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Cell death.
Newton, Kim; Strasser, Andreas; Kayagaki, Nobuhiko; Dixit, Vishva M.
Affiliation
  • Newton K; Physiological Chemistry Department, Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080, USA. Electronic address: knewton@gene.com.
  • Strasser A; WEHI: Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia; Department of Medical Biology, The University of Melbourne, Melbourne, VIC 3010, Australia. Electronic address: strasser@wehi.edu.au.
  • Kayagaki N; Physiological Chemistry Department, Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080, USA. Electronic address: kayagaki@gene.com.
  • Dixit VM; Physiological Chemistry Department, Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080, USA. Electronic address: dixit@gene.com.
Cell ; 187(2): 235-256, 2024 01 18.
Article in En | MEDLINE | ID: mdl-38242081
ABSTRACT
Cell death supports morphogenesis during development and homeostasis after birth by removing damaged or obsolete cells. It also curtails the spread of pathogens by eliminating infected cells. Cell death can be induced by the genetically programmed suicide mechanisms of apoptosis, necroptosis, and pyroptosis, or it can be a consequence of dysregulated metabolism, as in ferroptosis. Here, we review the signaling mechanisms underlying each cell-death pathway, discuss how impaired or excessive activation of the distinct cell-death processes can promote disease, and highlight existing and potential therapies for redressing imbalances in cell death in cancer and other diseases.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Signal Transduction / Cell Death Limits: Humans Language: En Journal: Cell Year: 2024 Type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Signal Transduction / Cell Death Limits: Humans Language: En Journal: Cell Year: 2024 Type: Article