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In mouse endostatin, however, the SGR sequence is seen in place of NGR.
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To endow the targeted S. typhimurium strain for secreting endostatin, we used the plasmid pSEndo, in which a mouse Endostatin cDNA was fused with a N-terminal FLAG epitope tag and a SopA N-terminal sequence (the first 95 residues of SopA) which directs protein secretion through T3SS (Fig. 3a).
There are 15 arginine residues in mouse endostatin of which 14 are conserved in human endostatin.
Endostatin, however, modulates focal adhesion and actin stress fibre formation.
The regulatory effect of endostatin, however, is not critical since endostatin alone does not modify the basal bone resorption.
Biologically active recombinant mouse endostatin was administered twice daily (the half-life of endostatin is estimated at 12 14 hours) to Col18a1−/− mice with CCl4-induced toxic liver injury.
Endostatin, however, inhibited osteoclastogenesis when compared to this maximal stimulus (achieved with the combination of M-CSF, RANKL, and VEGF-A).
Endostatin is however susceptible to degradation by intracellular proteases and if tissue injury accompanies inflammation, endostatin may be degraded, allowing angiogenesis to occur.
Mouse, however, has vanished.
Its mouse, however, was not.
By 20 h, when the experiment was terminated, endostatin had however been degraded.
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