Melittin, a major component of bee venom, sensitizes human hepatoce...
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2009 Feb 6;284(6):3804-13. doi: 10.1074/jbc.M. Epub
2008 Dec 12.Melittin, a major component of bee venom, sensitizes human hepatocellular carcinoma cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by activating CaMKII-TAK1-JNK/p38 and inhibiting IkappaBalpha kinase-NFkappaB.1, , , , , , , .1Department of Integrative Medicine, Changhai Hospital, Second Military Medical University, Shanghai, China.AbstractPromoting apoptosis is a strategy for cancer drug discovery. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in a wide range of malignant cells. However, several cancers, including human hepatocellular carcinoma (HCC), exhibit a major resistance to TRAIL-induced cell death. Melittin, a water-soluble 26-amino acid peptide derived from bee venom of Apis mellifera, can exert toxic or inhibitory effects on many types of tumor cells. Here we report that melittin can induce apoptosis of HCC cells by activating Ca2+/calmodulin-dependent protein kinase, transforming growth factor-beta-activated kinase 1 (TAK1), and JNK/p38 MAPK. We show that melittin-induced apoptosis can be inhibited by calcium chelator, by inhibitors for Ca2+/calmodulin-dependent protein kinase, JNK and p38, and by dominant negative TAK1. In the presence of melittin, TRAIL-induced apoptosis is significantly increased in TRAIL-resistant HCC cells, which may be attributed to melittin-induced TAK1-JNK/p38 activation and melittin-mediated inhibition of IkappaBalpha kinase-NFkappaB. Our data suggest that melittin can synergize with TRAIL in the induction of HCC cell apoptosis by activating the TAK1-JNK/p38 pathway but inhibiting the IkappaBalpha kinase-NFkappaB pathway. Therefore, the combination of melittin with TRAIL may be a promising therapeutic approach in the treatment of TRAIL-resistant human cancer.PMID:
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External link. Please review our .上个月月底托人在香港买回来的ipad air，序列号是：DQTLV1ANFK15，好心人帮忙查询一下是不是正品？_百度知道
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中国(富士康)常见型号，正常现象& & &nbsp，即可查询& &nbsp，所以产地是显示中国销售往香港就叫港版是否有锁，可以给苹果线商店和售后支持免费打电话咨询：过关需要提前激活; 对应查询的颜色。 &nbsp，看网页不舒服　　----DQVL;F17 F2N开头：日 - 日生产工厂，颜色不对即是卖家私自翻新的 &KH是韩国版 &TA是台湾 &顺手采纳或评价为满意答案 & &nbsp。为售后换机（官方翻新机）返修机/官翻机：全新的机器; &nbsp，质量比较好;　　根据序列号鉴别阴阳屏的方法如下：　　----DMQL;& & & &nbsp：CH国行 ZP港版 LL美版 J日版 B英国版 C加拿大版 F法国版 &nbsp: 全新苹果设备有三个月有效期; && & & &序列号; &&也就是常说的销售地区或是版本号 除了 CH是国行 其他统称为水货&注; &nbsp，但12年12月就激活的水货的机器，是时差的关系，参考上面查询的信息; &nbsp。产地中国; & & & & &nbsp：一般是指全新的机子在保修期内出现毛病;&nbsp，再核对自己的购买激活日期苹果设备序列号查询地址百度搜索【“维维苹果序列号查询】”或搜索“【果粉查询】”打开后复制序列号进去;B是英国版 &nbsp：已激活（日）电话支持;本机的型号只有自己在机器才能查到版本【手机——设置——通用——关于本机】查看型号 &nbsp，维修好了之后卖给下一个顾客质量是有保障的; &nbsp：CCP C7G C3K DYJ DQG DQH & & & &nbsp，即是13年1月20日& DN是德国版 &F是法国版 & & &nbsp，全冷荧屏; & 比如13年5月生产的; & 购买保修到14年1月19日如果购买延保的 保修则是两年二手的机器; & & &ZP是港版 & & & &nbsp，查询结果激活日期早于生产日期的; &nbsp，价格略低于全新机& Y是为西班牙& & 如果是激活日期比购买日期提前一天，是否全新或翻新; & &例如】苹果型号MD513CH/A国行机 系统升级6：DQTLV1ANFK15设备名称; & & &最近购买的是【 全新正品机子】序 列 号，例如还没未生产就已经先激活&nbsp，左边发黄明显：未过期（日）硬件保修，小部分偏暖　　----DMPL; &苹果设备具体情况请; & & & &nbsp：（手机）一般来说; & & & &nbsp: 苹果机子几乎是中国富士康代工生产的:即是生产日期比激活日期还要晚;& &nbsp，轻微阴阳; &nbsp，用卡贴 则有锁& C是加拿大 & &nbsp，所以激活日期比购买激活日期提前在一个月内是没有问题的; &nbsp: 是否有锁.1以上则带/A&nbsp：iPad Air Wi-Fi激活状态，轻微阴阳：如果显示已过期 则机器使用过一年; &LL是美国版 &电话支持，颜色轻微偏黄　　----DLXL，基本阴阳屏—————————— &J是日本 &nbsp，质量最高; &nbsp：未过期（日）生产日期:硬件保修; &nbsp，可以放心使用，返厂维修; & & & &nbsp，一般查不到详细的激活日期& & & &翻新的机器; &nbsp:激活状态 至 硬件保修是显示一年整; & &nbsp，左边些许发黑　　----DQTL; & &nbsp机子全新 正品&nbsp
哦，谢谢！那我这个算是比较严重的阴阳屏了吗？为什么偏偏让我碰上了啊！！唉，这个除了去换货还有其他什么解决办法吗？我现在不方便去香港啊，我给北京直营店打电话说他们不给换啊，怎么办？？？好失望啊
----DQTL，左边发黄明显，看网页不舒服除了自己去换 不然无法的顺手采纳
国内换不了是吧？？现在没法去香港啊
你国内找售后 试试看顺手采纳
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出门在外也不愁Role of atypical protein kinase C in activation of sterol regulator...
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):. doi: 10.-009-1336-5. Epub
2009 Apr 9.Role of atypical protein kinase C in activation of sterol regulatory element binding protein-1c and nuclear factor kappa B (NFkappaB) in liver of rodents used as a model of diabetes, and relationships to hyperlipidaemia and insulin resistance.1, , , , , , , , .1Research Service, James A Haley Veterans Hospital, Tampa, FL 33612, USA.AbstractAIMS/HYPOTHESIS: Previous findings in rodents used as a model of diabetes suggest that insulin activation of atypical protein kinase C (aPKC) is impaired in muscle, but, unexpectedly, conserved in liver, despite impaired hepatic protein kinase B (PKB/Akt) activation. Moreover, aPKC at least partly regulates two major transactivators: (1) hepatic sterol receptor binding protein-1c (SREBP-1c), which cont and (2) nuclear factor kappa B (NFkappaB), which promotes inflammation and systemic insulin resistance.METHODS: In Goto-Kakizaki rats used as a model of type 2 diabetes, we examined: (1) whether differences in hepatic aPKC and PKB activation reflect differences in activation of IRS-1- and IRS-2-dependent phosphatidylinositol 3-kinase (PI3K); (2) whether hepatic SREBP-1c and NFkappaB are excessively activated by aPKC; and (3) metabolic consequences of excessive activation of hepatic aPKC, SREBP-1c and NFkappaB.RESULTS: In liver, as well as in muscle, IRS-2/PI3K activation by insulin was intact, whereas IRS-1/PI3K activation by insulin was impaired. Moreover, hepatic IRS-2 is known to control hepatic aPKC during insulin activation. Against this background, selective inhibition of hepatic aPKC by adenoviral-mediated expression of mRNA encoding kinase-inactive aPKC or short hairpin RNA targeting Irs2 mRNA and partially depleting hepatic IRS-2 diminished hepatic SREBP-1c production and NFkappaB activities, concomitantly improving serum lipids and insulin signalling in muscle and liver. Similar improvements in SREBP-1c, NFkappaB and insulin signalling were seen in ob/ob mice following inhibition of hepatic aPKC.CONCLUSIONS/INTERPRETATION: In diabetic rodent liver, diminished PKB activation may largely reflect impaired IRS-1/PI3K activation, while conserved aPKC activation reflects retained IRS-2/PI3K activity. Hepatic aPKC may also contribute importantly to excessive SREPB-1c and NFkappaB activities. Excessive hepatic aPKC-dependent activation of SREBP-1c and NFkappaB may contribute importantly to hyperlipidaemia and systemic insulin resistance.PMID:
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External link. Please review our .Transcriptional regulation of the bcl-x gene encoding the anti-apop...
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):595-601.Transcriptional regulation of the bcl-x gene encoding the anti-apoptotic Bcl-xL protein by Ets, Rel/NFkappaB, STAT and AP1 transcription factor families.1, , , .1Institute of Signalisation, Developmental Biology and Cancer, Université de Nice, Faculté des Sciences, France.AbstractTranscription factors play an essential role in determining the fate of a cell by affecting the expression of target genes involved in proliferation, in differentiation and in programmed cell death. Under certain conditions, some of these factors are capable of deregulating expression of genes involved in the cell cycle and/or in programmed cell death resulting in uncontrolled proliferation of the cell. The focus of this review is on the transcriptional regulation of the bcl-x gene encoding the anti-apoptotic Bcl-xL protein. Since 1999, several papers have implicated members of the Ets, Rel/NFkappaB, STAT and AP-1 families as transcription factors regulating bcl-x expression. A specific emphasis of these different transcription factor families on bcl-x regulation in hematopoietic cells is discussed.PMID:
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