1         The loss of mTORC2 has been shown to abrogate the activation of Akt, a critical downstream co

2 y using a selective small-molecule inhibitor abrogates the activation of c-Met, Gab1 and AKT, in resp

3  of Claspin from egg extracts only partially abrogates the activation of Chk1 in response to chromati

4 We found that an inhibitory anti-TF antibody abrogated the activation of coagulation but had no effec

5 on in a dose-dependent manner and completely abrogated the activation of downstream targets Akt and E

6    Last, blockade of TLR4 and TLR9 signaling abrogated the activation of healthy donor B cells by cir

7 of the hedgehog coreceptor Smoothened (Smo), abrogated the activation of hedgehog signaling and prote

8  or cnNfat3 that inhibited their interaction abrogated the activation of hypertrophy-associated gene

9 ralizing antibody to IFNbeta also completely abrogated the activation of interferon stimulation respo

10 in isolated endothelial cells (H-Ras siRNA), abrogated the activation of MMP-9 and prevented the redu

11 he JNK-interacting protein 3 (JIP3) and thus abrogated the activation of NADPH oxidase and oxidant ge

12                          Finally, octreotide abrogated the activation of phosphorylation of Akt, mTOR

13 -LR) presented on an Ig molecule (Ig-PLP-LR) abrogates the activation of T cells stimulated with free

14 e resulting inhibition of ATR/Chk1 signaling abrogates the activation of the G2 DNA damage checkpoint

15                       Overexpression of FHL2 abrogates the activation of the TGF-beta1 promoter, wher