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Interacting protein identification

ABSTRACT: Identification of interacting proteins with Herpes Simplex Virus

OTHER RELATED OMICS DATASETS IN: PRJNA412975PRJNA390133

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell

DISEASE(S): Disease Free

SUBMITTER: Yue Chen

LAB HEAD: Yue Chen

PROVIDER: PXD008108 | Pride | 2019-11-12

REPOSITORIES: pride

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	txt.zip	Other
	yuechen_lerber_20170906_aCFIm25.raw	Raw
	yuechen_lerber_20170906_aWT.raw	Raw

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Publications

Nudt21 Controls Cell Fate by Connecting Alternative Polyadenylation to Chromatin Signaling.

Brumbaugh Justin J Di Stefano Bruno B Wang Xiuye X Borkent Marti M Forouzmand Elmira E Clowers Katie J KJ Ji Fei F Schwarz Benjamin A BA Kalocsay Marian M Elledge Stephen J SJ Chen Yue Y Sadreyev Ruslan I RI Gygi Steven P SP Hu Guang G Shi Yongsheng Y Hochedlinger Konrad K

Cell 20171214 1-2

Cell fate transitions involve rapid gene expression changes and global chromatin remodeling, yet the underlying regulatory pathways remain incompletely understood. Here, we identified the RNA-processing factor Nudt21 as a novel regulator of cell fate change using transcription-factor-induced reprogramming as a screening assay. Suppression of Nudt21 enhanced the generation of induced pluripotent stem cells, facilitated transdifferentiation into trophoblast stem cells, and impaired differentiation ...[more]

PMID: 29249356

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2017-04-20 | PXD005104 | Pride

Sequencing of HSV-1 genomic DNA to identify genomic variation resulting from selective pressure imposed by mutation of the PP1 binding site in the pUL21 gene

Project description:The pUL21 gene is essential for efficient replication and dissemination in herpes simplex virus 1 (HSV-1) but the molecular basis for its function is not well understood. Experimental work revealed that pUL21 is a virus-encoded adaptor of protein phosphatase 1 (PP1). Mutation of the specific motif in pUL21 responsible for PPI recruitment, followed by propagation in cell culture, was performed in order to identify the impact of preventing PP1 recruitment on the viral genome. This allowed identification of compensatory mutations disrupting the viral kinase gene pUS3, which restored viral growth and spread, revealing that pUL21 directly antagonises pUS3. Three mutant strains of HSV-1 were generated, mutating the conserved residues F242 and V243 in the PP1 binding sequence, individually and in combination (pUL21F242E, pUL21V243D, pUL21FV242AA), along with a knockout strain lacking pUL21 (ΔpUL21). These four virus stocks, plus wild-type HSV-1, were propagated in Vero cells for three passages. Genomic DNA was extracted from the P3 viruses and sequenced with Illumina. Reads were trimmed and mapped to an edited version of the HSV-1 genome (based on JQ673480.1) and read depth and variants were quantified.

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Whole-cell and plasma membrane proteomics of herpes simplex virus-1 infection reveals cell surface remodelling via pUL56-mediated GOPC degradation

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