TY - JOUR
T1 - RumMAGE-D the members
T2 - Structure and function of a new adaptor family of MAGE-D proteins
AU - Sasaki, Aya
AU - Hinck, Lindsay
AU - Watanabe, Ken
N1 - Funding Information:
Authors (AS and KW) thank Drs. Yoshiko Masuda and Kyoji Ikeda for contribution in the series of our study on MAGE-D1. This work was supported in part by grant NS39572 from the NIH (to LH) and a grant for the Program for Promotion of Fundamental Studies in Health Sciences of the Organization for Pharmaceutical Safety and Research of Japan (to KW).
PY - 2005
Y1 - 2005
N2 - MAGE genes were first described as cancer-testis antigens, which are silenced in normal adult tissues but aberrantly expressed in tumor cells. The short peptides, derived from the degradation of MAGE transcripts, are the source of antigens that cause tumor rejection reactions when presented in the context of major histocompatibility complex. The recent discovery of a subset of genes that contain the structurally conserved MAGE homology domain (MHD) has accelerated the investigation into the normal function of MAGE genes. This new type of MAGE gene is normally expressed in embryonal and adult tissue, especially the brain. MAGE-D1, also known as NRAGE or Dlxin-1, functions as an adaptor protein that mediates multiple signaling pathways, including NGFR (p75NTR) and UNC5H1-induced apoptosis and Dlx/Msx-mediated transcription. Loss of a different MAGE family member, Necdin, which works as a cell cycle regulator, may play a role in the pathogenesis of Prader-Willi syndrome, a neurobehavioral disorder. In this article, the authors discuss recent findings concerning the structure and function of new MAGE genes, primarily focusing on MAGE-D1. Because some MAGE-D subfamily proteins share significant homology within the MHD, these recent discoveries on MAGE-D1 may give insight into the function of other MAGE-D proteins.
AB - MAGE genes were first described as cancer-testis antigens, which are silenced in normal adult tissues but aberrantly expressed in tumor cells. The short peptides, derived from the degradation of MAGE transcripts, are the source of antigens that cause tumor rejection reactions when presented in the context of major histocompatibility complex. The recent discovery of a subset of genes that contain the structurally conserved MAGE homology domain (MHD) has accelerated the investigation into the normal function of MAGE genes. This new type of MAGE gene is normally expressed in embryonal and adult tissue, especially the brain. MAGE-D1, also known as NRAGE or Dlxin-1, functions as an adaptor protein that mediates multiple signaling pathways, including NGFR (p75NTR) and UNC5H1-induced apoptosis and Dlx/Msx-mediated transcription. Loss of a different MAGE family member, Necdin, which works as a cell cycle regulator, may play a role in the pathogenesis of Prader-Willi syndrome, a neurobehavioral disorder. In this article, the authors discuss recent findings concerning the structure and function of new MAGE genes, primarily focusing on MAGE-D1. Because some MAGE-D subfamily proteins share significant homology within the MHD, these recent discoveries on MAGE-D1 may give insight into the function of other MAGE-D proteins.
KW - Apoptosis
KW - Dlx/Msx
KW - MAGE-D
KW - NGFR (p75NTR)
KW - Necdin
KW - UNC5H
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U2 - 10.1080/10799890500210511
DO - 10.1080/10799890500210511
M3 - Article
C2 - 16194933
AN - SCOPUS:26444451086
SN - 1079-9893
VL - 25
SP - 181
EP - 198
JO - Journal of Receptors and Signal Transduction
JF - Journal of Receptors and Signal Transduction
IS - 3
ER -
