PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19903766-0 2009 Nicotine enhances the antiapoptotic function of Mcl-1 through phosphorylation. Nicotine 0-8 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 48-53 19903766-7 2009 Mechanistically, nicotine-induced Mcl-1 phosphorylation significantly enhances the half-life of Mcl-1, which renders Mcl-1 a long-term survival activity. Nicotine 17-25 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 96-101 19903766-8 2009 Specific depletion of Mcl-1 by RNA interference blocks nicotine-stimulated survival and enhances apoptotic cell death. Nicotine 55-63 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 22-27 19903766-9 2009 Thus, nicotine-enhanced survival of lung cancer cells may occur through activation of Mcl-1 by phosphorylation at T163 site, which may contribute to development of human lung cancer and/or chemoresistance. Nicotine 6-14 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 86-91 19903766-5 2009 Here, we found that nicotine induces Mcl-1 phosphorylation through activation of extracellular signal-regulated kinase 1/2 in association with increased chemoresistance of human lung cancer cells. Nicotine 20-28 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 37-42 19903766-6 2009 Since nicotine stimulates Mcl-1 phosphorylation and survival in cells expressing wild-type but has no such effects in cells expressing T163A Mcl-1 mutant, this indicates that nicotine induces Mcl-1 phosphorylation exclusively at the T163 site and that phosphorylation of Mcl-1 at T163 is required for nicotine-induced survival. Nicotine 6-14 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 26-31 19903766-7 2009 Mechanistically, nicotine-induced Mcl-1 phosphorylation significantly enhances the half-life of Mcl-1, which renders Mcl-1 a long-term survival activity. Nicotine 17-25 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 34-39 19903766-7 2009 Mechanistically, nicotine-induced Mcl-1 phosphorylation significantly enhances the half-life of Mcl-1, which renders Mcl-1 a long-term survival activity. Nicotine 17-25 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 96-101 31956373-0 2020 Nicotine Upregulates the Level of Mcl-1 through STAT3 in H1299 Cells. Nicotine 0-8 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 34-39 31956373-1 2020 Background: Nicotine contributes to development of human lung cancer and chemoresistance through activation of myeloid cell leukemia-1 (Mcl-1). Nicotine 12-20 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 111-134 31956373-1 2020 Background: Nicotine contributes to development of human lung cancer and chemoresistance through activation of myeloid cell leukemia-1 (Mcl-1). Nicotine 12-20 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 136-141 31956373-3 2020 Therefore, we examined the STAT3 cascade in nicotine regulation of Mcl-1 transcription in human lung cancer cells. Nicotine 44-52 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 67-72 31956373-4 2020 Methods: The effects of nicotine on the expression of STAT3 and Mcl-1 were determined using western blot. Nicotine 24-32 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 64-69 31956373-7 2020 Results: STAT3 was constitutively activated (i.e., tyrosine-phosphorylated, serine-phosphorylated and nuclear translocation), meanwhile the expression and transcriptional activity of Mcl-1 were up-regulated in lung cancer cells following treatment with nicotine. Nicotine 253-261 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 183-188 31956373-9 2020 Deleted mutagenesis of a putative STAT3 consensus binding sequence decreased Mcl-1 promoter activity and eliminated the increase of Mcl-1 promoter activity induced by nicotine. Nicotine 167-175 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 132-137 31956373-12 2020 Conclusions: We have demonstrated that nicotine induces up-regulation of Mcl-1 through STAT3, which process may be independent on JAKs and not only dependent on the phosphorylation of Y705. Nicotine 39-47 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 73-78 30741422-0 2019 Nicotine induces cell survival and chemoresistance by stimulating Mcl-1 phosphorylation and its interaction with Bak in lung cancer. Nicotine 0-8 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 66-71 30741422-2 2019 Our previous data found that nicotine promotes cell survival in lung cancer by affecting the expression of antiapoptotic protein Mcl-1, suggesting that the Mcl-1 may be a therapeutic target for patients with lung cancer. Nicotine 29-37 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 129-134 30741422-2 2019 Our previous data found that nicotine promotes cell survival in lung cancer by affecting the expression of antiapoptotic protein Mcl-1, suggesting that the Mcl-1 may be a therapeutic target for patients with lung cancer. Nicotine 29-37 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 156-161 30741422-3 2019 In this study, we found that the effects of drug resistance on nicotine-induced lung cancer cell lines were shown to influence the phosphorylation of Mcl-1. Nicotine 63-71 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 150-155 30741422-4 2019 Moreover, nicotine induces Mcl-1 phosphorylation exclusively at the T163 site, which results in enhancement of the antiapoptotic activity of Mcl-1 and increased cell survival. Nicotine 10-18 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 27-32 30741422-4 2019 Moreover, nicotine induces Mcl-1 phosphorylation exclusively at the T163 site, which results in enhancement of the antiapoptotic activity of Mcl-1 and increased cell survival. Nicotine 10-18 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 141-146 30741422-5 2019 Meanwhile, nicotine can reduce the sensitivity of H1299 cells to CDDP via enhancement of the binding of Mcl-1 to Bak, which inhibits the proapoptotic effect of Bak and ultimately leads to increased survival and drug resistance of lung cancer cells. Nicotine 11-19 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 104-109 30741422-6 2019 Thus, nicotine-induced cell survival and chemoresistance may occur in a mechanism by stimulating Mcl-1 phosphorylation and its interaction with Bak, which may contribute to improving the efficacy of chemotherapy in the treatment of human lung cancer. Nicotine 6-14 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 97-102