Proteomics

Dataset Information

0

IP-MS analysis


ABSTRACT: It has recently been shown that HSV-1 infection induces widespread defect in host gene transcription termination while viral genes are unaffected. However, The underlying mechanism remain poorly understood. According to our sequencing data, ICP27 as an immediate early protein of HSV-1 was involved in disrupting host transcription termination. To elucidate the underlying mechanism, we performed IP-MS to figure out interaction proteins with ICP27. Other than export proteins, 3’ end processing factors strongly associated with ICP27 based on this IP-MS data. Pre-mRNA 3’ end processing is required for transcription termination. As expected, this MS data as well as our in vitro and in vivo data suggested that ICP27 functions in pre-mRNA 3’ end processing to regulate transcription termination in a sequence dependent manner.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Yue Chen  

LAB HEAD: Yue Chen

PROVIDER: PXD012837 | Pride | 2020-05-26

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
maxquanttxt.zip Other
yuechen_lerber_20170830_a27_KOS.raw Raw
yuechen_lerber_20170830_a27_lacZ.raw Raw
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Publications


Infection by viruses, including herpes simplex virus-1 (HSV-1), and cellular stresses cause widespread disruption of transcription termination (DoTT) of RNA polymerase II (RNAPII) in host genes. However, the underlying mechanisms remain unclear. Here, we demonstrate that the HSV-1 immediate early protein ICP27 induces DoTT by directly binding to the essential mRNA 3' processing factor CPSF. It thereby induces the assembly of a dead-end 3' processing complex, blocking mRNA 3' cleavage. Remarkably  ...[more]

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