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Julie A. Jarrett

Bio: Julie A. Jarrett is an academic researcher from Genentech. The author has contributed to research in topics: Transforming growth factor & Peptide sequence. The author has an hindex of 3, co-authored 3 publications receiving 2826 citations.

Papers
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Journal ArticleDOI
01 Aug 1985-Nature
TL;DR: The cDNA sequence indicates that the 112-amino acid monomeric form of the natural TGF-β homodimer is derived proteolytically from a much longer precursor polypeptide which may be secreted.
Abstract: The partial amino-acid sequence of purified human transforming growth factor-beta (TGF-beta) was used to identify a series of cDNA clones encoding the protein. The cDNA sequence indicates that the 112-amino acid monomeric form of the natural TGF-beta homodimer is derived proteolytically from a much longer precursor polypeptide which may be secreted. TGF-beta messenger RNA is synthesized in various normal and transformed cells.

1,716 citations

Journal ArticleDOI
01 Dec 1984-Nature
TL;DR: Purified recombinant lymphotoxin shows cytotoxic activity on murine and human tumour cell lines in vitro and causes necrosis of certain murine sarcomas in vivo.
Abstract: A chemically-synthesized gene and natural complementary DNA coding for human lymphotoxin were isolated and engineered for expression in Escherichia coli. Purified recombinant lymphotoxin shows cytotoxic activity on murine and human tumour cell lines in vitro and causes necrosis of certain murine sarcomas in vivo.

656 citations

Journal ArticleDOI
TL;DR: Two areas of the precursor exhibit a marked degree of homology to the human counterpart and suggests an important biological function for this area of TGF-beta, which can act, often in cooperation with other growth factors, as a mitogenic factor for a variety of cells.

481 citations


Cited by
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Journal ArticleDOI
TL;DR: The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms and mutations in these pathways are the cause of various forms of human cancer and developmental disorders.
Abstract: The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms. Work over the past few years has led to the elucidation of a TGF-beta signal transduction network. This network involves receptor serine/threonine kinases at the cell surface and their substrates, the SMAD proteins, which move into the nucleus, where they activate target gene transcription in association with DNA-binding partners. Distinct repertoires of receptors, SMAD proteins, and DNA-binding partners seemingly underlie, in a cell-specific manner, the multifunctional nature of TGF-beta and related factors. Mutations in these pathways are the cause of various forms of human cancer and developmental disorders.

7,710 citations

Journal ArticleDOI
23 Feb 2001-Cell
TL;DR: The authors regret the inability to cite all of the primary literature contributing to this review due to length considerations, but wish to thank F. Chan, T. Migone, and J. Wang for insightful comments on the manuscript.

3,756 citations

Journal ArticleDOI
TL;DR: Two different tumour-necrosis factors, first isolated in 1984, were found to be cytotoxic to tumour cells and to induce tumour regression in mice, and blockers of TNF have been approved for human use in treating TNF-linked autoimmune diseases.
Abstract: Two different tumour-necrosis factors (TNFs), first isolated in 1984, were found to be cytotoxic to tumour cells and to induce tumour regression in mice. Research during the past two decades has shown the existence of a superfamily of TNF proteins consisting of 19 members that signal through 29 receptors. These ligands, while regulating normal functions such as immune responses, haematopoiesis and morphogenesis, have also been implicated in tumorigenesis, transplant rejection, septic shock, viral replication, bone resorption, rheumatoid arthritis and diabetes; so indicating their role as 'double-edged swords'. These cytokines either induce cellular proliferation, survival, differentiation or apoptosis. Blockers of TNF have been approved for human use in treating TNF-linked autoimmune diseases in the United States and other countries.

2,582 citations

Journal ArticleDOI
08 Nov 1985-Science

2,505 citations