G
Gary M. Hellmann
Researcher at R. J. Reynolds Tobacco Company
Publications - 8
Citations - 293
Gary M. Hellmann is an academic researcher from R. J. Reynolds Tobacco Company. The author has contributed to research in topics: Squalene & Complementary DNA. The author has an hindex of 7, co-authored 8 publications receiving 286 citations.
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Journal ArticleDOI
Variations in the VPg Protein Allow a Potyvirus to Overcome va Gene Resistance in Tobacco
TL;DR: It was demonstrated that a domain within the VPg protein is responsible for overcoming va resistance in TN 86, compatible with the hypothesis that VPg must assume an appropriate configuration in order to interact with appropriate host components and facilitate systemic virus movement.
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Gene expression profiling of cultured human bronchial epithelial and lung carcinoma cells.
TL;DR: A commercially available human cDNA array is employed to systematically screen for alterations in the expression of 600 genes in normal human bronchial epithelial cells as well as in several lung carcinoma lines to increase the understanding of the molecular basis for human pulmonary carcinogenesis.
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Molecular cloning, in vitro expression and characterization of a plant squalene synthetase cDNA.
Kathleen M. Hanley,Olivier Nicolas,Timothy B. Donaldson,Constance Smith-Monroy,Gordon William Robinson,Gary M. Hellmann +5 more
TL;DR: Comparison of the deduced primary amino acid sequences of plant, yeast, rat and human squalene synthetase revealed regions of conservation that may indicate similar functions within each polypeptide.
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Regeneration of salvia sclarea via organogenesis
TL;DR: A system for regeneration of clary sage, (Salvia sclarea L.) via organogenesis using plant tissue culture techniques in a multistage culturing medium containing 2,4-dichlorophenoxyacetic acid (2, 4-D) is provided.
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Increased DNA methylation in the HoxA5 promoter region correlates with decreased expression of the gene during tumor promotion.
TL;DR: Increased DNA methylation contributes to the downregulation of HoxA5, and combined with hypermethylation of p16 or MGMT, this might facilitate the clonal expansion of increasingly aberrant cells during promotion.