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| 1 | The p53/miR-34 axis in development and disease显示文摘肿瘤 suppressor p53 是在人的癌症的最经常变异的基因之一。MicroRNAs (miRNAs ) 是在 post-transcriptional 水平上调整基因表示的小 non-proteincoding RNA。最近, p53 调整几 miRNAs 的 theexpression,这被显示出,从而代表 p53 发信号的重要机制。几个独立人士作为最流行的导致 p53 的 miRNAs 学习 miR-34 家庭的 identifiedthe 成员。miR-34s 经常是在 tumorentities 的变化的 silenced,建议他们是重要肿瘤 suppressors。确实, miR-34s 的宫外的表示禁止增长,对各种各样的癌症房间实体的间充质的转变,移植,侵略,和转移上皮。而且, miR-34 的 deliveryor 重新表示在癌症老鼠模型导致肿瘤生长和转移的著名压抑,并且可以 thereforerepresent 为未来癌症治疗学的有效策略。除他们在癌症的关键函数以外, themiR-34 家庭的成员也在精子发生,干细胞区别, neuronal 开发,老化,和 cardiovascularfunctions 起重要作用。因而, miR-34 也在各种各样的非癌的疾病被含有,例如大脑混乱,骨质疏松症,和心血管的复杂并发症。 | Matjaz Rokavec Huihui Li Longchang Jiang and Heiko Hermeking | 2014 | Journal of Molecular Cell Biology2014，8，3： | 27 |
| 2 | The role of epigenetic inactivation of 14-3-3σ in human cancer显示文摘Cancer cells show characteristic alterations in DNA methylation patterns. Aberrant CpG methylation of specificpromoters results in inactivation of tumor suppressor genes and therefore plays an important role in carcinogenesis. Thep53-regulated gene 14-3-3σ undergoes frequent epigenetic silencing in several types of cancer, including carcinoma ofthe breast, prostate, and skin, suggesting that the loss of 14-3-3σ expression may be causally involved in tumor progression.Functional studies demonstrated that 14-3-3σ is involved in cell-cycle control and prevents the accumulation of chro-mosomal damage. The recent identification of novel 14-3-3σ-associated proteins by a targeted proteomics approachimplies that 14-3-3σ regulates diverse cellular processes, which may become deregulated after silencing of 14-3-3σexpression in cancer cells. | Dmitri LODYGIN Heiko HERMEKING | 2005 | Cell Research2005，15，4： | 8 |
| 3 | The crystal structure of the non-liganded 14-3-3σ protein: insights into determinants of isoform specific ligand binding and dimerization显示文摘Seven different, but highly conserved 14-3-3 proteins are involved in diverse signaling pathways in human cells. It isunclear how the 14-3-3σ isoform, a transcriptional target of p53, exerts its inhibitory effect on the cell cycle in thepresence of other 14-3-3 isoforms, which are constitutively expressed at high levels. In order to identify structuraldifferences between the 14-3-3 isoforms, we solved the crystal structure of the human 14-3-3σ protein at a resolutionof 2.8 ? and compared it to the known structures of 14-3-3ζ and 14-3-3τ. The global architecture of the 14-3-3σ foldis similar to the previously determined structures of 14-3-3ζ and 14-3-3τ: two 14-3-3σ molecules form a cup-shapeddimer. Significant differences between these 14-3-3 isoforms were detected adjacent to the amphipathic groove, whichmediates the binding to phosphorylated consensus motifs in 14-3-3-ligands. Another specificity determining region islocalized between amino-acids 203 to 215. These differences presumably select for the interaction with specific ligands,which may explain the different biological functions of the respective 14-3-3 isoforms. Furthermore, the two 14-3-3σmolecules forming a dimer differ by the spatial position of the ninth helix, which is shifted to the inside of the ligandinteraction surface, thus indicating adaptability of this part of the molecule. In addition, 5 non-conserved residues arelocated at the interface between two 14-3-3σ proteins forming a dimer and represent candidate determinants of homo-and hetero-dimerization specificity. The structural differences among the 14-3-3 isoforms described here presumablycontribute to isoform-specific interactions and functions. | Anne BENZINGER Grzegorz M. POPOWICZ Joma K. JOY Sudipta MAJUMDAR Tad A. HOLAK Heiko HERMEKING | 2005 | Cell Research2005，15，4： | 6 |
| 4 | p53 Enters the MicroRNA World显示文摘 | Heiko Hermeking | 2007 | Cancer Cell2007，，5： | 2 |
| 5 | 14-3-3 proteins in cell cycle regulation显示文摘 | Heiko Hermeking Anne Benzinger | 2006 | Seminars in Cancer Biology2006，，3： | 1 |
| 6 | The miR- 34 family in cancer and apoptosis 显示文摘 | Hermeking H | 2010 | Cell Death Differ2010，17，2： | 1 |
| 7 | The MYC oncogene as a cancer drug target 显示文摘 | Hermeking H | 2003 | Curr Cancer Drug Targets2003，3，3： | 1 |
| 8 | The 14-3-3 Cancer Connection显示文摘 | Hermeking H | 2003 | Nature Reviews Cancer2003，3，12： | 1 |
| 9 | p53 Enters the microRNA world显示文摘 | Hermeking H | 2007 | Cancer Cell2007，12，5： | 1 |
| 10 | Serial Analysis of Gene Expression and Cancer显示文摘 | HERMEKING H | 2003 | Curt Opin Oncol2003，15，1： | 1 |
| 11 | The 14-3-3 cancer connection显示文摘 | Hermeking H | 2003 | Nat Rev Cancer2003，3，： | 1 |
| 12 | The 14-3-3 cancer connection显示文摘 | Heiko Hermeking | 2003 | Nature Reviews Cancer2003，3，12： | 1 |
| 13 | The miR-34 family in cancer and apoptosis 显示文摘 | Hermeking H | 2010 | Cell Death Differ2010，17，2： | 1 |
| 14 | p53 enters the microRNA world 显示文摘 | Hermeking H | 2007 | Cancer Cell2007，12，5： | 1 |
| 15 | The miR-34 family in cancer and apoptosis显示文摘 | Hermeking H | 2010 | Cell Death Differ2010，17，2： | 1 |
| 16 | p53 enters the microRNA world显示文摘 | HERMEKING H | | 0，，05： | 1 |
| 17 | Characterization of the cMYC-regulated Transcriptomes with SAGE 显示文摘 | MENSSEN A HERMEKING H | 2002 | Proc Natl Acad Sci2002，99，9： | 1 |
| 18 | The miR - 34 family in cancer and apoptosis 显示文摘 | HERMEKING H | 2010 | Cell Death Differ2010，17，2： | 1 |
| 19 | The14-3-3cancer connection显示文摘 | Hermeking H | 2003 | Nat Rev Cancer2003，3，12： | 1 |
| 20 | The miR-34 family in cancer and apoptosis 显示文摘 | Hermeking H | 2010 | Cell Death Differ2010，17，2： | 1 |
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