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Open AccessJournal ArticleDOI

TGF-beta signal transduction.

TLDR
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.

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Journal ArticleDOI

Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus

TL;DR: Current understanding on the mechanisms of TGF-β signaling from cell membrane to the nucleus is presented and the transcriptional regulation of target gene expression is reviewed.
Journal ArticleDOI

Two-component signal transduction

TL;DR: Detailed analyses of a relatively small number of representative proteins provide a foundation for understanding this large family of signaling proteins, which consists of two conserved components, a histidine protein kinase and a response regulator protein.
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Mammalian Mitogen-Activated Protein Kinase Signal Transduction Pathways Activated by Stress and Inflammation

TL;DR: This review focuses on the biochemical components and regulation of mammalian stress-regulated mitogen-activated protein kinase (MAPK) pathways, and the nuclear factor-kappa B pathway, a second stress signaling paradigm.
Journal ArticleDOI

Regulation of Wound Healing by Growth Factors and Cytokines

TL;DR: This review summarizes the results of expression studies that have been performed in rodents, pigs, and humans to localize growth factors and their receptors in skin wounds and reports on genetic studies addressing the functions of endogenous growth factors in the wound repair process.
References
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Journal ArticleDOI

Signal transduction by receptors with tyrosine kinase activity

TL;DR: Cet article synthese montre comment des recepteurs membranaires a activite tyrosine kinase peuvent etre impliques dans la transduction and notamment jouent le role de signal de the transduction.
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Regulation of skeletal muscle mass in mice by a new TGF-beta superfamily member.

TL;DR: Results suggest that GDF-8 functions specifically as a negative regulator of skeletal muscle growth, which is significantly larger than wild-type animals and show a large and widespread increase in skeletal muscle mass.
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GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons

TL;DR: In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake and did not increase total neuron or astrocyte numbers or transmitter uptake.
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Targeted disruption of the mouse transforming growth factor-β1 gene results in multifocal inflammatory disease

TL;DR: TGF-β1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.
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