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John L. Cleveland

Researcher at Scripps Research Institute

Publications -  257
Citations -  29431

John L. Cleveland is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Apoptosis & Gene. The author has an hindex of 83, co-authored 241 publications receiving 27222 citations. Previous affiliations of John L. Cleveland include Ben-Gurion University of the Negev & W. Alton Jones Cell Science Center.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Daniel J. Klionsky, +235 more
- 16 Feb 2008 - 
TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
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Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization

TL;DR: MEFs that survive myc overexpression sustain p53 mutation or ARF loss during the process of establishment and become immortal, and ARF regulates a p53-dependent checkpoint that safeguards cells against hyperproliferative, oncogenic signals.
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Toll-like receptor signalling in macrophages links the autophagy pathway to phagocytosis

TL;DR: It is shown that a particle that engages TLRs on a murine macrophage while it is phagocytosed triggers the autophagosome marker LC3 to be rapidly recruited to the phagosome in a manner that depends on theAutophagy pathway proteins ATG5 and ATG7; this process is preceded by recruitment of beclin 1 and phosphoinositide-3-OH kinase activity.
Journal Article

Constitutive c-myc expression in an IL-3-dependent myeloid cell line suppresses cell cycle arrest and accelerates apoptosis.

TL;DR: The premature induction of apoptosis in cells harboring a deregulated c-myc gene suggests that apoptosis may be an important mechanism in the elimination of hematopoietic cells Harboring mutations, such as constitutive c- myc expression, which imbalance normal cell cycle regulatory controls.
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Puma is an essential mediator of p53-dependent and -independent apoptotic pathways

TL;DR: It is reported that Puma is essential for hematopoietic cell death triggered by ionizing radiation, deregulated c-Myc expression, and cytokine withdrawal, and required for IR-induced death throughout the developing nervous system and accounts for nearly all of the apoptotic activity attributed to p53 under these conditions.