Disease relevance of UCS15A

• One of the biological consequences of src-inhibition by UCS15A was its ability to inhibit the bone resorption activity of osteoclasts in vitro [1].
• Our previous studies showed that UCS15A, produced by Streptomyces species, inhibited PLPI [2].

High impact information on UCS15A

• In the present study we have examined the ability of UCS15A to disrupt the interaction of Src-SH3 with Sam68, both in vivo and in vitro [3].
• However, UCS15A was unable to disrupt the non-SH3-mediated protein-protein interactions of beta-catenin, with E-cadherin and alpha-catenin [3].
• Previous studies have identified an unconventional, small-molecule, Src signal transduction inhibitor, UCS15A [3].
• In vitro analyses suggested that UCS15A did not bind to the SH3 domain itself but rather may interact directly with the target proline-rich domains [3].
• UCS15A, a non-kinase inhibitor of Src signal transduction [1].

Chemical compound and disease context of UCS15A

• These data suggest that UCS15A may inhibit the bone resorption activity of osteoclasts, not by inhibiting src tyrosine kinase activity, but by disrupting the interaction of proteins associated with src, thereby modulating downstream events in the src signal transduction pathway [1].

Biological context of UCS15A

• UCS15A was found to inhibit the src specific tyrosine phosphorylation of numerous proteins in v-src-transformed cells [1].

References