Words similar to arp
Example sentences for: arp
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Antibodies used: rabbit Arp3 antibodies (gift from C. Egile using the same peptide as described [ 33 ] ) used at 1:500 dilution, mouse actin antibodies (Santa Cruz SC-8432) used at 1:10,000 dilution, rabbit VASP antibodies (gift from F. Southwick) used at 1:100, rabbit WAVE1 antibodies (gift from S. Eden as described [ 26 ] ) used at 1:100 and Alexa-dye labeled secondary antibodies, goat anti-rabbit and goat anti-mouse (Molecular Probes).
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 ] .
We found that 20 mM BDM does not affect movement of bacteria inside treated cells [Figure 3A] consistent with a previous report [ 4 ] . Interestingly, localization of Arp3 in Listeria comet tails is unaffected with BDM treatment [Figure 3B] though Arp3 localization at the leading edge of these cells is disrupted.
For Arp3 immunofluorescence, cells were post-fixed in methanol (-20°C) for 2 minutes.
No effect was seen on the polymerization of actin alone or as stimulated by VCA-activated Arp2/3 complex, using a pyrene-actin polymerization assay (data not shown).
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