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1 l molecule c-FLIP (cellular homolog of viral FLICE inhibitory protein).
2 ellular inhibitor of apoptosis protein-2 and FLICE inhibitory protein.
3 were attenuated by the forced expression of FLICE-inhibitory protein.
4 , inhibitor of apoptosis proteins, and viral FLICE-inhibitory proteins.
5 lly downregulates expression of the cellular FLICE inhibitory protein, a negative regulator of death
6 002 decreases expression of c-FLIP (cellular FLICE inhibitory protein), an inhibitor of caspase-8 act
8 rotein that is homologous to cellular FLIPs (FLICE-inhibitory proteins) and is proposed to inhibit Fa
9 riety of anti-apoptotic molecules, including FLICE inhibitory protein, Bcl-2, and Mcl-1, which protec
10 ntly attenuated, but the expression level of FLICE inhibitory protein c-FLIP(L), which had been shown
12 The Fas apoptosis inhibitor molecule and FLICE inhibitory protein (c-FLIP) proteins are up-regula
13 d T cells led to down-regulation of cellular FLICE inhibitory protein (c-FLIP), an inhibitor of apopt
14 Fas-ligand interleukin-1-converting enzyme (FLICE)-inhibitory protein (c-FLIP), an endogenous antago
16 receptor, and reduces the levels of cellular FLICE-inhibitory protein (c-FLIP) (both the long and sho
17 ib down-regulated the expression of cellular FLICE-inhibitory protein (c-FLIP), a major negative regu
18 oxib action based on degradation of cellular FLICE-inhibitory protein (c-FLIP), a major regulator of
23 companied by the down-regulation of cellular FLICE-inhibitory protein (c-FLIP, I-FLICE) without evide
24 aminin, but not collagen, expressed cellular FLICE inhibitory protein (cFLIP) and TNFalpha stimulatio
25 ated death domain (FADD) protein or cellular FLICE inhibitory protein (cFLIP), other proteins associa
28 ible or permanent) with deletion of cellular FLICE-inhibitory protein (cFlip) or caspase-8 in the int
29 coy receptors and the antiapoptotic cellular FLICE-inhibitory protein (cFLIP) was inconsistent across
30 ell leukemia-1 (Mcl-1) and caspase 8 homolog FLICE-inhibitory protein (cFLIP), and induced G2M cell-c
31 ll death and caspase activation by promoting FLICE-inhibitory protein degradation and mitochondrial r
33 short isoform of the caspase-8 inhibitor, c-FLICE inhibitory protein (FLIP(S)), and that FLIP(S) exp
34 ersely related to the intracellular level of FLICE inhibitory protein (FLIP) but not that of death re
35 P, an inhibitor of apoptosis, and disrupting FLICE inhibitory protein (FLIP) expression through the A
36 n of NO and concomitant decrease in cellular FLICE inhibitory protein (FLIP) expression without signi
37 ine, was associated with increased levels of FLICE inhibitory protein (FLIP), and was overcome by cyc
38 ncoding the inhibitor of caspase activation, FLICE inhibitory protein (FLIP), appears to be a direct
39 cies (ROS) generation and down-regulation of FLICE inhibitory protein (FLIP); however, the relationsh
40 D)-like interleukin-1beta-converting enzyme (FLICE) inhibitory protein (FLIP), leading to apoptosis.
41 rleukin 1 beta (IL-1beta)-converting enzyme (FLICE)-inhibitory protein (FLIP) has been reported to in
42 ysis showed higher transcript levels for the FLICE-inhibitory protein (FLIP(L)) in resistant cells an
43 ates the degradation of the long form of the FLICE-inhibitory protein (FLIP(L)), an inhibitor of deat
45 Levels of DcR1 and DcR2 or levels of the FLICE-inhibitory protein (FLIP) did not correlate with T
49 ndent and correlated with down-regulation of FLICE-inhibitory protein (FLIP), an intracellular caspas
50 for various apoptosis inhibitors, including FLICE-inhibitory protein (FLIP), and lower procaspase-8
51 decoy recepter 2) or antiapoptotic proteins (FLICE-inhibitory protein (FLIP), inhibitor of apoptosis
54 ibited expression of the caspase-8 inhibitor FLICE-inhibitory protein (FLIP), which functions downstr
55 ity correlated with a progressive decline in Flice-inhibitory protein (FLIP), which was induced withi
58 apoptotic effectors such as Bcl-2, p53, and FLICE inhibitory protein in cancer cell anoikis is also
59 sociated herpesvirus (KSHV) K13/vFLIP (viral Flice-inhibitory protein) induces transcription of numer
61 -associated herpesvirus (KSHV)-encoded viral FLICE inhibitory protein K13 interacts with a cytosolic
64 own that the antiapoptotic molecule cellular-FLICE-inhibitory protein long isoform [c-FLIP(L)] is nec
65 wn to encode proteins with DEDs (also called FLICE inhibitory proteins or vFLIPs) which have the abil
68 (KSHV) genomes encode a homolog of cellular FLICE-inhibitory proteins (termed v-FLIP) that activates
69 ption is regulated by the KSHV-encoded viral FLICE inhibitory protein (vFLIP) and by viral IFN regula
70 -associated herpesvirus (KSHV)-encoded viral FLICE inhibitory protein (vFLIP) enhances IRF4-mediated
72 characterized the role of KSHV-encoded viral FLICE inhibitory protein (vFLIP) K13 in the modulation o
73 -associated herpesvirus (KSHV)-encoded viral FLICE inhibitory protein (vFLIP) K13 is a potent activat
74 sarcoma-associated herpesvirus-encoded viral FLICE inhibitory protein (vFLIP) K13 was originally beli
75 he human herpes virus 8 (HHV8)-encoded viral FLICE inhibitory protein (vFLIP), also known as K13, is
76 Human herpesvirus 8 (HHV-8) encodes a viral FLICE inhibitory protein (vFLIP), called K13, with homol
77 e interferon converting enzyme or caspase 8 (FLICE) inhibitory protein (vFLIP) that prevents death re
78 Here, we have revealed the role of viral FLICE-inhibitory protein (vFLIP) in the initiation of PE
81 levels of cellular inhibitors of apoptosis (FLICE inhibitory protein, X chromosome-linked inhibitor
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