keywords: cyclin T1 knockdown

2008-07-31 | GSE10738 | GEO

CTDG in non-activated Jurkat cells

Project description:Cyclin T1-dependent genes in non-activated Jurkat cells. HIV-1 is dependent upon cellular co-factors to mediate its replication cycle in CD4+ T cells and macrophages, the two major cell types infected by the virus in vivo. One critical co-factor is Cyclin T1, a subunit of a general RNA polymerase II elongation factor known as P-TEFb. Cyclin T1 is targeted directly by the viral Tat protein to activate proviral transcription. Cyclin T1 is up-regulated when resting CD4+ T cells are activated and during macrophage differentiation or activation, conditions that are also necessary for high levels of HIV-1 replication. Because Cyclin T1 is a subunit of a transcription factor, the up-regulation of Cyclin T1 in these cells results in the induction of cellular genes, some of which might be HIV-1 co-factors. Using shRNA depletions of Cyclin T1 and transcriptional profiling, we identified 54 cellular mRNAs that are Cyclin T1-dependent for their induction in activated CD4+ T cells and during macrophage differentiation and activation. The promoters for these Cyclin T1-dependent genes (CTDGs) are over-represented in two transcription factor binding sites, SREBP1 and ARP1. Notably, 10 of these CTDGs have been reported to be involved in HIV-1 replication, a significant over-representation of such genes when compared to randomly generated lists of 54 genes (p value < 0.00021). SiRNA depletions of two CTDGs identified here, CDK11 and Casein kinase1gamma1, suggest that these genes are also involved in HIV-1 replication. It is therefore likely that the 54 CTDGs identified here include novel HIV-1 co-factors. The presence of CTDGs in the protein space that was available for HIV-1 to sample during its evolution and acquisition of Tat function may provide an explanation for why CTDGs are enriched in viral co-factors. Keywords: cyclin T1 knockdown

2008-07-31 | GSE10737 | GEO

CTDG in PMA-activated Jurkat cells

Project description:Cyclin T1-dependent genes in activated Jurkat cells. HIV-1 is dependent upon cellular co-factors to mediate its replication cycle in CD4+ T cells and macrophages, the two major cell types infected by the virus in vivo. One critical co-factor is Cyclin T1, a subunit of a general RNA polymerase II elongation factor known as P-TEFb. Cyclin T1 is targeted directly by the viral Tat protein to activate proviral transcription. Cyclin T1 is up-regulated when resting CD4+ T cells are activated and during macrophage differentiation or activation, conditions that are also necessary for high levels of HIV-1 replication. Because Cyclin T1 is a subunit of a transcription factor, the up-regulation of Cyclin T1 in these cells results in the induction of cellular genes, some of which might be HIV-1 co-factors. Using shRNA depletions of Cyclin T1 and transcriptional profiling, we identified 54 cellular mRNAs that are Cyclin T1-dependent for their induction in activated CD4+ T cells and during macrophage differentiation and activation. The promoters for these Cyclin T1-dependent genes (CTDGs) are over-represented in two transcription factor binding sites, SREBP1 and ARP1. Notably, 10 of these CTDGs have been reported to be involved in HIV-1 replication, a significant over-representation of such genes when compared to randomly generated lists of 54 genes (p value < 0.00021). SiRNA depletions of two CTDGs identified here, CDK11 and Casein kinase1gamma1, suggest that these genes are also involved in HIV-1 replication. It is therefore likely that the 54 CTDGs identified here include novel HIV-1 co-factors. The presence of CTDGs in the protein space that was available for HIV-1 to sample during its evolution and acquisition of Tat function may provide an explanation for why CTDGs are enriched in viral co-factors. Keywords: shrna knockdown

2008-07-31 | GSE10232 | GEO

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