Example sentences for: overexpressing

How can you use “overexpressing” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • , 1998), it has been proposed that there is a need for caution in interpreting p53 function on the basis of cells transiently overexpressing this protein.

  • c- myc was upregulated in K562 cells overexpressing BP1, and c-Myc protein is highly expressed in more than half of breast cancer patients [ 36 ] . Cyclin D2, downregulated on the array, is repressed in breast cancer [ 37 ] . It will be important to determine whether either of those genes is a target for BP1 in breast cancer.

  • The increase in the Her2/neu overexpressing cells is more than 40-fold.

  • In this respect we note that we have not been able to recover F9 cell lines significantly overexpressing TBP suggesting that TBP overexpression is toxic.

  • 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 ] .

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