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Transforming growth factor beta 1 directly and reversibly inhibits the initial cell divisions of long-term repopulating hematopoietic stem cells.

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TLDR
It is shown that the continuous presence of TGF-beta 1 directly inhibits the cell division of essentially all low Ho/Rh cells during their 0 to 5th cell division in vitro, which must directly inhibit the proliferation of LTR-HSC contained within these low Ho-Rh cells.
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This article is published in Blood.The article was published on 1996-07-01 and is currently open access. It has received 201 citations till now. The article focuses on the topics: Cellular differentiation & Stem cell factor.

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Journal ArticleDOI

STEM CELL NICHE: Structure and Function

TL;DR: A comparative summary of the differences and commonalities of different stem cell niches in Drosophila ovary/testis and Caenorhabditis elegans distal tip as well as in mammalian bone marrow, skin/hair follicle, intestine, brain, and testis is compared.
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The stem cell niches in bone.

TL;DR: The architecture of the osteoblastic and vascular niches in bone marrow is compared and the function of osteoblasts in maintaining a quiescent HSC microenvironment and the likely role of the vascular niche in regulating stem cell proliferation, differentiation, and mobilization is highlighted.
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Hematopoietic stem cell: self-renewal versus differentiation

TL;DR: This review focuses on the hierarchical structure of the hematopoietic system, the current understanding of microenvironment and molecular cues regulating self‐renewal and differentiation of adult HSCs, and the currently emerging systems approaches to understand HSC biology.
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Aging hematopoietic stem cells decline in function and exhibit epigenetic dysregulation.

TL;DR: These studies show that hematopoietic stem cells are not protected from aging, and loss of epigenetic regulation at the chromatin level may drive both functional attenuation of cells, as well as other manifestations of aging, including the increased propensity for neoplastic transformation.
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Homeostatic expansion of T cells during immune insufficiency generates autoimmunity.

TL;DR: It is shown that reduced T cell numbers and the resulting exaggerated homeostatic-type proliferation of T cells generate autoimmunity and that poor T cell survival and lymphopenia precipitate autoimmune disease.
References
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Journal ArticleDOI

Purification and Characterization of Mouse Hematopoietic Stem Cells

TL;DR: Mouse bone marrow hematopoietic stem cells were isolated with the use of a variety of phenotypic markers and thirty of these cells are sufficient to save 50 percent of lethally irradiated mice, and to reconstitute all blood cell types in the survivors.
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Transforming growth factor beta induces the cyclin-dependent kinase inhibitor p21 through a p53-independent mechanism

TL;DR: It is demonstrated that a single extracellular antiproliferative signal, TGF-beta, can act through multiple signaling pathways to elicit a growth arrest response, suggesting that p21 can respond to both intracellular and extacellular signals for cell cycle arrest.
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Growth inhibition by TGF-β linked to suppression of retinoblastoma protein phosphorylation

TL;DR: TGF- beta 1 and RB appear to function in a common growth-inhibitory pathway in which TGF-beta 1 acts to retain RB in the underphosphorylated, growth-suppressive state.
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TGF-β1 inhibition of c-myc transcription and growth in keratinocytes is abrogated by viral transforming proteins with pRB binding domains

TL;DR: Observations indicate that pRB or another protein that interacts with this binding domain mediates TGF-beta 1 regulation of c-myc gene expression and growth inhibition.
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Negative regulation of G1 in mammalian cells: inhibition of cyclin E-dependent kinase by TGF-beta

TL;DR: The effects of TGF-beta, which correlated with the inhibition of retinoblastoma protein phosphorylation, suggest that mammalian G1 cyclin-dependent kinases, like their counterparts in yeast, are targets for negative regulators of the cell cycle.
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