W
W.D. Fairlie
Researcher at La Trobe University
Publications - 25
Citations - 1334
W.D. Fairlie is an academic researcher from La Trobe University. The author has contributed to research in topics: Cancer & Cell. The author has an hindex of 13, co-authored 25 publications receiving 1211 citations. Previous affiliations of W.D. Fairlie include Walter and Eliza Hall Institute of Medical Research & University of Melbourne.
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Journal ArticleDOI
Crystal structure of ABT-737 complexed with Bcl-xL: implications for selectivity of antagonists of the Bcl-2 family
Erinna F. Lee,Erinna F. Lee,Peter E. Czabotar,Brian J. Smith,Kurt Deshayes,Kerry Zobel,Peter M. Colman,W.D. Fairlie +7 more
TL;DR: The crystal structure of ABT-737 complexed with Bcl-x L has implications for selectivity of antagonists of the BCl-2 family and for the design of new drugs for this class of drugs.
Journal ArticleDOI
Vaccinia virus anti-apoptotic F1L is a novel Bcl-2-like domain-swapped dimer that binds a highly selective subset of BH3-containing death ligands.
Marc Kvansakul,Hong Yang,W.D. Fairlie,Peter E. Czabotar,S F Fischer,Matthew A. Perugini,David C.S. Huang,Peter M. Colman +7 more
TL;DR: It is reported that the crystal structure of F1L reveals a Bcl-2-like fold with an unusual N-terminal extension, and a novel sequence signature that redefines the BH4 domain as a structural motif present in both pro- and anti-apoptotic BCl-2 members, including viral B cl- 2-like proteins.
Journal ArticleDOI
The role of BH3-only protein Bim extends beyond inhibiting Bcl-2–like prosurvival proteins
Delphine Merino,Maybelline Giam,Maybelline Giam,Peter Hughes,Owen M. Siggs,Klaus Heger,Lorraine A. O'Reilly,Jerry M. Adams,Andreas Strasser,Erinna F. Lee,W.D. Fairlie,Philippe Bouillet +11 more
TL;DR: Analysis of mice showed that Bim's proapoptotic activity is not solely caused by its ability to engage its prosurvival relatives or solely to its binding to Bax, and initiation of apoptosis in vivo appears to require features of both models.
Journal ArticleDOI
Bcl-2, Bcl-x(L), and Bcl-w are not equivalent targets of ABT-737 and navitoclax (ABT-263) in lymphoid and leukemic cells.
Delphine Merino,Delphine Merino,Seong Lin Khaw,Stephan P. Glaser,Stephan P. Glaser,Daniel Anderson,Lisa D. Belmont,Chihunt Wong,Peng Yue,Mikara Robati,Belinda Phipson,Belinda Phipson,W.D. Fairlie,W.D. Fairlie,Erinna F. Lee,Erinna F. Lee,Kirsteen J. Campbell,Cassandra J. Vandenberg,Cassandra J. Vandenberg,Suzanne Cory,Suzanne Cory,Andrew W. Roberts,Andrew W. Roberts,Andrew W. Roberts,Mary J. C. Ludlam,David C.S. Huang,David C.S. Huang,Philippe Bouillet,Philippe Bouillet +28 more
TL;DR: It is found that Bcl-2 is the critical target in vivo for antitumor efficacy in vivo, suggesting that patients with tumors overexpressing B cl-2 will probably benefit and the use of these compounds can be optimized for treating lymphoid malignancies.
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The BH3 mimetic compound, ABT-737, synergizes with a range of cytotoxic chemotherapy agents in chronic lymphocytic leukemia.
Kylie D. Mason,Seong Lin Khaw,Seong Lin Khaw,Kathleen C. Rayeroux,E Chew,Erinna F. Lee,W.D. Fairlie,Andrew Grigg,Andrew Grigg,John F. Seymour,John F. Seymour,Jeff Szer,Jeff Szer,David C.S. Huang,Andrew W. Roberts +14 more
TL;DR: It is reported that ABT-737 is highly effective as a single agent against most CLL samples, but that a sizable minority is relatively insensitive, and a potential role for combination therapies that include BH3 mimetics for the treatment of this disease is suggested.