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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.
8                For example, the well studied IkappaBalpha protein actively shuttles between the nucle
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
14                                              IkappaBalpha protein, but not RNA, expression was reduce
15 -1 cells did not prevent the augmentation of IkappaBalpha protein by Dex.
16                      By Western blotting, no IkappaBalpha protein can be detected in extracts of RC-K
17 ive effect was mediated by the inhibition of IkappaBalpha protein degradation.
18 ation which results in a diminished level of IkappaBalpha protein, despite an upregulated IkappaBalph
19 41 which blocks intracellular degradation of IkappaBalpha proteins, downregulates the expression of b
20      Dexamethasone (Dex), which up-regulates IkappaBalpha protein, enhances blockade of NF-kappaB act
21  to have any effect on the relative level of IkappaBalpha protein expression over 24 h.
22 e-specific and total NFKBIA mRNA expression, IkappaBalpha protein expression, and TLR responsiveness;
23 of NFKBIA influenced NFKBIA gene expression, IkappaBalpha protein expression, and TLR-mediated inflam
24                      BMP9/10 increased basal IkappaBalpha protein expression, but did not alter p65/R
25 kappaBalpha phosphorylation that targets the IkappaBalpha protein for degradation and inhibited NF-ka
26 g cardiac-restricted expression of a mutated IkappaBalpha protein (IkappaBalphaDeltaN) that prevents
27  stabilized form of the NF-kappaB-inhibiting IkappaBalpha protein (IkappaBalphaSR) in breast tumor ce
28 ntributes to the constitutive degradation of IkappaBalpha protein in 3T3-L1 fibroblasts.
29 B subunits, we expressed a dominant-negative IkappaBalpha protein in p50(-/-)RelA(-/-) MEFs to inhibi
30                               The absence of IkappaBalpha protein in RC-K8 cells appears to be due to
31 ha-MSH-induced preservation of expression of IkappaBalpha protein in the brain.
32 duces stable nuclear localization of p65 and IkappaBalpha proteins in the absence of additional pro-i
33 elevated levels of lung IkappaBbeta (but not IkappaBalpha) protein in the absence of elevated mRNA fo
34              The inhibitor of kappa B alpha (IkappaBalpha) protein is able to shuttle between the cyt
35 verexpression of a mutant, dominant negative IkappaBalpha protein led to the suppression of SSAT indu
36                 CD437 was unable to decrease IkappaBalpha protein levels and up-regulate DR4 expressi
37  achieved this effect through maintenance of IkappaBalpha protein levels in the face of phorbol ester
38                                No changes in IkappaBalpha protein levels were detected.
39 y), increased JNK activity, and up-regulated IkappaBalpha protein levels, a potent stimulator of apop
40 urned toward baseline, whereas that of total IkappaBalpha protein remained lower than the correspondi
41 V-1 stimulated the degradation of regulatory IkappaBalpha protein, resulting in nuclear translocation
42 ne 305 is associated with an increase of the IkappaBalpha protein stability.
43 e kinetic analysis of the phosphorylation of IkappaBalpha protein substrates catalyzed by constitutiv
44 cocorticoids, we did not detect induction of IkappaBalpha protein that could prevent nuclear transloc
45  study of IkappaBalpha degradation, we fused IkappaBalpha protein to enhanced green fluorescent prote
46                       The use of a truncated IkappaBalpha protein to prevent NF-kappaB-mediated gene
47 ree IkappaBalpha and NFkappaB/Rel-associated IkappaBalpha proteins to CRM1.