Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HOXB13 interactome in prostate cancer PC3 cell line

ABSTRACT: Transcription factors are one of the major groups of proteins whose suppression leads to tumor growth arrest. Different types of cancer express a specific set of transcription factors that establish and maintain specific gene expression patterns. In prostate cancer cells, one of the key transcriptional regulators is the HOXB13 protein, but its function has not been well characterized. In the present study, we searched for protein partners of HOXB13 by co-immunoprecipitation followed by high-throughput mass spectrometric analysis (IP/LC-MS) using the PC3 cell line as a source. This analysis revealed that the major partners of HOXB13 were transcription factors with different types of DNA-binding domains.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

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

SUBMITTER: Rustam Ziganshin

LAB HEAD: Maksim Erokhin

PROVIDER: PXD059115 | Pride | 2025-11-06

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20220103_050_RZ_ME-85.raw	Raw
	20220103_052_RZ_ME-86.raw	Raw
	Search_results.zip	Other
	checksum.txt	Txt

Items per page:

1 - 4 of 4

Similar Datasets

DNMT3B targets in RKO cells by ChIP-on-chip

Project description:Chromatin immunoprecipitation with DNMT3B specific antibody followed by CGI microarray identified genes with or without CGIs, repeat elements and genomic contigs in RKO cells. ChIP-Chop analysis showed that majority of the target genes including P16, DCC, DISC1, SLIT1, CAVEOLIN1, TBX5, TBX18, HOXB13 and some histone variants, that harbor CGI in their promoters, were methylated in multiple colon cancer cell lines but not in normal colon epithelial cells. Further, these genes were reactivated in RKO cells after treatment with 5-aza-2â-deoxycytidine, a DNA hypomethylating agent. COBRA and bisulfite genomic sequencing showed that the CGIs encompassing the transcription start sites (TSS) of DCC, TBX5, TBX18, SLIT1 were also methylated in primary colorectal tumors compared to matching normal tissues whereas GNA11 was methylated in both. MassARRAY analysis demonstrated that the CGI located ~4.5 kb upstream of HOXB13 +1 site was tumor-specifically hypermethylated in primary colorectal cancers and cancer cell lines. Analysis of tumor suppressor properties of two aberrantly methylated transcription factors, HOXB13 and TBX18, revealed that both inhibited growth and clonogenic survival of colon cancer cells in vitro, but only HOXB13 abolished tumor growth in nude mice. Chromatin immunoprecipitation with DNMT3B specific antibody in RKO cells was compared to control antibody.

2010-05-06 | E-GEOD-18929 | biostudies-arrayexpress

Comparative analysis of PRE DNA-binding factors interactomes: purification of Combgap, Zeste, Psq and Adf1 associated proteins

Project description:The Polycomb group (PcG) and Trithorax group (TrxG) proteins are key epigenetic regulators controlling silenced and active states of genes in multicellular organisms, respectively. In Drosophila PcG/TrxG proteins are recruited to chromatin via binding to specialized DNA-elements termed Polycomb Response Elements (PREs). While precise mechanisms of PcG/TrxG proteins recruitment remains unknown, the important role is suggested to belong to sequence specific DNA-binding factors. Here, using affinity purification coupled with high throughput mass spectrometry (IP/MS), we isolated factors associated with Combgap, Psq, Zeste and Adf1 PRE DNA-binding Drosophila proteins. As a control we used unspecific IgG. For affinity purification the nuclear extract from Drosophila S2 cells and polyclonal antibodies against Combgap, Psq, Zeste and Adf1 were used.

2024-05-22 | PXD029459 | Pride

The p53-regulated long noncoding RNA, lincRNA-p21 promotes the expression of Polycomb target genes and enforces the G1/S checkpoint by activating p21 in cis [ChIP-seq]

Project description:The p53-regulated long non-coding RNA, lincRNA-p21, has been proposed to promote apoptosis and to repress in trans the expression of genes in the p53 transcriptional network. Here, we report the generation of a conditional knockout mouse model developed to further examine lincRNA-p21 function. Using this genetic approach, we find that the primary function of lincRNA-p21 is to activate in cis the expression of its neighboring gene, the cyclin-dependent kinase inhibitor p21. Mechanistically, we show that lincRNA-p21 acts in concert with hnRNP-K as a co-activator for p53-dependent transcription of p21. Additional phenotypes of lincRNA-p21 deficiency, including deregulated expression and altered chromatin state of a set of Polycomb target genes, defective G1/S checkpoint, increased proliferation rates, and enhanced reprogramming efficiency could be attributed to diminished p21 levels. This study reveals a novel paradigm, whereby the long non-coding RNA lincRNA-p21 affects global gene expression and influences events in the p53 tumor suppressor pathway by acting in cis as a locus-restricted transcriptional co-activator for p53-mediated expression of p21. Examination of 2 different histone modifications (H3K4me3 and H3K27me3) in 2 cell types (WT and lincRNA-p21 KO) in the presence and absence of Doxorubicin.

2014-05-22 | E-GEOD-52956 | biostudies-arrayexpress

Mapping of genome-wide action sites of topoisomerase IIbeta by a functional ChIP-chip technique (eTIP-tiling array)

Project description:DNA topoisomerase II (topo II) catalyzes a strand passage reaction in that one duplex is passed through a transient brake in another. Completion of late stages of neuronal development depends on the presence of active isoform (topo IIbeta). We identified topo IIbeta action sites on 7 selected genomic regions (about 79 Mb in total), each containing at least one gene that is controlled by topo IIbeta in neuronal differentiation. We used a novel method, etoposide-mediated topoisomerase immunoprecipitation (eTIP), followed by identification of precipitated DNA fragments on genomic tiling arrays. These DNA fragments were first fractionated by concentrated salt prior to the array analysis. The 0.5 M NaCl-released fraction was analyzed as P2 and the salt-resistant fraction wad analyzed as P1. The genomic DNA fractions from the immunoprecipitate (P1 or P2) were co-hybridized with a reference DNA isolated from the input of immunoprecipitation.

2010-05-15 | E-GEOD-13145 | biostudies-arrayexpress

The p53-regulated long noncoding RNA, lincRNA-p21 promotes the expression of Polycomb target genes and enforces the G1/S checkpoint by activating p21 in cis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-05-22 | E-GEOD-52958 | biostudies-arrayexpress

Methylome analysis of 123 epiRILs, WT and ddm1 mutant aerial part

Project description:DNA methylation profiling in 123 epiRILs, WT and ddm1 mutant aerial part (epiRIL008 - epiRIL011 - epiRIL014 - epiRIL018 - epiRIL020 - epiRIL024 - epiRIL036 - epiRIL046 - epiRIL052 - epiRIL053 - epiRIL054 - epiRIL055 - epiRIL060 - epiRIL062 - epiRIL064 - epiRIL069 - epiRIL070 - epiRIL071 - epiRIL073 - epiRIL092 - epiRIL093 - epiRILv94 - epiRIL095 - epiRIL098 - epiRIL099 - epiRIL101 - epiRIL108 - epiRIL112 - epiRIL114 - epiRIL118 - epiRIL122 - epiRIL137 - epiRIL144 - epiRIL147 - epiRIL148 - epiRIL150 - epiRIL159 - epiRIL164 - epiRIL166 - epiRIL169 - epiRIL170 - epiRIL172 - epiRIL183 - epiRIL193 - epiRIL195 - - epiRIL202 - epiRIL208 - epiRIL215 - epiRIL216 - epiRIL218 - epiRIL222 - epiRIL225 - epiRIL229 - epiRIL232 - epiRIL238 - epiRIL244 - epiRIL252 - epiRIL257 - epiRIL258 - epiRIL260 - epiRIL262 - epiRIL275 - epiRIL276 - epiRIL277 - epiRIL297 - epiRIL305 - epiRIL315 - epiRIL323 - epiRIL326 - epiRIL333 - epiRIL340 - epiRIL344 - epiRIL350 - epiRIL356 - epiRIL362 - epiRIL361 - epiRIL363 - epiRIL366 - epiRIL368 - epiRIL371 - epiRIL375 - epiRIL391 - epiRIL393 - epiRIL394 - epiRIL400 - epiRIL408 - epiRIL410 - epiRIL425 - epiRIL432 - epiRIL434 - epiRIL437 - epiRIL438 - epiRIL439 - epiRIL454 - epiRIL458 - epiRIL466 - epiRIL467 - epiRIL471 - epiRIL473 - epiRIL477 - epiRIL480 - epiRIL488 - epiRIL492 - epiRIL493 - epiRIL494 - epiRIL495 - epiRIL497 - epiRIL500 - epiRIL503 - epiRIL506 - epiRIL508 - epiRIL523 - epiRIL538 - epiRIL539 - epiRIL556 - epiRIL558 - epiRIL559 - epiRIL561 - epiRIL567 - epiRIL570 - epiRIL572 - epiRIL573 - epiRIL579 - wt - ddm1 mutant) Keywords: Genome binding/occupancy profiling by genome tiling array 1 biological replicate in dye-swap - MeDIP-chip

2012-09-03 | E-GEOD-37284 | biostudies-arrayexpress

Methylome analysis of nerd1-1 mutant seedlings

Project description:DNA methylation profiling in nerd1-1 mutant seedlings 2 biological replicates in dye-swap - MeDIP-chip

2012-12-20 | E-GEOD-35344 | biostudies-arrayexpress

A functional genomics approach identifies the GATA factor SERPENT as a tissue-specific partner of CLOCK/CYCLE in the Drosophila circadian clock

Project description:Broadly expressed transcriptions factors (TFs) control tissue-specific programs of gene expression through interactions with local TF networks. Prime examples are the circadian clock TFs CLOCK (CLK) and CYCLE (CYC or BMAL1): while they control a core transcriptional circuit throughout animal bodies, downstream clock target genes and circadian physiology are tissue-specific. Here, we use ChIP-seq to determine the regulatory targets of Drosophila CLK and CYC, which we epitope-tagged by homologous recombination. Both TFs have distinct binding sites in heads versus bodies, suggesting that they directly control tissue-specific downstream target genes. Analysis of these context-specific binding sites revealed distinct sequence motifs for putative clock partner factors, including a motif for the GATA factor SERPENT (SRP). SRP indeed synergistically enhances CLK/CYC-mediated activity of a cis-regulatory region bound by CLK/CYC specifically in bodies. These results reveal how universal clock circuits can generate tissue-specific outputs and demonstrate an approach to dissect regulatory interactions more generally. We sequenced ChIP and input samples, as well as M-bM-^@M-^\mockM-bM-^@M-^] samples for which we performed ChIP with the V5 antibody from wildtype w- flies (not carrying the V5 tag) for two independent biological replicates each, summing to 24 libraries in total.

2013-06-01 | E-GEOD-40467 | biostudies-arrayexpress

Chromatin immunopreciptation genome wide location of H2A.Z binding sites in yeast yeast

Project description:genome wide location of H2A.Z binding sites in yeast Saccharomyces cerevisiae. Nucleosome density controled with H2B ChIP. Hybridization control ChIP H2AZ/H2AZ and H2A/H2B.

2005-12-31 | E-MEXP-396 | biostudies-arrayexpress

The IRE1a-XBP1 pathway promotes T helper cell differentiation by resolving secretory stress and accelerating proliferation (ChIP-seq)

Project description:The IRE1a-XBP1 pathway, a conserved adaptive response to the unfolded protein response, is indispensable for development of the secretory cells. It maintains endoplasmic reticulum homeostasis by enhancing protein folding and the secretory capacity of the cells. Here, we used a modified ChIP-seq protocol (ChIPmentation) to investigate the genome-wide binding events of the transcription factor XBP1 in differentiated mouse Th2 cells.

2018-10-06 | E-MTAB-6327 | biostudies-arrayexpress