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Example sentences for: capping
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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 ] .
Although the plasmid-encoded capping enzyme genes are under the control of a regulated nmt1* promoter, which can be repressed by inclusion of 5 μg/ml thiamine in the growth medium [ 19 ] , we observed that the growth of the plasmid-dependent strains was not affected by exogenous thiamine.
Although the three capping reactions are universal in eukaryotes, there is a surprising diversity in the genetic organization of the capping enzymes as well as a complete divergence in the structure and catalytic mechanism of the RNA triphosphatase component in "lower" versus "higher" eukaryotic species [ 1 ] . Metazoans and plants have a two-component capping system consisting of a bifunctional triphosphatase-guanylyltransferase polypeptide and a separate methyltransferase polypeptide, whereas fungi contain a three-component system consisting of separate triphosphatase, guanylyltransferase, and methyltransferase gene products.
[ 25 ] had previously generated a single allele knockout in C. albicans of the guanylyltransferase component of the capping apparatus (Cgt1) using the URA-blaster technique and noted a variety of pleiotrophic effects on stress response, hygromycin sensitivity, and colony morphology in the CGT1/cgt1Δ heterozygote, but they found that the heterozygote was just as virulent as the wild-type strain in animal models of systemic candidiasis.
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