Pub. Date : 2003 Jan 17
PMID : 12421819
12 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | A functional role for nicotine in Bcl2 phosphorylation and suppression of apoptosis. | Nicotine | BCL2 apoptosis regulator | Homo sapiens |
| 2 | It is possible that nicotine may regulate Bcl2 to stimulate cell survival. | Nicotine | BCL2 apoptosis regulator | Homo sapiens |
| 3 | Here we report that nicotine can induce Bcl2 phosphorylation exclusively at the serine 70 site in association with prolonged survival of SCLC H82 cells expressing wild-type but not the phosphorylation-deficient S70A mutant Bcl2 after treatment with chemotherapeutic agents (i.e. cisplatin or VP-16). | Nicotine | BCL2 apoptosis regulator | Homo sapiens |
| 4 | Here we report that nicotine can induce Bcl2 phosphorylation exclusively at the serine 70 site in association with prolonged survival of SCLC H82 cells expressing wild-type but not the phosphorylation-deficient S70A mutant Bcl2 after treatment with chemotherapeutic agents (i.e. cisplatin or VP-16). | Nicotine | BCL2 apoptosis regulator | Homo sapiens |
| 5 | Nicotine induces activation of PKC alpha and the MAPKs ERK1 and ERK2, which are physiological Bcl2 kinases. | Nicotine | BCL2 apoptosis regulator | Homo sapiens |
| 6 | Furthermore, ET-18-OCH3, a specific phospholipase C (PLC) inhibitor, blocks nicotine-stimulated Bcl2 phosphorylation and promotes apoptosis, suggesting that PLC may be involved in nicotine activation of Bcl2 kinases. | Nicotine | BCL2 apoptosis regulator | Homo sapiens |
| 7 | Furthermore, ET-18-OCH3, a specific phospholipase C (PLC) inhibitor, blocks nicotine-stimulated Bcl2 phosphorylation and promotes apoptosis, suggesting that PLC may be involved in nicotine activation of Bcl2 kinases. | Nicotine | BCL2 apoptosis regulator | Homo sapiens |
| 8 | Furthermore, ET-18-OCH3, a specific phospholipase C (PLC) inhibitor, blocks nicotine-stimulated Bcl2 phosphorylation and promotes apoptosis, suggesting that PLC may be involved in nicotine activation of Bcl2 kinases. | Nicotine | BCL2 apoptosis regulator | Homo sapiens |
| 9 | Furthermore, ET-18-OCH3, a specific phospholipase C (PLC) inhibitor, blocks nicotine-stimulated Bcl2 phosphorylation and promotes apoptosis, suggesting that PLC may be involved in nicotine activation of Bcl2 kinases. | Nicotine | BCL2 apoptosis regulator | Homo sapiens |
| 10 | Thus, nicotine-induced cell survival results, at least in part, from a mechanism that involves Bcl2 phosphorylation. | Nicotine | BCL2 apoptosis regulator | Homo sapiens |
| 11 | Therefore, novel therapeutic strategies for lung cancer in which Bcl2 is expressed may be used to abrogate the anti-apoptotic activity of Bcl2 by inhibiting multiple upstream nicotine-activated pathways. | Nicotine | BCL2 apoptosis regulator | Homo sapiens |
| 12 | Therefore, novel therapeutic strategies for lung cancer in which Bcl2 is expressed may be used to abrogate the anti-apoptotic activity of Bcl2 by inhibiting multiple upstream nicotine-activated pathways. | Nicotine | BCL2 apoptosis regulator | Homo sapiens |