Changes in BiP (GRP78) levels upon HSV-1 infection are strain dependent

Hanwen Mao; Diana Palmer; Kenneth S. Rosenthal

doi:10.1016/S0168-1702(01)00257-X

Changes in BiP (GRP78) levels upon HSV-1 infection are strain dependent

Hanwen Mao, Diana Palmer, Kenneth S. Rosenthal

Research output: Contribution to journal › Article › peer-review

9 Scopus citations

Abstract

BiP (grp78) is a chaperone protein which can also regulate the unfolded protein response of the cell. Levels of BiP increased in cells infected by the small plaque producing, cell associated, neuroinvasive strains of HSV-1 (SP7, 490) but decreased in cells infected with KOS, a large plaque, attenuated strain. BiP protein synthesis continued early in infection and BiP was sequestered and its degradation was limited during SP7 infection. BiP protein synthesis stopped and the protein was degraded in KOS infected cells. These viral strain dependent differences in BiP concentration may influence other aspects of the viral interaction with the target cell and its host.

Original language	English (US)
Pages (from-to)	127-135
Number of pages	9
Journal	Virus Research
Volume	76
Issue number	2
DOIs	https://doi.org/10.1016/S0168-1702(01)00257-X
State	Published - 2001
Externally published	Yes

Keywords

BiP
ER stress
HSV
Strain dependence

ASJC Scopus subject areas

Cancer Research
Virology
Infectious Diseases

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/S0168-1702(01)00257-X

Cite this

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title = "Changes in BiP (GRP78) levels upon HSV-1 infection are strain dependent",

abstract = "BiP (grp78) is a chaperone protein which can also regulate the unfolded protein response of the cell. Levels of BiP increased in cells infected by the small plaque producing, cell associated, neuroinvasive strains of HSV-1 (SP7, 490) but decreased in cells infected with KOS, a large plaque, attenuated strain. BiP protein synthesis continued early in infection and BiP was sequestered and its degradation was limited during SP7 infection. BiP protein synthesis stopped and the protein was degraded in KOS infected cells. These viral strain dependent differences in BiP concentration may influence other aspects of the viral interaction with the target cell and its host.",

keywords = "BiP, ER stress, HSV, Strain dependence",

author = "Hanwen Mao and Diana Palmer and Rosenthal, {Kenneth S.}",

note = "Funding Information: We thank Martin Snyder and Tom Kim for their advice and help and Richard Vernell for assistance with the Northern Blots. Research done in our laboratory is supported by a grant from the National Institutes of Health, NS-40324.",

year = "2001",

doi = "10.1016/S0168-1702(01)00257-X",

language = "English (US)",

volume = "76",

pages = "127--135",

journal = "Virus Research",

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number = "2",

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T1 - Changes in BiP (GRP78) levels upon HSV-1 infection are strain dependent

AU - Mao, Hanwen

AU - Palmer, Diana

AU - Rosenthal, Kenneth S.

N1 - Funding Information: We thank Martin Snyder and Tom Kim for their advice and help and Richard Vernell for assistance with the Northern Blots. Research done in our laboratory is supported by a grant from the National Institutes of Health, NS-40324.

PY - 2001

Y1 - 2001

N2 - BiP (grp78) is a chaperone protein which can also regulate the unfolded protein response of the cell. Levels of BiP increased in cells infected by the small plaque producing, cell associated, neuroinvasive strains of HSV-1 (SP7, 490) but decreased in cells infected with KOS, a large plaque, attenuated strain. BiP protein synthesis continued early in infection and BiP was sequestered and its degradation was limited during SP7 infection. BiP protein synthesis stopped and the protein was degraded in KOS infected cells. These viral strain dependent differences in BiP concentration may influence other aspects of the viral interaction with the target cell and its host.

AB - BiP (grp78) is a chaperone protein which can also regulate the unfolded protein response of the cell. Levels of BiP increased in cells infected by the small plaque producing, cell associated, neuroinvasive strains of HSV-1 (SP7, 490) but decreased in cells infected with KOS, a large plaque, attenuated strain. BiP protein synthesis continued early in infection and BiP was sequestered and its degradation was limited during SP7 infection. BiP protein synthesis stopped and the protein was degraded in KOS infected cells. These viral strain dependent differences in BiP concentration may influence other aspects of the viral interaction with the target cell and its host.

KW - BiP

KW - ER stress

KW - HSV

KW - Strain dependence

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JO - Virus Research

JF - Virus Research

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ER -

Changes in BiP (GRP78) levels upon HSV-1 infection are strain dependent

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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