J
Jacalyn H. Pierce
Researcher at National Institutes of Health
Publications - 142
Citations - 15069
Jacalyn H. Pierce is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Tyrosine phosphorylation & Receptor tyrosine kinase. The author has an hindex of 63, co-authored 142 publications receiving 14881 citations. Previous affiliations of Jacalyn H. Pierce include Harvard University & University of Massachusetts Medical School.
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Journal ArticleDOI
Mast cell lines produce lymphokines in response to cross-linkage of Fc epsilon RI or to calcium ionophores.
Marshall Plaut,Jacalyn H. Pierce,Cynthia J. Watson,J. Hanley-Hyde,Richard P. Nordan,William E. Paul +5 more
TL;DR: It is shown that cross-linkage of FcεRI on a series of non-transformed murine mast cell lines, or treatment of these cells with calcium ionophores, stimulates increased messenger RNA levels and secretion of a group of lymphokines classically produced by a subset of murine T cell lines (TH2cells).
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erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells
TL;DR: A new mechanism for acquisition of oncogenic properties by genes encoding growth factor receptor-like proteins is demonstrated and a functional basis for the role of their overexpression in the development of human malignancies is provided.
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Role of IRS-2 in insulin and cytokine signalling
Xiao Jian Sun,Ling Mei Wang,Yitao Zhang,Lynne Yenush,Martin G. Myers,Erin Glasheen,William S. Lane,Jacalyn H. Pierce,Morris F. White +8 more
TL;DR: The discovery of a second IRS-signalling protein, IRS-2, which is expressed in many cells, including tissues from IRS-1 −/− mice, and may be essential for signalling by several receptor systems, is provisionally resolved.
Journal Article
Induction of WAF1/CIP1 by a p53-independent Pathway
TL;DR: The results suggest the existence of two separate pathways for the induction of WAF1/CIP1, a p53-dependent one activated by DNA damage and a p 53-independent oneactivated by mitogens at the entry into the cell cycle.
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Overexpression of the human EGF receptor confers an EGF-dependent transformed phenotype to NIH 3T3 cells
Pier Paolo Di Fiore,Jacalyn H. Pierce,Timothy P. Fleming,Rachel B. Hazan,Axel Ullrich,C. Richter King,Joseph Schlessinger,Stuart A. Aaronson +7 more
TL;DR: EGF receptor overexpression appears to amplify normal EGF signal transduction, and high levels of EGFR expression, which conferred a transformed phenotype to NIH 3T3 cells in the presence of ligand were demonstrated in representative human tumor cell lines that contained amplified copies of the EGFR gene.