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Mao Yang

Researcher at St. Jude Children's Research Hospital

Publications -  17
Citations -  2031

Mao Yang is an academic researcher from St. Jude Children's Research Hospital. The author has contributed to research in topics: Autophagy & Biology. The author has an hindex of 10, co-authored 12 publications receiving 1338 citations.

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ESCRT-III Acts Downstream of MLKL to Regulate Necroptotic Cell Death and Its Consequences

TL;DR: It is shown that, during necroptosis, MLKL-dependent calcium (Ca2+) influx and phosphatidylserine (PS) exposure on the outer leaflet of the plasma membrane preceded loss of PM integrity.
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Noncanonical autophagy inhibits the autoinflammatory, lupus-like response to dying cells

TL;DR: In this paper, the authors describe the consequences of defective LC3-associated phagocytosis in vivo and show that mice lacking any of several components of the LAP pathway show increased serum levels of inflammatory cytokines and autoantibodies, glomerular immune complex deposition, and evidence of kidney damage.
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LC3-associated endocytosis facilitates β-amyloid clearance and mitigates neurodegeneration in murine Alzheimer’s Disease

TL;DR: The data support a protective role for LANDO in microglia in neurodegenerative pathologies resulting from β-amyloid deposition, and identify a novel non-canonical function of several autophagy proteins in the conjugation of LC3 to Rab5+, clathrin+ endosomes containing β-amide.
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LC3-Associated Phagocytosis in Myeloid Cells Promotes Tumor Immune Tolerance.

TL;DR: It is found that the anti-tumor effects of LAP impairment require tumor-infiltrating T cells, dependent upon STING and the type I interferon response, and autophagy proteins in the myeloid cells of the tumor microenvironment contribute to immune suppression of T lymphocytes by effecting LAP.
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BOK Is a Non-canonical BCL-2 Family Effector of Apoptosis Regulated by ER-Associated Degradation.

TL;DR: BOK is a bona fide yet unconventional effector of MOMP that can trigger apoptosis in the absence of both BAX and BAK, but unlike the canonical effectors, BOK appears to be constitutively active and unresponsive to antagonistic effects of the antiapoptotic BCL-2 proteins.