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1 , and the phosphorylation and degradation of IkappaBalpha protein.
2 lated with decreased levels of the inhibitor IkappaBalpha protein.
3 ppaB) kinase activity and the degradation of IkappaBalpha protein.
4 its function by modulating the stability of IkappaBalpha protein.
5 hat of the degradation of the phosphorylated IkappaBalpha protein.
6 e and the phosphorylation and degradation of IkappaBalpha protein.
7 ress moderate levels of endogenous bcl-2 and IkappaBalpha proteins.
9 te that the IkappaBepsilon protein, like the IkappaBalpha protein, actively shuttles between the nucl
10 irement for the fast degradation of the free IkappaBalpha protein; alteration of free IkappaBalpha de
11 PI3K-Akt activation mediated degradation of IkappaBalpha protein and impaired NF-kappaB self-negativ
12 hat CD437 activates NF-kappaB via decreasing IkappaBalpha protein and thereby induces DR4 expression
13 SV infection, there was no reaccumulation of IkappaBalpha protein, as infected cells produced only a
17 ation which results in a diminished level of IkappaBalpha protein, despite an upregulated IkappaBalph
18 41 which blocks intracellular degradation of IkappaBalpha proteins, downregulates the expression of b
21 e-specific and total NFKBIA mRNA expression, IkappaBalpha protein expression, and TLR responsiveness;
22 of NFKBIA influenced NFKBIA gene expression, IkappaBalpha protein expression, and TLR-mediated inflam
24 kappaBalpha phosphorylation that targets the IkappaBalpha protein for degradation and inhibited NF-ka
25 g cardiac-restricted expression of a mutated IkappaBalpha protein (IkappaBalphaDeltaN) that prevents
26 stabilized form of the NF-kappaB-inhibiting IkappaBalpha protein (IkappaBalphaSR) in breast tumor ce
28 B subunits, we expressed a dominant-negative IkappaBalpha protein in p50(-/-)RelA(-/-) MEFs to inhibi
31 duces stable nuclear localization of p65 and IkappaBalpha proteins in the absence of additional pro-i
32 elevated levels of lung IkappaBbeta (but not IkappaBalpha) protein in the absence of elevated mRNA fo
34 verexpression of a mutant, dominant negative IkappaBalpha protein led to the suppression of SSAT indu
36 achieved this effect through maintenance of IkappaBalpha protein levels in the face of phorbol ester
38 y), increased JNK activity, and up-regulated IkappaBalpha protein levels, a potent stimulator of apop
39 urned toward baseline, whereas that of total IkappaBalpha protein remained lower than the correspondi
40 V-1 stimulated the degradation of regulatory IkappaBalpha protein, resulting in nuclear translocation
42 cocorticoids, we did not detect induction of IkappaBalpha protein that could prevent nuclear transloc
43 study of IkappaBalpha degradation, we fused IkappaBalpha protein to enhanced green fluorescent prote
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