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Identification of interacting proteins of Pdcd7 (U11-59K)

ABSTRACT: In order to identify interacting proteins of Pdcd7 (U11-59K), pCMV6-Pdcd7-Myc was transfected in HEK293T cells, followed by UV cross-linking and immunoprecipitation with Myc antibody. Samples were then analysed on Thermo Scientific Q Exactive HF mass spectrometer.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

SUBMITTER: Rahul Kanadia

LAB HEAD: Rahul Kanadia

PROVIDER: PXD019428 | Pride | 2021-09-09

REPOSITORIES: Pride

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	jlb20190703_AOlthof_4IPs_LCMSresults.xml	Xml
	jlb20190703_AOlthof_Kanadia_IP1_FASP.raw	Raw
	jlb20190703_AOlthof_Kanadia_IP2_FASP.raw	Raw
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Publications

Disruption of exon-bridging interactions between the minor and major spliceosomes results in alternative splicing around minor introns.

Olthof Anouk M AM White Alisa K AK Mieruszynski Stephen S Doggett Karen K Lee Madisen F MF Chakroun Almahdi A Abdel Aleem Alice K AK Rousseau Justine J Magnani Cinzia C Roifman Chaim M CM Campeau Philippe M PM Heath Joan K JK Kanadia Rahul N RN

Nucleic acids research 20210401 6

Vertebrate genomes contain major (>99.5%) and minor (<0.5%) introns that are spliced by the major and minor spliceosomes, respectively. Major intron splicing follows the exon-definition model, whereby major spliceosome components first assemble across exons. However, since most genes with minor introns predominately consist of major introns, formation of exon-definition complexes in these genes would require interaction between the major and minor spliceosomes. Here, we report that minor spliceo ...[more]

PMID: 33660780

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A benzimidazole inhibitor attenuates sterile inflammation induced in a model of systemic autoinflammation

Project description:Sterile stimuli can trigger inflammatory responses, and in some cases can lead to a variety of acute or chronic diseases. In this study, we hypothesize that a benzimidazole inhibitor may be used as a therapeutic in the treatment of sterile inflammation. In vitro, this inhibitor blocks TLR signalling and inflammatory responses. The benzimidazole inhibitor does not prevent mouse macrophage activation after stimulation with 2, 6, 10, 14-tetramethylpentadecane (TMPD, also known as pristane), a hydrocarbon oil that mimics features of sterile inflammation when injected in vivo. However, C57BL/6 female mice treated with the benzimidazole inhibitor exhibited a significant reduction of pristane-dependent induction of splenocyte number and weight. Conversely, no significant difference was observed in males. Using mass spectrometry, we found that the urine of pristane-injected mice contained increased levels of putative markers for several inflammatory diseases, which were reduced by the benzimidazole inhibitor. To study the mechanism, we showed that pristane-injected mice had increased cell free DNA in serum, which was not impacted by inhibitor treatment. However, chemokine release (e.g. MCP-1, RANTES and TARC) was significantly reduced in inhibitor-treated mice. Thus, the benzimidazole inhibitor might be used as a new drug to block the recruitment of immune cells during sterile inflammatory diseases in humans.

2020-07-27 | PXD017492 | Pride

Myc correlates globally with transcription complexes rather than specific DNA elements

Project description:The Myc-Max heterodimer has been thought of as a sequence specific DNA binding protein that regulates transcription of a large number of genes. We demonstrate here that the positions of the human genome occupied by Myc-Max correlate with the RNA polymerase II (Pol II) transcription complex rather than to the canonical DNA binding sequence element CACGTG. The heterodimer is positioned slightly upstream of essentially all promoter proximal paused polymerases and is found throughout the transcribed regions of genes. Using a multi-genome analysis of promoter regions we show that the heterodimers are oriented with respect to the direction of transcription with Myc downstream of Max. In strong support of a model in which the Myc is recruited by transcription complexes rather than specific DNA sequences, we found that the difference in affinities of Myc-Max heterodimers for CACGTG versus non-specific DNA is not great enough to drive the pattern of genome occupancy exhibited. A total of 2 ChIP-Seq data for Myc and Max in human HeLa cell.

2013-01-02 | E-GEOD-43227 | biostudies-arrayexpress

Long-range joining of intra-chromosomal DNA double-strand breaks

Project description:Antibody class switch recombination (CSR) in B lymphocytes joins two DNA double-strand breaks (DSBs) lying 100 to 200 kilobases (kb) apart within switch (S) regions in the immunoglobulin heavy chain locus (IgH). CSR-activated B lymphocytes generate multiple S-region DSBs in the donor Sm and in a downstream acceptor S region, with a DSB in Sm being joined to a DSB in the acceptor S region at sufficient frequency to drive CSR in a large fraction of activated B cells. Such frequent joining of widely separated CSR DSBs could be promoted by IgH-specific or B cell-specific processes or by general aspects of chromosome architecture and DSB repair. Previously, we found that B cells with two yeast I-SceI endonuclease targets in place of Sg1 undergo I-SceI-dependent class switching from IgM to IgG1 at 5-10% of normal levels. Now, we report that B cells in which Sg1 is replaced with a 28 I-SceI target array, designed to increase I-SceI DSB frequency, undergo I-SceI-dependent class switching at almost normal levels. High-throughput genome-wide translocation sequencing revealed that I-SceI-generated DSBs introduced in cis at Sm and Sg1 sites are joined together in T cells at levels similar to those of B cells. Such high joining levels also occurred between I-SceI-generated DSBs within c-myc and I-SceI- or CRISPR/Cas9-generated DSBs 100 kb downstream within Pvt1 in B cells or fibroblasts, respectively. We suggest that CSR exploits a general propensity of intra-chromosomal DSBs separated by several hundred kb to be frequently joined together and discuss relevance of this finding for recurrent interstitial deletions in cancer. Comparison of frequency of long-range joining between I-SceI-induced DSBs at IgH and c-myc loci in different cell types by HTGTS

2014-01-03 | E-GEOD-53755 | biostudies-arrayexpress

Effcts of Zbp1 in B-cell lymphoma

Project description:B-cell lymphomas arising in Zbp1-/-Eu-Myc mice were compared to B-cell lymphomas arising in Zbp1+/+Eu-Myc mice

2014-04-01 | E-MTAB-2354 | biostudies-arrayexpress

The ubiquitin ligase HUWE1 regulates hematopoietic stem cell maintenance and lymphoid commitment [microarray]

Project description:We identified the ubiquitin ligase Huwe1 as a crucial regulator of hematopoietic stem cell (HSC) functions. We generated Huwe1 conditional knock-out mice and discovered that the loss of this ligase causes an increased proliferation and stem cell exhaustion, together with a decreased lymphoid specification in vivo. We observed that the ubiquitin ligase Huwe1 is controlling the expression of N-myc at the level of the most immature stem and progenitor hematopoietic populations, mediating the described effects. Hematopoietic stem cells (HSC) from the bone marrow of transgenic animals carrying a N-myc/mCherry fusion gene were sorted according to N-myc expression (defined by mCherry) into N-myc high and low subpopulations. Each of these 2 populations was subjected to microarray gene expression profiling.

2016-08-20 | E-GEOD-85832 | biostudies-arrayexpress

Identification of WRKY22 direct targets under submergence in Arabidopsis with ChIP

Project description:To identify direct targets of WRKY22, we created a transgenic Arabidopsis line that expresses a c-myc epitope-tagged WRKY22 and used ChIP followed by microarray hybridization (ChIP-chip) to screen for candidates and validate the in vivo protein-DNA interactions with ChIP followed by quantitative PCR (ChIP-Q-PCR). The WRKY22 and c-myc epitope tag fusion construct was generated and transformed into wrky22-ko2 plants. The resulting transgenic lines should have better ChIP efficiency than the wild-type background, due to the reduced competition for WRKY22 binding sites from endogenous WRKY22. ChIP-enriched DNA fragments were identified using criteria of a window of +300 to M-oM-<M-1200 of a gene for a promoter, a width of 4 probes or more, and a false discovery rate (FDR) < 0.1. The ChIP-chip experiments were repeated six times, i.e., six biological replicas. Candidates were defined by the presence of the promoter in three out of six biological replicas. Candidates were then classified based on their hypoxic responsiveness with a positive response defined as gene expression levels exhibiting > 2 or < 0.5-fold induction in any time point under submergence treatments in expression array data. Comparison of c-myc tagged WRKY22 transgenic plants vs wild-type (Columbia) plants. Both materials were submergence treated for 3 hours.

2013-07-03 | E-GEOD-40138 | biostudies-arrayexpress

Human Cardiac Fibroblast BioID2 Interactome for SKI and TAZ(WWTR1)

Project description:We used adenoviral-mediated overexpression of MYC-BioID2, MYC-BioID2-SKI, MYC-BioID2-WWTR1 (TAZ) in human primary cardiac fibroblasts to elucidate the interaction between SKI and the Hippo signaling pathway. Original data is also available on the Global Proteome Machine (http://hs2.proteome.ca/tandem/thegpm_tandem.html). Datasets are identified as follows: GPM10000002938 and 2939 are untreated negative control cell lysates; GPM10000002941 and 2942 are "empty" MYC-BioID2 vector; GPM10000002943 and 2944 are MYC-BioID2-SKI; and GPM10000002944 and 2945 are MYC-BioID2-WWTR1(TAZ).

2021-09-09 | PXD018246 | Pride

MYC multimers shield stalled replication forks from RNA polymerase

Project description:Oncoproteins of the MYC family drive the development of numerous human tumors. In unperturbed cells, MYC proteins bind to virtually all active promoters and control transcription by RNA Polymerase II (RNAPII). MYC proteins can also coordinate transcription with DNA replication and promote the repair of transcription-associated DNA damage, but how they exert these mechanistically diverse functions is unknown. Here we show that MYC dissociates from many of its binding sites in active promoters and forms multimeric, often sphere-like structures in response to perturbation of transcription elongation, mRNA splicing or inhibition of the proteasome. Multimerization is accompanied by a global change in the MYC interactome towards proteins involved in transcription termination and RNA processing. MYC multimers accumulate on chromatin immediately adjacent to stalled replication forks and surround FANCD2, ATR and BRCA1 proteins, which are located at stalled forks. MYC multimerization is triggered in a HUWE1- and ubiquitylation-dependent manner. At active promoters, MYC multimers block antisense transcription and stabilize FANCD2 association with chromatin. This limits DNA double-strand break formation during S phase, suggesting that multimerization of MYC enables tumor cells to proliferate under stressful conditions.

2022-10-27 | PXD036674 | Pride

H3 occupancy

Project description:Chromatin plays roles in processes governed by different time scales. To assay the dynamic behaviour of chromatin in living cells, we used genomic tiling arrays to measure histone H3 turnover in G1-arrested S. cerevisiae at single-nucleosome resolution over 4% of the genome, and over the entire genome at lower (~265 bp) resolution. We find that nucleosomes at promoters are replaced more rapidly than at coding regions, and that replacement rates over coding regions correlate with polymerase density. In addition, rapid histone turnover is found at known chromatin boundary elements. These results suggest that rapid histone turnover serves to functionally separate chromatin domains and prevent spread of histone states. Keywords: Chip-chip, H3 ChIP-chip for Myc-H3 vs WCE.

2007-05-16 | E-GEOD-6669 | biostudies-arrayexpress

Ratios for G1 arrested cells (Printed array)

2010-06-11 | E-GEOD-6665 | biostudies-arrayexpress