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1 wth/survival factor for RA synoviocytes to a death factor.
2 elease of cytochrome c, a pro-apoptotic cell death factor.
3 Caspase-2 or Bax, up to 79% coexpressed both death factors.
4  until it is killed by an unknown cascade of death factors.
5 ting that dying cells can release long-range death factors.
6 hway would protect tissues by reducing a pro-death factor (2',3'-cAMP) while increasing a retaliatory
7 death factor in the Bcl-2 family of survival/death factors, and were also negative for p53, a tumor-s
8                        Furthermore, the axon-death factor Axed is only partially required for self-de
9 ectively immunopositive for the bcl-2 family death factor, Bax, and for the protease Caspase-2 (Nedd2
10                                          The death factor Fas/Apo-1 and its ligand (FasL) play pivota
11 itochondrial dysfunction and release of cell death factors from mitochondria, and protected against A
12 dings suggest that BAD is more than an inert death factor in healthy cells; it is also a pro-survival
13 f the MIS cascade to function as a paracrine death factor in Mullerian duct regression.
14 cells of the tongue were negative for Bax, a death factor in the Bcl-2 family of survival/death facto
15 cal expression of mitochondrial dynamics and death factors in cardiomyocytes wherein mitochondrial mo
16 onversion of BAD from an anti-death to a pro-death factor, including alternative splicing that produc
17                                Extracellular death factor is a quorum-sensing pentapeptide that relay
18 apoptotic member of the Bcl-2 family of cell death factors, is strongly induced in response to hypoxi
19 ease from IkappaBalpha led to an increase in death factor processing during HSV-1(F) infection.
20                                      (ii) No death factor processing or apoptotic morphological chang
21 criptional inhibitor actinomycin D prevented death factor processing upon infection with the apoptoti
22            (i) No viral protein synthesis or death factor processing was detected after infection wit
23                        (v) Finally, complete death factor processing was observed upon infection with
24              (iv) Apoptotic morphologies and death factor processing were not observed following infe
25 chromatin, and patterns of specific cellular death factor processing.
26 ring apoptosis to promote the release of pro-death factors sequestered in the mitochondrial intermemb
27 f viral Bcl-2 proteins can be converted into death factors, similar to their cellular counterparts, f
28 poptosis triggered by the overproduction of "death factors" such as TNF-alpha or Fas ligand (FasL) ma
29 as potentially contributory factors to their deaths--factors that can largely be ameliorated.
30 stimulation via PKCdelta-mediated release of death factors, the involvement of PKCepsilon in this res
31 n using immunocytochemistry to seek putative death factors, we observed that squamous epithelial cell