G
Gavan Holloway
Researcher at University of Melbourne
Publications - 23
Citations - 1185
Gavan Holloway is an academic researcher from University of Melbourne. The author has contributed to research in topics: Rotavirus & NSP1. The author has an hindex of 15, co-authored 23 publications receiving 1085 citations.
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Journal ArticleDOI
The type III effectors NleE and NleB from enteropathogenic E. coli and OspZ from Shigella block nuclear translocation of NF-kappaB p65
Hayley J. Newton,Jaclyn S. Pearson,Luminita Badea,Michelle Kelly,Mark Lucas,Gavan Holloway,Kylie M. Wagstaff,Michelle A. Dunstone,Joan Sloan,James C. Whisstock,James B. Kaper,Roy M. Robins-Browne,David A. Jans,Gad Frankel,Alan D. Phillips,Barbara S. Coulson,Elizabeth L. Hartland +16 more
TL;DR: Overall the data show that EPEC and Shigella have evolved similar T3SS-dependent means to manipulate host inflammatory pathways by interfering with the activation of selected host transcriptional regulators.
Journal ArticleDOI
Sialic acid dependence in rotavirus host cell invasion
Thomas Haselhorst,Fiona E. Fleming,Jeffrey Clifford Dyason,Regan David Hartnell,Xing Yu,Gavan Holloway,Kim Santegoets,Milton J. Kiefel,Helen Blanchard,Barbara S. Coulson,Mark von Itzstein +10 more
TL;DR: It is shown that N-acetylneuraminic acid is a key determinant for binding of these rotaviruses and the glycans of gangliosides G(M1) and G(D1a) are determined by NMR spectroscopy and molecular modeling.
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Human immunodeficiency virus type 1 Nef binds to tumor suppressor p53 and protects cells against p53-mediated apoptosis
Alison L. Greenway,Dale A. McPhee,Kelly Allen,Ricky W. Johnstone,Gavan Holloway,John Mills,Ahmed A. Azad,Sonia E. Sankovich,Paul F. Lambert +8 more
TL;DR: The data show that HIV-1 Nef may augment HIV replication by prolonging the viability of infected cells by blocking p53-mediated apoptosis and p53 DNA binding activity and transcriptional activation.
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Rotavirus Activates JNK and p38 Signaling Pathways in Intestinal Cells, Leading to AP-1-Driven Transcriptional Responses and Enhanced Virus Replication
TL;DR: It is shown that maximal RRV-induced IL-8 and c-jun transcription required JNK and p38 activity, highlighting the importance of JNK or p38 activation in RRv-induced, AP-1-driven gene expression.
Journal ArticleDOI
Rotavirus Antagonizes Cellular Antiviral Responses by Inhibiting the Nuclear Accumulation of STAT1, STAT2, and NF-κB
TL;DR: It is shown that the monkey rotav virus RRV and human rotavirus Wa also block gene expression induced by type I and II IFNs through a mechanism allowing signal transducer and activator of transcription 1 (STAT1) and STAT2 activation but preventing their nuclear accumulation.