Words similar to monomers
Example sentences for: monomers
How can you use “monomers” in a sentence? Here are some example sentences to help you improve your vocabulary:
The terminal residues of both monomers were also protonated (Pro 1, Pro 1', Phe 99 and Phe 99').
Even reversible aggregation of monomers in undersaturated solutions is known to affect pK
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 ] .
A 50% decrease in p53 monomers can easily be imagined to result in a greater than 50% decrease in functional tetramers, which in turn increases the chances of these cells becoming cancerous.
Loss of Hnt1 enzymatic activity also renders cells hypersensitive to mutations in the cyclin H homolog Ccl1, the MAT1 homolog Tfb3, and to Cak1, the activating kinase for Kin28, all of which lead to destabilized Kin28 complexes and a likely increase in concentration of Kin28 monomers [ 30].
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