Home
|
Learning Center
|
中文版
Publications
站内成果搜索:
搜索
八五九灌区水生态环境分析与评价
八五八农场水稻钾肥施肥分区的研究
八五五农场打造水产养殖的可行性分析
八五五农场的场县共建模式初探
八五新潮文化选择对写意花鸟画的影响
把物理实验融入初中物理课堂
把物理思想注入于数学之中——以黏性流体力学的Navier-Stokes方程的求解为例,谈剑桥大学G.K.Batchelor教授的一个学术思想
八五二农场和平村水库坝址洪水分析
Bawu Decoction Ameliorates Benign Prostatic Hyperplasia in Rats
八五三农场清河灌区渠道防渗方案比较
把五大发展理念贯穿于文化发展改革全过程
八五思潮影响下的广州当代艺术
八五○农场水稻品种筛选试验
Bax expression remains unchanged following antisense treatment directed against BCL-2
Bax Is Essential for Drp1-Mediated Mitochondrial Fission But Not for Mitochondrial Outer Membrane Permeabilization Caused by Photodynamic Therapy
Bax inhibitor-1 is a pH-dependent regulator of Ca(2+) channel activity in the endoplasmic reticulum
Bax inhibitor-1 mediates apoptosis-resistance in human nasopharyngeal carcinoma cells
Bax activation by Bim?
Bax inhibitor-1 regulates endoplasmic reticulum stress-associated reactive oxygen species and heme oxygenase-1 expression
Bax mRNA therapy using cationic liposomes for human malignant melanoma
Bax siRNA promotes survival of cultured and allografted granule cell precursors through blockade of caspase-3 cleavage
Bax dimerizes via a symmetric BH3:groove interface during apoptosis
Bax Crystal Structures Reveal How BH3 Domains Activate Bax and Nucleate Its Oligomerization to Induce Apoptosis
Bax and Bak have critical roles in ischemic acute kidney injury in global and proximal tubule-specific knockout mouse models
Bax Inhibitor-1-Mediated Inhibition of Mitochondrial Ca2+ Intake Regulates Mitochondrial Permeability Transition Pore Opening and Cell Death
Bax deficiency prolongs cerebellar neurogenesis, accelerates medulloblastoma formation and paradoxically increases both malignancy and differentiation
Bax Exists in a Dynamic Equilibrium between the Cytosol and Mitochondria to Control Apoptotic Priming
Bax and Bak function as the outer membrane component of the mitochondrial permeability pore in regulating necrotic cell death in mice
Bax phosphorylation association with nucleus and oligomerization after neonatal Hypoxia-ischemia
Bax Interacting Factor-1 Promotes Survival and Mitochondrial Elongation in Neurons
Bax protein may influence the invasion of colorectal cancer
Bax Delta 2 Promotes Apoptosis through Caspase-8 Activation in Microsatellite-Unstable Colon Cancer
Bax Inhibitor-1 Is Likely a pH-Sensitive Calcium Leak Channel, Not a H+/Ca2+ Exchanger
Bax Inhibitor-1-mediated Ca2+ leak is decreased by cytosolic acidosis
Bax induces cytochrome c release by multiple mechanisms in mitochondria from MCF7 cells
Bax Contains Two Functional Mitochondrial Targeting Sequences and Translocates to Mitochondria in a Conformational Change- and Homo-oligomerization-driven Process
bax mRNA和蛋白产物与常见舌苔舌上皮细胞凋亡关系的研究
Bax assembly into rings and arcs in apoptotic mitochondria is linked to membrane pores
Bax deficiency extends the survival of Ku70 knockout mice that develop lung and heart diseases
Bax and Bif-1 proteins interact on Bilayer Lipid Membrane and form pore
Bax Inhibitor 1 Increases Cell Adhesion through Actin Polymerization: Involvement of Calcium and Actin Binding
Bax Forms an Oligomer via Separate, Yet Interdependent, Surfaces
Bax is upregulated by p53 signal pathway in the SPE B-induced apoptosis
Bax Inhibitor-1 regulates hepatic lipid accumulation via ApoB secretion
Bax Expression in Untreated Breast Cancer: An Immunocytometric Study of 255 Cases
Bax is necessary for PGC1 alpha pro-apoptotic effect in colorectal cancer cells
Bax distribution into mitochondrial detergent-resistant microdomains is related to ceramide and cholesterol content in postischemic hearts
Bax Inhibitor-1, a Conserved Cell Death Suppressor, Is a Key Molecular Switch Downstream from a Variety of Biotic and Abiotic Stress Signals in Plants
Bax Predicts Outcome in Gastric Cancer Patients Treated with 5-fluorouracil, Leucovorin, and Oxaliplatin Palliative Chemotherapy
Bax and the mitochondrial permeability transition cooperate in the release of cytochrome c during endoplasmic reticulum-stress-induced apoptosis
Bax deficiency in mice increases cartilage production during fracture repair through a mechanism involving increased chondrocyte proliferation without changes in apoptosis