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Transforming growth factor-β signalling: role and consequences of Smad linker region phosphorylation

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TLDR
Key factors including the identification of the kinases that phosphorylate individual Smad residues, the upstream agents that activate these kinases, the cellular location of the phosphorylation event and the importance of the linker region in regulation and expression of genes induced by TGF-β are covered.
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This article is published in Cellular Signalling.The article was published on 2013-10-01. It has received 227 citations till now. The article focuses on the topics: Serine/threonine-specific protein kinase & MAP2K7.

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TGF-β: the master regulator of fibrosis

TL;DR: Studies over the past 5 years have identified additional mechanisms that regulate the action of TGF-β1/Smad signalling in fibrosis, including short and long noncoding RNA molecules and epigenetic modifications of DNA and histone proteins.
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Alternatively activated microglia and macrophages in the central nervous system.

TL;DR: Cumulative evidence shows that microglia may undergo the alternative activation pathway, express M2-type markers and contribute to neuroprotection, and in the approaches available for its identification.
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MicroRNA and mRNA cargo of extracellular vesicles from porcine adipose tissue-derived mesenchymal stem cells

TL;DR: Gene ontology analysis indicates that these miRNAs target transcription factors and genes that participate in several cellular pathways, including angiogenesis, cellular transport, apoptosis, and proteolysis.
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The changing role of TGFβ in healthy, ageing and osteoarthritic joints.

TL;DR: In this Review, the changing role of TGFβ in normal joint homeostasis, ageing and osteoarthritis is discussed: TGF β counteracts pathological changes in a young healthy joint, alters its signalling during ageing and is a driving force of pathology in osteoartritic joints.
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The GSK-3 family as therapeutic target for myocardial diseases

TL;DR: Glycogen synthase kinase-3 is one of the few signaling molecules that regulate a truly astonishing number of critical intracellular signaling pathways and its expanding role in the heart is focused on, concentrating primarily on recent studies that have used cardiomyocyte- and fibroblast-specific conditional gene deletion in mouse models.
References
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Journal ArticleDOI

TGF-beta signal transduction.

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.
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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.
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Mammalian MAP kinase signalling cascades

TL;DR: Recent studies have begun to shed light on the physiological functions of MAPK cascades in the control of gene expression, cell proliferation and programmed cell death.
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Smad-dependent and Smad-independent pathways in TGF-beta family signalling.

TL;DR: Transforming growth factor-β (TGF-β) proteins regulate cell function, and have key roles in development and carcinogenesis, and combinatorial interactions in the heteromeric receptor and Smad complexes, receptor-interacting and Smadracing proteins, and cooperation with sequence-specific transcription factors allow substantial versatility and diversification of TGF- β family responses.
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Oncogenic kinase signalling

TL;DR: How oncogenic conversion of protein kinases results from perturbation of the normal autoinhibitory constraints on kinase activity is emphasized and an update is provided on the role of deregulated PI(3)K/Akt and mammalian target of rapamycin/p70S6K signalling in human malignancies.
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