Words similar to capping
Example sentences for: capping
How can you use “capping” in a sentence? Here are some example sentences to help you improve your vocabulary:
Although a coordinated climate and air quality policy appeared to lower costs compared to a series of separate policy initiatives, the EIA assessment indicated significant costs associated with capping emissions.
The triphosphatase (Cet1), guanylyltransferase (Ceg1), and methyltransferase (Abd1) components of the capping apparatus are essential for cell growth in the budding yeast S. cerevisiae [ 1 4 5 6 ] . Mutations of the RNA triphosphatase Cet1 that abrogate catalytic activity in vitro are lethal in vivo [ 7 8 9 ] ; thus, it is reasonable to think that pharmacological inhibition of Cet1 function in vivo would impede cell growth.
is expressed in skeletal muscle, with a less abundant ~7 kb transcript expressed in both skeletal and cardiac muscle [ 8 ] . Whereas tropomodulins or the Arp 2/3 complex cap the pointed end of actin filaments, the barbed end can be capped by CapZ, α, β, and γ adducins as well as gelsolin [ 9 10 11 ] . Control of thin filament length is critical for maintaining proper sarcomere function and length [ 12 ] . Inhibition of Tmod1's capping activity - either by using an antibody to its C-terminal end or by decreasing expression using an antisense Tmod1 transcript - results in elongated thin filaments and decreased cardiac contractility [ 13 14 ] . Tmod1 overexpression in rat cardiomyocytes causes shortening of the thin filaments and sarcomere disorganization, resulting in myofibril degeneration [ 14 ] . Likewise, mice overexpressing TMOD1 in the heart show disrupted sarcomere organization with shortened thin filaments, leading to myofibril degeneration and dilated cardiomyopathy [ 15 ] . Recently, Littlefield and colleagues showed that overexpression of GFP-Tmod1 in chick cardiac myocytes results in shortening of thin filaments; the authors proposed that excess Tmod1 decreases the affinity between actin monomers and pointed ends, leading to monomer dissociation and filament shortening [ 42 ] . Mutations in many proteins making up the cardiac sarcomere have been shown to cause cardiac hypertrophy [ 16 17 18 19 ] :mutations in the TPM1 gene, for example, cause type 3 familial hypertrophic cardiomyopathy (CMH3), and a transgenic mouse expressing a CMH3 mutation develops ventricular myocyte disarray and hypertrophy [ 20 ] . Mutations in myosin heavy chain 7 are estimated to account for 40-50% of the cases of hypertrophic cardiomyopathy [ 21 ] .
RNA triphosphatase is an attractive therapeutic target for fungal infections because: (i) the active site structure and catalytic mechanism of fungal RNA triphosphatase are completely different from the RNA triphosphatase domain of the metazoan capping enzyme and (ii) metazoans encode no identifiable homologs of the fungal RNA triphosphatases.
In this case all the components function with full efficiency: first, a complex of telomerase and binder/cutter bind to the binding site, then cutting of the cut-site ensues with immediate, coupled telomerase capping of the MAC-destined end, with no interposed erosion.
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