P
Paul J. Higgins
Researcher at Albany Medical College
Publications - 166
Citations - 8873
Paul J. Higgins is an academic researcher from Albany Medical College. The author has contributed to research in topics: Regulation of gene expression & Plasminogen activator. The author has an hindex of 45, co-authored 159 publications receiving 8226 citations. Previous affiliations of Paul J. Higgins include Kettering University & Brigham and Women's Hospital.
Papers
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Control selection for RNA quantitation.
TL;DR: The uses and pitfalls of the most popular of these controls, glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and beta-actin, are discussed, with special emphasis on precautions associated with the use of GAPDH.
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Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence
TL;DR: It is reported that suppression of the p53 target gene encoding plasminogen activator inhibitor-1 (PAI-1) by RNA interference leads to escape from replicative senescence both in primary mouse embryo fibroblasts and primary human BJ fibro Blasts.
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Reaction of monosaccharides with proteins: possible evolutionary significance.
H F Bunn,Paul J. Higgins +1 more
TL;DR: The emergence of glucose as the primary metabolic fuel may be due in part to the high stability of its ring structure which limits potentially deleterious nonenzymatic glycosylation of proteins.
Journal Article
Suppression of experimental autoimmune encephalomyelitis by oral administration of myelin basic protein and its fragments.
Paul J. Higgins,Howard L. Weiner +1 more
TL;DR: It is reported that experimental autoimmune encephalomyelitis can be suppressed in Lewis rats by the oral administration of myelin basic protein (MBP), suggesting that suppressor determinants exist in the MBP molecule distinct from the encephalitogenic region.
Journal ArticleDOI
Suppression of experimental autoimmune encephalomyelitis by oral administration of myelin basic protein and its fragments
Paul J. Higgins,Howard L. Weiner +1 more
TL;DR: In this paper, the authors showed that experimental autoimmune encephalomyelitis, a T cell-mediated autoimmune disease studied as a model for multiple sclerosis, can be suppressed in Lewis rats by the oral administration of myelin basic protein (MBP).