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David A.D. Parry
Researcher at Massey University
Publications - 204
Citations - 16262
David A.D. Parry is an academic researcher from Massey University. The author has contributed to research in topics: Keratin & Protein structure. The author has an hindex of 68, co-authored 200 publications receiving 15751 citations. Previous affiliations of David A.D. Parry include Commonwealth Scientific and Industrial Research Organisation.
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Journal ArticleDOI
Retinoblastoma-protein-dependent cell-cycle inhibition by the tumour suppressor p16
Jiri Lukas,David A.D. Parry,Louise Aagaard,David J. Mann,Jirina Bartkova,Michael A. Strauss,Gordon Peters,Jiri Bartek +7 more
TL;DR: It is shown that wild-type pi6 arrests normal diploid cells in late Gl, whereas a tumour-associated mutant of pi6 does not, and the ability ofpi6 to induce cell-cycle arrest is lost in cells lacking functional RB, including primary fibroblasts from Rb-/- mouse embryos.
Journal ArticleDOI
New consensus nomenclature for mammalian keratins
Jürgen Schweizer,Paul Edward Bowden,Pierre A. Coulombe,Lutz Langbein,E. Birgitte Lane,Thomas M. Magin,Lois J. Maltais,M. Bishr Omary,David A.D. Parry,Michael A. Rogers,Mathew W. Wright +10 more
TL;DR: This revised nomenclature accommodates functional genes and pseudogenes, and although designed specifically for the full complement of human keratins, it offers the flexibility needed to incorporate additional keratin proteins from other mammalian species.
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α‐Helical coiled coils and bundles: How to design an α‐helical protein
Carolyn Cohen,David A.D. Parry +1 more
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Raf-induced proliferation or cell cycle arrest is determined by the level of Raf activity with arrest mediated by p21Cip1.
TL;DR: The ability of Raf to elicit cell cycle arrest is strongly associated with its ability to induce the expression of the cyclin-dependent kinase inhibitor p21Cip1 in a manner that bears analogy to alpha-factor arrest in Saccharomyces cerevisiae.
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Lack of cyclin D-Cdk complexes in Rb-negative cells correlates with high levels of p16INK4/MTS1 tumour suppressor gene product
TL;DR: It is suggested that in cells in which the function of Rb has been compromised, p16 competes with D cyclins for binding to Cdk4 and Cdk6 and prevents formation of active complexes, and DNA tumour virus oncoproteins do not disrupt cyclin D1‐Cdk4 complexes in cells lacking p16.