共 19 条
[1]
Bad is a BH-3 domain-contain-ing protein that forms aninactivating dimer with Bcl-xL. Kelekar A,Chang BS,Harlan JE,et al. Molecular and Cellular Biology . 1997
[2]
Akt phosphorylation of BAD couplessurvival signals to the cell-intrinsic-death machinery. Datta SR,Dudek H,Tao X,et al. Cell . 1997
[3]
Phenylephrine Promotes Phospho-rylation of Bad in Cardiac Myocytes Through the Extracellular Signal-regulated Kinases1/2 and Protein Kinase A. Valks DM,Cook SA,Pham FH,et al. Journal of Molecular and Cellular Cardiology . 2002
[4]
Activition of Bcl-2 associat-ed death protein and counter-response of Akt within cell populationduring seizure-induced neuronal death. Henshall DC,Araki T,Schindler CK,et al. The Journal of Neuroscience . 2002
[5]
Bcl-2 family members and themitochondria in apoptosis. Gross A,McDonnell JM,Korsmeyer SJ. Genes and Development . 1999
[6]
Over expression of copper/zinc su-peroxide dismutase intransgenic mice protects against neuronal celldeath after transient focal ischemia by blocking action of the Bad celldeath signaling pathway. Saito A,Hayashi T,Okuno S,et al. The Journal of Neuroscience . 2003
[7]
BAD Ser-155 phosphorylation reg-ulates BAD/Bcl-xL interaction and cell survival. Tan Y,Demeter MR,Ruan J,et al. Journal of Biological Chemistry . 2000
[8]
Leukemia[P]. 英国专利:GB0221802D0,2002-10-30
[9]
Seizure-like activity leads tothe release of BAD from 14-3-3 protein and cell death in hippocampalneurons in vitro. Meller R,Schindler CK,Chu XP,et al. Cell Death and Differentiation . 2003
[10]
Differential neuro-protection by cyclosporin A and FK 506 following ischemia correspondswith different abilities to inhibit calcineurin and the mitochondrial per-meability transition. Uchino H,Minamikawa-Tachino R,Kristian T,et al. Neurobiology of Disease . 2002