T
Thomas Maciag
Researcher at Maine Medical Center
Publications - 92
Citations - 10515
Thomas Maciag is an academic researcher from Maine Medical Center. The author has contributed to research in topics: Fibroblast growth factor & Notch signaling pathway. The author has an hindex of 50, co-authored 92 publications receiving 10356 citations. Previous affiliations of Thomas Maciag include American Red Cross & Saint Francis University.
Papers
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Journal ArticleDOI
The heparin-binding (fibroblast) growth factor family of proteins.
Wilson H. Burgess,Thomas Maciag +1 more
Journal ArticleDOI
Human endothelial cell growth factor: cloning, nucleotide sequence, and chromosome localization
Michael C. Jaye,Richard S. Howk,Wilson H. Burgess,George A. Ricca,Ing-Ming Chiu,Mark W. Ravera,Stephen J. O'Brien,William S. Modi,Thomas Maciag,William N. Drohan +9 more
TL;DR: The complete amino acids sequence of human ECGF was deduced from the nucleic acid sequence of these clones; it encompasses all the well-characterized acidic endothelial cell polypeptide mitogens described by several laboratories.
Journal ArticleDOI
Cyclooxygenase is an immediate-early gene induced by interleukin-1 in human endothelial cells.
TL;DR: The data suggest that Cox is an immediate-early gene induced by IL-1 in HUVEC and may contribute to the regulation of the endothelial cell differentiation pathway in vitro.
Journal ArticleDOI
Molecular mechanisms of angiogenesis: fibroblast growth factor signal transduction.
Robert Friesel,Thomas Maciag +1 more
TL;DR: Recent insights into the pathways used for the regulation of FGF secretion and cellular trafficking as well as signaling by FGFRs are described.
Journal ArticleDOI
Induction of cyclooxygenase-2 by interleukin-1 alpha. Evidence for post-transcriptional regulation.
TL;DR: Analysis of the effect of interleukin-1 alpha on the expression of Cox-2 in a human cell line and post-transcriptional mechanisms are suggested to be important in the sustained induction of thecox-2 mRNA suggest that IL-1alpha may increase the stability of the Cox- 2 transcript.