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TGF-β and the TGF-β Family: Context-Dependent Roles in Cell and Tissue Physiology

TLDR
TGF-β is introduced as the best-studied factor among the TGF- β family proteins, with its diversity of roles in the control of cell proliferation and differentiation, wound healing and immune system, and its key roles in pathology, for example, skeletal diseases, fibrosis, and cancer.
Abstract
The transforming growth factor-β (TGF-β) is the prototype of the TGF-β family of growth and differentiation factors, which is encoded by 33 genes in mammals and comprises homo- and heterodimers. This review introduces the reader to the TGF-β family with its complexity of names and biological activities. It also introduces TGF-β as the best-studied factor among the TGF-β family proteins, with its diversity of roles in the control of cell proliferation and differentiation, wound healing and immune system, and its key roles in pathology, for example, skeletal diseases, fibrosis, and cancer.

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New insights into TGF-β/Smad signaling in tissue fibrosis.

TL;DR: An overview of the molecular mechanisms of TGF-β/Smad signaling pathway in renal, hepatic, pulmonary and cardiac fibrosis is presented and particular challenges are presented and placed within the context of future applications against tissue fibrosis.
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Specificity, versatility, and control of TGF-β family signaling.

TL;DR: The exquisite nature of TGF-β family signaling in its roles in diverse and context-specific cellular behaviors is described and the mechanisms through which proteins called Smads act as intracellular effectors of ligand-induced gene expression responses are introduced, showing that the specificity and impressive versatility of Smad signaling depend on cross-talk from other pathways.
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Tissue-specific contribution of macrophages to wound healing

TL;DR: This review evaluates how macrophages in two fundamentally distinct tissues, i.e. the lung and the skin, differentially contribute to the process of wound healing.
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Zinc in Wound Healing Modulation.

TL;DR: Investigations on the cellular and molecular mechanisms of zinc in modulating the wound healing process and how these findings can be translated into future clinical management of wound healing are discussed.
References
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A genetic model for colorectal tumorigenesis

TL;DR: A model for the genetic basis of colorectal neoplasia that includes the following salient features is presented, which may be applicable to other common epithelial neoplasms, in which tumors of varying stage are more difficult to study.
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The basics of epithelial-mesenchymal transition

TL;DR: Processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias and the identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes.
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The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells

TL;DR: It is reported that the induction of an EMT in immortalized human mammary epithelial cells (HMLEs) results in the acquisition of mesenchymal traits and in the expression of stem-cell markers, and it is shown that those cells have an increased ability to form mammospheres, a property associated with mammARY epithelial stem cells.
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Cancer Genome Landscapes

TL;DR: This work has revealed the genomic landscapes of common forms of human cancer, which consists of a small number of “mountains” (genes altered in a high percentage of tumors) and a much larger number of "hills" (Genes altered infrequently).
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