G
Gregory I.L. Veitch
Researcher at University of Western Ontario
Publications - 4
Citations - 578
Gregory I.L. Veitch is an academic researcher from University of Western Ontario. The author has contributed to research in topics: Oculodentodigital dysplasia & Connexin. The author has an hindex of 4, co-authored 4 publications receiving 562 citations.
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Journal ArticleDOI
A Gja1 missense mutation in a mouse model of oculodentodigital dysplasia
Ann M. Flenniken,Lucy R. Osborne,Lucy R. Osborne,Nicole M. Anderson,Nadia Ciliberti,Craig Fleming,Joanne E. I. Gittens,Xiang-Qun Gong,Lois B. Kelsey,Crystal S. Lounsbury,Luisa Moreno,Brian J. Nieman,Katie Peterson,Dawei Qu,Wendi A. Roscoe,Qing Shao,Dan Tong,Gregory I.L. Veitch,Irina Voronina,Igor Vukobradovic,Geoffrey A. Wood,Yonghong Zhu,Ralph A Zirngibl,Jane E. Aubin,Jane E. Aubin,Donglin Bai,Benoit G. Bruneau,Marc D. Grynpas,Marc D. Grynpas,Janet E. Henderson,R. Mark Henkelman,Colin McKerlie,Colin McKerlie,John G. Sled,William L. Stanford,William L. Stanford,Dale W. Laird,Gerald M. Kidder,S. Lee Adamson,S. Lee Adamson,Janet Rossant,Janet Rossant +41 more
TL;DR: In vivo and in vitro studies revealed that the mutant Cx43 protein acts in a dominant-negative fashion to disrupt gap junction assembly and function, and these mutant mice represent an experimental model with which to explore the clinical manifestations of ODDD and to evaluate potential intervention strategies.
Journal ArticleDOI
Down-regulation of Cx43 by Retroviral Delivery of Small Interfering RNA Promotes an Aggressive Breast Cancer Cell Phenotype
TL;DR: Results suggest that Cx43 is required for maintaining cell differentiation and the regulation of molecules important in angiogenesis.
Journal ArticleDOI
Oculodentodigital dysplasia-causing connexin43 mutants are non-functional and exhibit dominant effects on wild-type connexin43.
Wendi A. Roscoe,Gregory I.L. Veitch,Xiang-Qun Gong,Emily M. Pellegrino,Donglin Bai,Elizabeth McLachlan,Qing Shao,Gerald M. Kidder,Dale W. Laird +8 more
TL;DR: These studies suggest that, although patients suffering from oculodentodigital dysplasia possess one wild-type Cx43 allele, it is likely that C x43-mediated gap junctional intercellular communication is reduced below 50% because of a dominant-negative effect of mutant Cx44 on wild- type Cx 43.
Journal ArticleDOI
Selective assembly of connexin37 into heterocellular gap junctions at the oocyte/granulosa cell interface
TL;DR: Results indicate that the growing murine oocyte is functionally coupled with granulosa cells by homotypic gap junctions composed of Cx37, and that the formation and/or stabilization of CX37 junctions is selectively induced at the oocyte-granulosa interface by cell contact.