Jeong M Oh

20080299104, Dec 4, 2008

May 23, 2008

12/126691

Mary B. Kennedy - Pasadena CA, US
Irene Knuesel - Zurich, CH
Jeong Oh - Thousand Oaks CA, US

A61K 38/45
A61K 38/00
A61K 31/7088
A61P 25/00

424 945, 514 2, 514 44

The invention provides methods of detecting and identifying agents which moduclate the expression or activity of synGAP, a brain-specific Ras/Rap GTPase activating protein. In vivo studies using knock-out and conditional knock-out transgenic animals show that the level of apoptosis in neurons correlates inversely with the level of synGAP protein, indicating that neuronal apoptosis is enhanced by reduction of synGAP. The invention also describes that synGAP is capable of modulating signal transduction pathways associated with the NMDA receptor and triggering apoptosis, including activation of Ras-GAP. Phosphorylation of synGAP by CaMKII increases its Ras GTPase-activating activity by about 70-95%. Moreover, when these and other phosphorylation sites in the synGAP carboxyl tail are mutated, stimulation of GAP activity after phosphorylation is reduced to about 215% as compared to about 70-95% for the wild type protein. Also, phosphosite-specific antibodies used to determine levels of synGAP phosphorylation are described herein.

20100037317, Feb 11, 2010

Aug 6, 2008

12/186681

Jeong Wook Oh - Irvine CA, US

G06F 21/00

726 23

A method for detecting attacks that exploit vulnerabilities in an external module of a primary application is disclosed. The method begins with receiving from the primary application an external module method call that includes a module identifier and a module parameter. Thereafter, the external module method call is intercepted prior to the instantiation of the external module. The external module method call, which may include various data, is compared to the signature rules that are correlated to an attack attempt. If there is a match, then a resulting action part defined in the signature rule is evaluated. Otherwise, the external module is invoked.