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排序方式: 共有242条查询结果,搜索用时 15 毫秒
241.
Morison IM Cramer Bordé EM Cheesman EJ Cheong PL Holyoake AJ Fichelson S Weeks RJ Lo A Davies SM Wilbanks SM Fagerlund RD Ludgate MW da Silva Tatley FM Coker MS Bockett NA Hughes G Pippig DA Smith MP Capron C Ledgerwood EC 《Nature genetics》2008,40(4):387-389
We report the first identified mutation in the gene encoding human cytochrome c (CYCS). Glycine 41, invariant throughout eukaryotes, is substituted by serine in a family with autosomal dominant thrombocytopenia caused by dysregulated platelet formation. The mutation yields a cytochrome c variant with enhanced apoptotic activity in vitro. Notably, the family has no other phenotypic indication of abnormal apoptosis, implying that cytochrome c activity is not a critical regulator of most physiological apoptosis. 相似文献
242.
Necroptosis and ferroptosis are alternative cell death pathways that operate in acute kidney failure
Tammo Müller Christin Dewitz Jessica Schmitz Anna Sophia Schröder Jan Hinrich Bräsen Brent R. Stockwell James M. Murphy Ulrich Kunzendorf Stefan Krautwald 《Cellular and molecular life sciences : CMLS》2017,74(19):3631-3645
Ferroptosis is a recently recognized caspase-independent form of regulated cell death that is characterized by the accumulation of lethal lipid ROS produced through iron-dependent lipid peroxidation. Considering that regulation of fatty acid metabolism is responsible for the membrane-resident pool of oxidizable fatty acids that undergo lipid peroxidation in ferroptotic processes, we examined the contribution of the key fatty acid metabolism enzyme, acyl-CoA synthetase long-chain family member 4 (ACSL4), in regulating ferroptosis. By using CRISPR/Cas9 technology, we found that knockout of Acsl4 in ferroptosis-sensitive murine and human cells conferred protection from erastin- and RSL3-induced cell death. In the same cell types, deletion of mixed lineage kinase domain-like (Mlkl) blocked susceptibility to necroptosis, as expected. Surprisingly, these studies also revealed ferroptosis and necroptosis are alternative, in that resistance to one pathway sensitized cells to death via the other pathway. These data suggest a mechanism by which one regulated necrosis pathway compensates for another when either ferroptosis or necroptosis is compromised. We verified the synergistic contributions of ferroptosis and necroptosis to tissue damage during acute organ failure in vivo. Interestingly, in the course of pathophysiological acute ischemic kidney injury, ACSL4 was initially upregulated and its expression level correlated with the severity of tissue damage. Together, our findings reveal ACSL4 to be a reliable biomarker of the emerging cell death modality of ferroptosis, which may also serve as a novel therapeutic target in preventing pathological cell death processes. 相似文献