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Genome-wide profile of cJun and p27 in breast cancer cells

ABSTRACT: Genome-wide profile of cJun and p27 in breast cancer cells

PROVIDER: PRJNA447897 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6908940.fastq.gz	Fastqsanger.gz
	SRR6908950.fastq.gz	Fastqsanger.gz
	SRR6908941.fastq.gz	Fastqsanger.gz
	SRR6908951.fastq.gz	Fastqsanger.gz
	SRR6908942.fastq.gz	Fastqsanger.gz

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Genome-wide profile of cJun and p27 in breast cancer cells

Project description:We report the genome-wide profile of cJun and p27 in _231 (a line selected for low metastatic ability), _231-1833 (its bone-tropic metastatic derivative line), _231p27CK-DD (a phosphomimetic cell line), and _231-1833shp27 (p27 knockdown cell line). It shows that cJun and p27 broadly binds to genomic DNA and their bindings are regulated by p27 phosphorylation-dependent patterns.

2019-03-19 | GSE112444 | GEO

Genome-wide profile of cJun and p27 and gene expression profile in breast cancer cells

Project description:Genome-wide profile of cJun and p27 and gene expression profile in breast cancer cells

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Genome-wide profile of cJun and p27 and gene expression profile in breast cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-03-19 | GSE112446 | GEO

p27-affinity-purified mass spectrometry anslysis

Project description:This project aims to identify p27 modification sites.

2023-01-05 | PXD039223 | Pride

Rhodococcus sp. P27

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bZIP dimers CREB1, ATF2, Zta, ATF3|cJun, and cFos|cJun prefer binding some DNA sequences containing 5-formylcytosine and 5-carboxylcytosine

Project description:In mammalian cells, 5-methylcytosine (5mC) occurs in genomic double-stranded DNA (dsDNA) and is enzymatically oxidized to 5-hydroxymethylcytosine (5hmC), then to 5-formylcytosine (5fC), and finally to 5-carboxylcytosine (5caC). These cytosine modifications are enriched in regulatory regions of the genome. The effect of these oxidative products on five bZIP dimers (CREB1, ATF2, Zta, ATF3|cJun, and cFos|cJun) binding to five types of dsDNA was measured using protein binding microarrays. The five dsDNAs contain either cytosine in both DNA strands or cytosine in one strand and either 5mC, 5hmC, 5fC, or 5caC in the second strand. Some sequences containing the CEBP half-site GCAA are bound more strongly by all five bZIP domains when dsDNA contains 5mC, 5hmC, or 5fC. dsDNA containing 5caC in some TRE (AP-1)-like sequences, e.g., TGACTAA, is better bound by Zta, ATF3|cJun, and cFos|cJun.

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Cisplatin induces the rearrangement of RBPs on CDKN1B/p27 mRNA

Project description:Cisplatin (CP) is a chemotherapeutic drug that is used to cure different types of cancer. CP induces DNA damage and leads to cell cycle arrest. The cyclin-dependent kinase inhibitor 1B (CDKN1B), also termed p27, plays an important role in the drug response ; and increased levels of p27 correlated with CP resistance. In HEK293 cells, we observed that p27 mRNAs levels increased whereas protein level drastically decreased in cells treated with CP; suggesting post-transcriptional regulatory events. To further understand the underlying mechanisms, we applied a biochemical approach combined with mass-spectrometry to systematically identify the RNA-binding proteins (RBPs) that are bound to the 3’UTR of p27 mRNAs in CP-treated versus non-treated cells in vivo. We found that 24 proteins, most of them known RBPs such HuR, hNRNPD, changed their association with p27 mRNA upon CP treatement. Furthermore, knock-down of a subset of the identified RBPs led to the inhibition of the CP-induced increase of p27 mRNA levels. In conclusion, these results highlight substantial rearrangement between RBPs and p27 mRNA upon CP treatment and corroborate the importance of post-transcriptional control in cellular drug response.

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p27 binds to promoters of multiple genes leading to their repression

2011-12-01 | GSE20068 | GEO

BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein

Project description:Coordinated BCR-ABL1 kinase-dependent and -independent mechanisms convert p27 from a nuclear tumor suppressor to a cytoplasmic oncogene. Persistence of oncogenic p27 functions despite effective inhibition of BCR-ABL1 may contribute to resistance to tyrosine kinase inhibitors. BCR-ABL1 induced p27 versus knockout, controlling with Empty vector p27 versus knock out

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