Words similar to abundant
Example sentences for: abundant
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The first evidence that chemokines are associated with wound healing in vivo was reported in 1990 using the chemokine cCAF (chicken Chemotactic and Angiogenic Factor; the product of the 9E3 gene), a CXC chemokine that is now known to be the ortologue for human IL-8 [ 9 ] . cCAF is expressed to high levels very shortly after wounding and during the first 24-48 hours after injury, and remains elevated for at least 16 days after wounding [ 6 10 ] . It is primarily expressed by the fibroblasts of the granulation tissue, especially where interstitial collagen (Coll) is abundant, but the levels are also high in the endothelial cells of the microvessels, in the healing epidermis and in the connective tissue beneath the skin [ 6 11 ] . In the chicken chorioallantoic membrane (CAM) assay, low concentration of cCAF results in chemotaxis of monocyte/macrophages and lymphocytes and the formation of a granulation-like tissue beneath the chemokine-containing pellet [ 3 ] . After four days of exposure to this chemokine, the ectoderm of the CAMs becomes thickened and the amount of fibrillar collagen in the tissue is markedly increased, strongly suggesting that cCAF is able to initiate some of the primary events that lead to granulation tissue formation [ 3 ] .
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 ] .
Alpha-Crystallin is comprised of two polypeptides, alphaA-crystallin (alphaA) and alphaB-crystallin (alphaB), which share 55% amino acid sequence homology [ 1 ] . They are the most abundant proteins in lens fiber cells [ 2 3 ] and exist as heteroaggregates of approximately 800 kDa that can undergo inter-aggregate subunit exchange [ 4 ] . The expression of these two proteins in the lens epithelium, however, is not uniform throughout different regions of the anterior epithelium.
However, scrutiny of the putative alignments indicated that most or all were based upon fortuitous fitting of the abundant acidic residues.
Exposure for six days showed expression in heart, no expression in the brain and abundant expression in placenta as shown in Figure 1. We observed a single transcript of approximately 7.2 Kb thus, the published sequence of the cDNA for the DLG5 gene was incomplete.
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