Cited by 376Cell death mechanisms and regulationCancer-related Molecular PathwaysClusterin in disease pathology

Survivin and IAP proteins in cell-death mechanisms

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Altieri, Dario C.·2010·Biochemical Journal

Abstract

From the realization that cell number homoeostasis is fundamental to the biology of all metazoans, and that deregulation of this process leads to human diseases, enormous interest has been devoted over the last two decades to map the requirements of cell death and cell survival. This effort has led to tangible progress, and we can now chart with reasonable accuracy complex signalling circuitries controlling cell-fate decisions. Some of this knowledge has translated into novel therapeutics, and the outcome of these strategies, especially in cancer, is eagerly awaited. However, the function of cell-death modifiers have considerably broadened over the last few years, and these molecules are increasingly recognized as arbiters of cellular homoeostasis, from cell division, to intracellular signalling to cellular adaptation. This panoply of functions is best exemplified by members of the IAP (inhibitor of apoptosis) gene family, molecules originally narrowly defined as endogenous caspase inhibitors, but now firmly positioned at the crossroads of multiple normal and transformed cellular responses.

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Authors
Altieri, D. C.
Affiliations
University of Massachusetts Chan Medical School (US)
Corresponding author
Altieri, Dario C.
Venue
Biochemical Journal
Published
2010-08-13
Volume
430
Issue
2
Pages
199-205
ISSN
  • 0264-6021 (ISSN-L)
  • 1470-8728
OpenAlex
W1971576831
Cited by
376
References
109
Citations by year
2026: 6 · 2025: 8 · 2024: 10 · 2023: 9 · 2022: 12 · 2021: 10 · 2020: 20 · 2019: 17 · 2018: 19 · 2017: 27 · 2016: 23 · 2015: 46 · 2014: 37 · 2013: 35 · 2012: 50
FWCI
3.71
Type
journal article
Language
en
Open access
Locations
  • Biochemical Journal (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (R01HL054131, R37HL054131, HL 54131)
  • National Cancer Institute (R01CA078810, CA-78810, R01CA090917, CA118005, CA-90917, R01CA118005)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Health Sciences › Medicine › Oncology › Clusterin in disease pathology
Keywords
survivin, inhibitor of apoptosis proteins, IAP family, cell death, apoptosis, cell survival, cell fate determination, caspase inhibitors, cancer therapeutics, cellular adaptation, intracellular signaling
MeSH terms
Animals, Humans, Microtubule-Associated Proteins, Neoplasms, Apoptosis, Inhibitor of Apoptosis Proteins

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