TY - JOUR
T1 - Characterization of monoclonal antibodies against GRIM-19, a novel IFNβ and retinoic acid-activated regulator of cell death
AU - Hu, Jiadi
AU - Angell, Jon E.
AU - Zhang, Jun
AU - Ma, Xinrong
AU - Seo, Taegun
AU - Raha, Abhijit
AU - Hayashi, Jun
AU - Choe, Joonho
AU - Kalvakolanu, Dhananjaya V.
PY - 2002
Y1 - 2002
N2 - A combination of interferonβ (IFNβ) and all-trans retinoic acid (IFN/RA) induces tumor cell apoptosis via some unknown mechanisms. Apoptosis is a gene-directed process that limits the proliferation of undesired cells. Several genes are required to regulate cell death in the higher-order animals. Earlier, we employed a gene expression knockout technique to isolate cell death-related genes. A novel gene, the gene associated with retinoid-interferon-induced mortality-19 (GRIM-19), was found to be essential for tumor cell death induced by IFN/RA. Here, we describe the development and characterization of three monoclonal antibodies (mAbs) against GRIM-19. GRIM-19 is present in the nucleus and cytoplasm. Its expression is induced by the IFN/RA combination. We also show that GRIM-19 inhibits the cell-transforming property of viral oncogenic protein viral IFN regulatory factor-1 (vIRF-1) via a physical interaction. mAbs developed in this study should be useful for studying the other physiologic roles of GRIM-19 and serve as a potent tool for studying tumor responses to IFN/RA therapy.
AB - A combination of interferonβ (IFNβ) and all-trans retinoic acid (IFN/RA) induces tumor cell apoptosis via some unknown mechanisms. Apoptosis is a gene-directed process that limits the proliferation of undesired cells. Several genes are required to regulate cell death in the higher-order animals. Earlier, we employed a gene expression knockout technique to isolate cell death-related genes. A novel gene, the gene associated with retinoid-interferon-induced mortality-19 (GRIM-19), was found to be essential for tumor cell death induced by IFN/RA. Here, we describe the development and characterization of three monoclonal antibodies (mAbs) against GRIM-19. GRIM-19 is present in the nucleus and cytoplasm. Its expression is induced by the IFN/RA combination. We also show that GRIM-19 inhibits the cell-transforming property of viral oncogenic protein viral IFN regulatory factor-1 (vIRF-1) via a physical interaction. mAbs developed in this study should be useful for studying the other physiologic roles of GRIM-19 and serve as a potent tool for studying tumor responses to IFN/RA therapy.
UR - http://www.scopus.com/inward/record.url?scp=0036440556&partnerID=8YFLogxK
U2 - 10.1089/107999002760624242
DO - 10.1089/107999002760624242
M3 - Article
C2 - 12433281
AN - SCOPUS:0036440556
SN - 1079-9907
VL - 22
SP - 1017
EP - 1026
JO - Journal of Interferon and Cytokine Research
JF - Journal of Interferon and Cytokine Research
IS - 10
ER -