PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15173009-1 2004 The activation of protein kinase G (PKG) by cGMP has become of considerable interest as a novel molecular mechanism for the induction of apoptosis in cancer cells, because sulindac sulfone (exisulind, Aptosyn) and certain derivatives that inhibit cGMP-phosphodiesterases and thereby increase cellular levels of cGMP appear to induce apoptosis via this mechanism. sulindac sulfone 172-188 protein kinase cGMP-dependent 1 Homo sapiens 18-34 16166323-3 2005 There is extensive evidence that treatment of SW480 human colon cancer cells with sulindac sulfone (Exisulind, Aptosyn) or the related derivative OSI-461, both of which inhibit cyclic GMP (cGMP)-phosphodiesterases but lack COX-2 inhibitory activity, causes an increase in intracellular levels of cGMP, thus activating protein kinase G (PKG), which then activates pathways that lead to apoptosis. sulindac sulfone 82-98 protein kinase cGMP-dependent 1 Homo sapiens 318-334 16166323-3 2005 There is extensive evidence that treatment of SW480 human colon cancer cells with sulindac sulfone (Exisulind, Aptosyn) or the related derivative OSI-461, both of which inhibit cyclic GMP (cGMP)-phosphodiesterases but lack COX-2 inhibitory activity, causes an increase in intracellular levels of cGMP, thus activating protein kinase G (PKG), which then activates pathways that lead to apoptosis. sulindac sulfone 82-98 protein kinase cGMP-dependent 1 Homo sapiens 336-339 16166323-3 2005 There is extensive evidence that treatment of SW480 human colon cancer cells with sulindac sulfone (Exisulind, Aptosyn) or the related derivative OSI-461, both of which inhibit cyclic GMP (cGMP)-phosphodiesterases but lack COX-2 inhibitory activity, causes an increase in intracellular levels of cGMP, thus activating protein kinase G (PKG), which then activates pathways that lead to apoptosis. sulindac sulfone 111-118 protein kinase cGMP-dependent 1 Homo sapiens 318-334 16166323-3 2005 There is extensive evidence that treatment of SW480 human colon cancer cells with sulindac sulfone (Exisulind, Aptosyn) or the related derivative OSI-461, both of which inhibit cyclic GMP (cGMP)-phosphodiesterases but lack COX-2 inhibitory activity, causes an increase in intracellular levels of cGMP, thus activating protein kinase G (PKG), which then activates pathways that lead to apoptosis. sulindac sulfone 111-118 protein kinase cGMP-dependent 1 Homo sapiens 336-339 15173009-1 2004 The activation of protein kinase G (PKG) by cGMP has become of considerable interest as a novel molecular mechanism for the induction of apoptosis in cancer cells, because sulindac sulfone (exisulind, Aptosyn) and certain derivatives that inhibit cGMP-phosphodiesterases and thereby increase cellular levels of cGMP appear to induce apoptosis via this mechanism. sulindac sulfone 172-188 protein kinase cGMP-dependent 1 Homo sapiens 36-39 12492113-5 2002 CP248-induced VASP phosphorylation was inhibited by a specific PKG inhibitor but not by a protein kinase A inhibitor. sulindac sulfone 0-5 protein kinase cGMP-dependent 1 Homo sapiens 63-66 11051267-4 2000 Other compounds that increase cellular levels of cGMP also activated JNK1, and an inhibitor of protein kinase G (PKG), Rp-8-pCPT-cGMPS, inhibited JNK1 activation by the sulindac sulfone derivatives. sulindac sulfone 169-185 protein kinase cGMP-dependent 1 Homo sapiens 95-111 11051267-4 2000 Other compounds that increase cellular levels of cGMP also activated JNK1, and an inhibitor of protein kinase G (PKG), Rp-8-pCPT-cGMPS, inhibited JNK1 activation by the sulindac sulfone derivatives. sulindac sulfone 169-185 protein kinase cGMP-dependent 1 Homo sapiens 113-116 11051267-6 2000 Thus, it appears that sulindac sulfone and related compounds induce apoptosis, at least in part, through activation of PKG, which then activates the MEKK1-SEK1-JNK1 cascade. sulindac sulfone 22-38 protein kinase cGMP-dependent 1 Homo sapiens 119-122 11278263-1 2001 We recently obtained evidence that treatment of human colon cancer cells with exisulind (sulindac sulfone) and related compounds induces apoptosis by activation of protein kinase G (PKG) and c-Jun kinase (JNK1). sulindac sulfone 89-105 protein kinase cGMP-dependent 1 Homo sapiens 164-180 11278263-1 2001 We recently obtained evidence that treatment of human colon cancer cells with exisulind (sulindac sulfone) and related compounds induces apoptosis by activation of protein kinase G (PKG) and c-Jun kinase (JNK1). sulindac sulfone 89-105 protein kinase cGMP-dependent 1 Homo sapiens 182-185