Roger Hurst

Prof. Dr. Roger Hurst

orcid

Research Focus & Metrics

Academic Career Length

40Years (1987-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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30 August 2007 in Cellular and Molecular Life Sciences
Verified
Journal Article
Closed access
PDF file
DSD. E. Stevenson
D. E. Stevenson
RHRoger Hurst
Roger Hurst

1 April 2007 in Gastroenterology
Verified
Journal Article
Closed access
TSTor C. Savidge
Tor C. Savidge
PNPaul Newman
Paul Newman
CPCharalabos Pothoulakis
Charalabos Pothoulakis
ARAnne Ruhl
Anne Ruhl
MNMichel Neunlist
Michel Neunlist
MSMichael V. Sofroniew
Michael V. Sofroniew

1 April 2005 in Toxicology in Vitro
Verified
Journal Article
Closed access
PGP. Garberg
P. Garberg
MBM. Ball
M. Ball
NBN. Borg
N. Borg
RCR. Cecchelli
R. Cecchelli
LTLaurence Tilloy-Fenart
Laurence Tilloy-Fenart
TÖT. Österberg
T. Österberg

1 December 2000 in The Plant Journal
Verified
Journal Article
Open access
PDF file
ACAndrew Clarke
Andrew Clarke
RDRadhika Desikan
Radhika Desikan
RHRoger Hurst
Roger Hurst
JHJohn T. Hancock
John T. Hancock
SNSteven J. Neill
Steven J. Neill
Summary: Recent research has implicated nitric oxide (NO) in the induction of the hypersensitive response (HR) during plant–pathogen interactions. Here we demonstrate that Arabidopsis suspension cultures generate elevated levels of NO in response to challenge by avirulent bacteria, and, using NO donors, show that these elevated levels of NO are sufficient to induce cell death in Arabidopsis cells independently of reactive oxygen species (ROS). We also provide evidence that NO‐induced cell death is a form of programmed cell death (PCD), requiring gene expression, and has a number of characteristics of PCD of mammalian cells: NO induced chromatin condensation and caspase‐like activity in Arabidopsis cells, while the caspase‐1 inhibitor, Ac‐YVAD‐CMK, blocked NO‐induced cell death. A well‐established second messenger mediating NO responses in mammalian cells is cGMP, produced by the enzyme guanylate cyclase. A specific inhibitor of guanylate cyclase blocked NO‐induced cell death in Arabidopsis cells, and this inhibition was reversed by the cell‐permeable cGMP analogue, 8Br‐cGMP, although 8Br‐cGMP alone did not induce cell death or potentiate NO‐induced cell death. This suggests that cGMP synthesis is required but not sufficient for NO‐induced cell death in Arabidopsis. In‐gel protein kinase assays showed that NO activates a potential mitogen‐activated protein kinase (MAPK), although a specific inhibitor of mammalian MAPK activation, PD98059, which blocked H2O2‐induced cell death, did not inhibit the effects of NO.

1 May 2002
Verified
Journal Article
Closed access
SNSteven J. Neill
Steven J. Neill
RDRadhika Desikan
Radhika Desikan
ACAndrew Clarke
Andrew Clarke
RHRoger Hurst
Roger Hurst
John HancockJohn Hancock
John Hancock

YMYanita Mcleay
Yanita Mcleay
MBMatthew John Barnes
Matthew John Barnes
Toby MündelToby Mündel
Toby Mündel
SHSuzanne M Hurst
Suzanne M Hurst
RHRoger Hurst
Roger Hurst
SSStephen R Stannard
Stephen R Stannard
Exercise-induced muscle damage (EIMD) is accompanied by localized oxidative stress / inflammation which, in the short-term at least, is associated with impaired muscular performance. Dietary antioxidants have been shown to reduce excessive oxidative stress; however, their effectiveness in facilitating recovery following EIMD is not clear. Blueberries demonstrate antioxidant and anti-inflammatory properties. In this study we examine the effect of New Zealand blueberries on EIMD after strenuous eccentric exercise.