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Joseph D. Mancias

Researcher at Harvard University

Publications -  82
Citations -  12860

Joseph D. Mancias is an academic researcher from Harvard University. The author has contributed to research in topics: Medicine & Cancer. The author has an hindex of 29, co-authored 61 publications receiving 9330 citations. Previous affiliations of Joseph D. Mancias include Brigham and Women's Hospital & Memorial Sloan Kettering Cancer Center.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Quantitative proteomics identifies NCOA4 as the cargo receptor mediating ferritinophagy

Joseph D. Mancias, +4 more
- 01 May 2014 - 
TL;DR: In this article, the authors identify a cohort of novel and known autophagosome-enriched proteins in human cells, including cargo receptors, and identify NCOA4 as a selective cargo receptor for autophagic turnover of ferritin (ferritinophagy), which is critical for iron homeostasis.
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KRAS: feeding pancreatic cancer proliferation

Kirsten L. Bryant, +3 more
- 01 Feb 2014 - 
TL;DR: A number of studies have shown that oncogenic KRAS plays a central role in controlling tumor metabolism by orchestrating multiple metabolic changes including stimulation of glucose uptake, differential channeling of glucose intermediates, reprogrammed glutamine metabolism, increased autophagy, and macropinocytosis.
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Autophagy promotes immune evasion of pancreatic cancer by degrading MHC-I

Keisuke Yamamoto, +20 more
- 22 Apr 2020 - 
TL;DR: It is shown that, in PDAC, MHC-I molecules are selectively targeted for lysosomal degradation by an autophagy-dependent mechanism that involves theAutophagy cargo receptor NBR1 and leads to improved antigen presentation, enhanced anti-tumour T cell responses and reduced tumour growth in syngeneic host mice.