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Lixin Zheng

Researcher at National Institutes of Health

Publications -  71
Citations -  13937

Lixin Zheng is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Programmed cell death & Apoptosis. The author has an hindex of 44, co-authored 66 publications receiving 12825 citations. Previous affiliations of Lixin Zheng include Government of the United States of America.

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Termination of autophagy and reformation of lysosomes regulated by mTOR

TL;DR: It is shown that mTOR signalling in rat kidney cells is inhibited during initiation of autophagy, but reactivated by prolonged starvation, and this generates proto-lysosomal tubules and vesicles that extrude from autolysosomes and ultimately mature into functional lysosomes, thereby restoring the full complement of lysosity in the cell.
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CD4+CD25+Foxp3+ regulatory T cells induce cytokine deprivation–mediated apoptosis of effector CD4+ T cells

TL;DR: It is shown that Treg cells induced apoptosis of effector CD4+ T cells in vitro and in vivo in a mouse model of inflammatory bowel disease and cytokine deprivation–induced apoptosis is a prominent mechanism by which T Reg cells inhibit effector T cell responses.
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Induction of apoptosis in mature T cells by tumour necrosis factor.

TL;DR: It is shown that tumour necrosis factor (TNF) can mediate mature T-cell receptor-induced apoptosis through the p75 TNF receptor and suggest that autoregulatory apoptosis of the mature T cells can occur by two distinct molecular mechanisms.
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Mature T lymphocyte apoptosis--immune regulation in a dynamic and unpredictable antigenic environment.

TL;DR: Immunological, cellular, and molecular evidence indicates that throughout the life of a T cell, apoptosis may be evoked in excessive, harmful, or useless clonotypes to preserve a healthy and balanced immune system.
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A domain in TNF receptors that mediates ligand-independent receptor assembly and signaling.

TL;DR: A conserved domain in the extracellular region of the 60- and 80-kilodalton tumor necrosis factor receptors was identified that mediates specific ligand-independent assembly of receptor trimers.