Words similar to kinase-
Example sentences for: kinase-
How can you use “kinase-” in a sentence? Here are some example sentences to help you improve your vocabulary:
These include p150 RhoA-binding kinase α and β (p150 ROKα and β) [ 40 41 ] , p160 Rho-associated coiled-coil containing protein kinase (Rho-p160ROCK) [ 42 ] , p164 Rho kinase [ 43 ] , p120 protein kinase N (p120 PKN) [ 44 45 ] , and PKC-related kinase-2 (PRK-2) [ 46 ] . These kinases specifically bind to the GTP bound form of Rho, except for PRK-2, which can bind both Rho and Rac GTPases.
Among the most highly induced were the genes encoding NFκB1, RelB, IκB-alpha (the inhibitor of NFκB1), IκKε (IκB kinase-epsilon), and NFκB-inducing kinase or Map-3-kinase-14 (NIK, MAP3K14).
A Xho1/HindIII (blunt) cassette containing the Tn5 neomycin phosphotransferase ( Neo )gene, that could confer resistance to G418 and whose expression in mammalian cells was directed by a phosphoglycerate kinase-1 ( pgk) promoter, was introduced into an XbaI (blunt) site between the Hnf3α genomic sequences [ 16, 25].
In comparison to the two general alternative mechanisms utilized by known transforming viruses to promote cell-cycle progression, namely, by activating or bypassing endogenous D-type cyclins (herein, referred to as "cyclin D"), it has not been established whether HIV-1 gene products trigger either cyclin D-dependent or cyclin D-independent proliferation in non-lymphoid tissues [ 15 ] . In infected renal epithelium, HIV-1 could disrupt the inhibitory binding of pRb to E2F independent of endogenous cyclin D, analogous to transforming viral mechanisms that bypass and down-regulate endogenous cyclin D, such as SV-40 T antigen binding to pRb [ 16 ] , HHV-8 v -cyclin binding to and activating cyclin-dependent kinase-6 (CDK) [ 17 ] , and activation of cyclin E by EBV-induced c -myc [ 18 ] . Alternatively, HIV-1 could activate cyclin D-dependent proliferation, as exemplified by RSV v -src-mediated signaling [ 19 ] . In most tissues, the selective activation of these cell-cycle pathways is readily discernable.
LiCl has previously been shown to mimic activation of Wnt-1 signaling by stabilizing beta-catenin through its inhibition of glycogen synthase kinase-3β (GSK-3β), a kinase that phosphorylates beta-catenin and promotes its degradation via the ubiquitin proteasome pathway [ 39 ] . C57mg cells treated with LiCl exhibited elevated levels of mesothelin but not SL-1 (Figure 2, left panel).
Loading...