Dataset Information

Human proteomics analysis of BRD4 targeted small-molecules in KSHV+ cells by Orbitrap Eclipse and MaxQuant

ABSTRACT: In this project, we used proteomics to identify and compare protein profile changed in SIM-1, MZ-1, or JQ-1 treated TIVE-LTC, a KSHV long-term infected immortalized endothelial cell line.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Endothelial Cell Of Umbilical Vein

SUBMITTER: Zhen Lin

LAB HEAD: Zhiqiang Qin

PROVIDER: PXD075129 | Pride | 2026-06-08

REPOSITORIES: Pride

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Publications

Targeting BRD2 and BRD4 inhibit the growth of KSHV-infected immortalized endothelial cells through suppression of LANA translation.

Chen Jungang J Fan Jiaojiao J Qin Margaret M Lin Zhen Z Mu Shengyu S Dai Lu L Qin Zhiqiang Z

PLoS pathogens 20260601 6

Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of several human cancers, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL), both of which still lack effective treatment options. Members of the bromodomain and extra-terminal domain (BET) family, especially bromodomain-containing protein 4 (BRD4), play important roles in RNA polymerase II-mediated transcriptional regulation and are required for the expression of many tumor-driving oncogenes in various cance ...[more]

PMID: 42224297

Similar Datasets

Project description:Kaposi’s sarcoma-associated herpesvirus (KSHV) is a g-herpesvirus which persists as circular extrachromasomal DNA in the nucleus during latent infection. During latency a limited number of viral proteins are expressed, including LANA (latency-associated nuclear antigen). LANA is a multi-functional protein known to interact with transcriptional regulators and chromatin remodelers, and to regulate the LANA and RTA promoters. We hypothesized that LANA may contribute to the establishment of latency through controlling chromatinization and histone modification of KSHV episomes. We performed ChIP-seq analysis and correlated H3K4me3, H3K27me3, polII, and LANA occupancy of the KSHV genome at nucleotide resolution. Epigenetic marks were analyzed in BCBL-1 lymphoid cells and in telomerase-immortalized vein endothelial TIVE-LTC cells. We found that the transcription active mark H3K4me3, but not silencing mark H3K27me3, was enriched at KSHV regions where LANA is bound. Co-occupancy of LANA and H3K4 was also detected on 167 host genes, of which 89 are actively transcribed. By comparing LANA occupancy with the profiling of 43 transcription factors from ENCODE, a subset of transcription factors was enriched at regions where LANA is bound, including znf143, CTCF, and Stat1. These results indicate that LANA also plays a role in modulating expression of host genes. Co-immunoprecipitation of LANA with the H3K4 methyltransferase hSET1 suggests that LANA recruits hSET1 to specific loci on the viral genome, leading to H3K4 methylation and ensuring transcription of latency-associated genes. Host gene expression may be regulated by the same mechanism. LANA binding was correlated with the distribution in the latent KSHV genome of the transcription active histone modification H3K4me3, the silencing mark H3K27me3, and RNA polymerase II, using cells of lymphoid and endothelial origin. A similar analysis was done for the human genome. Biological replicates (BR) and technical replicates (TR) were included.

			Action	DRS
	2023_04_UniProt_Homo_sapiens.fasta	Fasta
	MaxQuant.zip	Other
	QinZ_102623_01.raw	Raw
	QinZ_102623_02.raw	Raw
	QinZ_102623_03.raw	Raw