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The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.

The MAGE proteins: Emerging roles in cell cycle progression, apoptosis, and neurogenetic disease

Barker, Philip A., Salehi, Amir·2002·Journal of Neuroscience Research

Abstract

Since the identification of the first MAGE gene in 1991, the MAGE family has expanded dramatically, and over 25 MAGE genes have now been identified in humans. The focus of studies on the MAGE proteins has been their potential for cancer immunotherapy, as a result of the finding that peptides derived from MAGE gene products are bound by major histocompatibility complexes and presented on the cell surface of cancer cells. However, the normal physiological role of MAGE proteins has remained a mystery. Recent studies are now beginning to provide insights into MAGE gene function. Necdin acts as a cell cycle regulatory protein and plays a key role in the pathogenesis of Prader‐Willi syndrome, a neurogenetic disorder. MAGE‐D1, identified as a binding partner for the p75 neurotrophin receptor, the apoptosis inhibitory protein XIAP, and Dlx/MSX homeodomain proteins, blocks cell cycle progression and enhances apoptosis. This review provides an overview of the human MAGE genes and proteins, summarizes recent findings on their cellular roles, and provides a baseline for future studies on this intriguing gene family. © 2002 Wiley‐Liss, Inc.

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Metadata

Authors
Barker, P. A., & Salehi, A.
Venue
Journal of Neuroscience Research
Publisher
Wiley
Published
2002-02-15
Volume
67
Issue
6
Pages
705-712
ISSN
  • 0360-4012 (ISSN-L)
  • 1097-4547
OpenAlex
W2036708294
Cited by
320
References
58
FWCI
7.27
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: The MAGE proteins: Emerging roles in cell cycle progression, apoptosis, and neurogenetic disease. https://app.cochat.ai/papers/10.1002/jnr.10160
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Barker, P. A., & Salehi, A. (2002). The MAGE proteins: Emerging roles in cell cycle progression, apoptosis, and neurogenetic disease. Journal of Neuroscience Research. https://doi.org/10.1002/jnr.10160

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