The antiapoptotic protein Api5 and its partner, high molecular weight FGF2, are up‐regulated in B cell chronic lymphoid leukemia
暂无分享,去创建一个
W. Wilcox | H. Laurell | B. Rosenbloom | P. Krejcí | K. Pejchalová | F. Rosenfelt | Elizabeth L. Tran | Kateřina Pejchalová
[1] A. Galloway,et al. Basic fibroblast growth factor (FGF‐2): The high molecular weight forms come of age , 2007, Journal of cellular biochemistry.
[2] Jun-Yuan Ji,et al. Functional Identification of Api5 as a Suppressor of E2F-Dependent Apoptosis In Vivo , 2006, PLoS genetics.
[3] A. Hampl,et al. FGF-2 abnormalities in B cell chronic lymphocytic and chronic myeloid leukemias , 2001, Leukemia.
[4] H Laurell,et al. FIF [fibroblast growth factor-2 (FGF-2)-interacting-factor], a nuclear putatively antiapoptotic factor, interacts specifically with FGF-2. , 2000, Molecular endocrinology.
[5] J. Kim,et al. AAC-11 Overexpression Induces Invasion and Protects Cervical Cancer Cells from Apoptosis , 2000, Laboratory Investigation.
[6] B. Ross,et al. AAC-11, a novel cDNA that inhibits apoptosis after growth factor withdrawal. , 1997, Cancer research.
[7] E. Calleja,et al. Elevated intracellular level of basic fibroblast growth factor correlates with stage of chronic lymphocytic leukemia and is associated with resistance to fludarabine. , 1996, Blood.
[8] H. Prats,et al. Alternative initiation of translation determines cytoplasmic or nuclear localization of basic fibroblast growth factor , 1991, Molecular and cellular biology.