Greg Matlashewski mainly investigates Leishmania donovani, Molecular biology, Virology, Gene and Antibody. His studies in Leishmania donovani integrate themes in fields like Amastigote and Immune system. His Molecular biology research incorporates elements of Transfection, Complementary DNA, Untranslated region, Tumor suppressor gene and Open reading frame.
His Virology study deals with Cell culture intersecting with Papillomaviridae, Monoclonal, Platelet-derived growth factor receptor and Growth factor. His Gene study contributes to a more complete understanding of Genetics. His research investigates the connection with Leishmaniasis and areas like Imiquimod which intersect with concerns in Drug resistance.
His main research concerns Visceral leishmaniasis, Leishmania donovani, Leishmaniasis, Leishmania and Molecular biology. His Leishmania donovani study incorporates themes from Macrophage, Amastigote, Leishmania major and Virology. His Virology research is multidisciplinary, relying on both Antibody, Immune system and Antigen.
His studies deal with areas such as Polymerase chain reaction, Microbiology and Virulence as well as Leishmania. His work deals with themes such as Gene expression, Transfection, Complementary DNA, Peptide sequence and Gene, which intersect with Molecular biology. To a larger extent, Greg Matlashewski studies Genetics with the aim of understanding Gene.
Leishmaniasis, Visceral leishmaniasis, Leishmania, Leishmania major and Leishmania donovani are his primary areas of study. His Leishmaniasis study also includes fields such as
Greg Matlashewski works mostly in the field of Leishmania, limiting it down to concerns involving Microbiology and, occasionally, Gene knockout. His Leishmania donovani study integrates concerns from other disciplines, such as Spleen, Vector and Immune system. His Cutaneous leishmaniasis study is related to the wider topic of Genetics.
His primary scientific interests are in Leishmaniasis, Virology, Genome editing, Gene and Leishmania. His Leishmaniasis research is multidisciplinary, incorporating elements of Disease Presentation and Neglected tropical diseases. When carried out as part of a general Virology research project, his work on Disease reservoir is frequently linked to work in Indian subcontinent, Development economics and Endemic diseases, therefore connecting diverse disciplines of study.
His study in Genome editing is interdisciplinary in nature, drawing from both Non-homologous end joining, Gene targeting, DNA and DNA Polymerase Theta. His Gene study is concerned with the field of Genetics as a whole. His Leishmania research includes themes of Parasite load, Antibody, Parasitemia and Antigen.
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Role of a p53 polymorphism in the development of human papillomavirus-associated cancer.
Alan Storey;Miranda Thomas;Ann Kalita;Catherine Harwood.
Nature (1998)
Two Polymorphic Variants of Wild-Type p53 Differ Biochemically and Biologically
Miranda Thomas;Ann Kalita;Sylvie Labrecque;David Pim.
Molecular and Cellular Biology (1999)
Isolation of human-p53-specific monoclonal antibodies and their use in the studies of human p53 expression
Lawrence Banks;Greg Matlashewski;Lionel Crawford.
FEBS Journal (1986)
Primary structure polymorphism at amino acid residue 72 of human p53
G J Matlashewski;S Tuck;D Pim;P Lamb.
Molecular and Cellular Biology (1987)
Human papillomavirus type 16 DNA cooperates with activated ras in transforming primary cells.
G. Matlashewski;J. Schneider;L. Banks;N. Jones.
The EMBO Journal (1987)
Isolation and characterization of a human p53 cDNA clone: expression of the human p53 gene.
G. Matlashewski;P. Lamb;D. Pim;J. Peacock.
The EMBO Journal (1984)
Mechanisms of p53 loss in human sarcomas.
Lois M. Mulligan;Greg J. Matlashewski;Heidi J. Scrable;Webster K. Cavenee.
Proceedings of the National Academy of Sciences of the United States of America (1990)
Intracellular infection by Leishmania donovani inhibits macrophage apoptosis
K J Moore;G Matlashewski.
Journal of Immunology (1994)
The human papilloma virus (HPV)-18 E6 oncoprotein physically associates with Tyk2 and impairs Jak-STAT activation by interferon-alpha.
Suiyang Li;S. Labrecque;M. C. Gauzzi;A. R. Cuddihy.
Oncogene (1999)
The E5 gene from human papillomavirus type 16 is an oncogene which enhances growth factor-mediated signal transduction to the nucleus.
P Leechanachai;L Banks;F Moreau;G Matlashewski.
Oncogene (1992)
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