Research Topics
Genomes and GenesSpecies | Heiko HermekingSummaryCountry: Germany Publications
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Publications
Characterization of the c-MYC-regulated transcriptome by SAGE: identification and analysis of c-MYC target genesAntje Menssen
Max-Planck-Institute of Biochemistry, Molecular Oncology, Independent Junior Research Group, Am Klopferspitz 18a, D-82152 Martinsried/Munich, Germany
Proc Natl Acad Sci U S A 99:6274-9. 2002..The c-MYC-regulated genes/tags identified here will help to define the set of bona fide c-MYC targets and may have potential therapeutic value for inhibition of cancer cell proliferation, tumor-vascularization, and restenosis...
The role of epigenetic inactivation of 14-3-3sigma in human cancerDmitri Lodygin
Molecular Oncology, Max Planck Institute of Biochemistry, Martinsried Munich, Germany
Cell Res 15:237-46. 2005....- p53 enters the microRNA worldHeiko Hermeking
Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152 Martinsried, Germany
Cancer Cell 12:414-8. 2007..The initial evidence suggesting that miR-34 genes are central mediators of p53 function is summarized here... - Serial analysis of gene expression and cancerHeiko Hermeking
Molecular Oncology, Max Planck Institute of Biochemistry, Martinreid Munich, Germany
Curr Opin Oncol 15:44-9. 2003..In addition, cancer diagnosis and treatment may benefit from a complementation between serial analysis of gene expression and quantitative proteomics in the future... - The MYC oncogene as a cancer drug targetHeiko Hermeking
Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
Curr Cancer Drug Targets 3:163-75. 2003..These and other recent developments, which address the use of myc genes as therapeutic targets for cancer treatment, are discussed in this review... - 14-3-3 proteins in cell cycle regulationHeiko Hermeking
Molecular Oncology, Independent Max Planck Research Group, Max Planck Institute of Biochemistry, Martinsried Munich, Germany
Semin Cancer Biol 16:183-92. 2006..Effects of 14-3-3 proteins on cell cycle progression and the regulation of 14-3-3 activity during the cell cycle are reviewed in this chapter... - The 14-3-3 cancer connectionHeiko Hermeking
Molecular Oncology, Max-Planck-Institute of Biochemistry, Am Klopferspitz 18a, D-82152 Martinsried, Germany
Nat Rev Cancer 3:931-43. 2003 - Inactivation of miR-34a by aberrant CpG methylation in multiple types of cancerDmitri Lodygin
Molecular Oncology, Max Planck Institute of Biochemistry, Martinsried, Germany
Cell Cycle 7:2591-600. 2008..These results show that miR-34a represents a tumor suppressor gene which is inactivated by CpG methylation and subsequent transcriptional silencing in a broad range of tumors... - c-MYC delays prometaphase by direct transactivation of MAD2 and BubR1: identification of mechanisms underlying c-MYC-induced DNA damage and chromosomal instabilityAntje Menssen
Molecular Oncology, Max Planck Institute of Biochemistry, Martinsried, Germany
Cell Cycle 6:339-52. 2007.... - Differential regulation of microRNAs by p53 revealed by massively parallel sequencing: miR-34a is a p53 target that induces apoptosis and G1-arrestValery Tarasov
Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152 Martinsried, Germany
Cell Cycle 6:1586-93. 2007..siRNAs corresponding to p53-induced miRNAs may have potential as cancer therapeutic agents as RNA interference based therapies are currently emerging... - Epigenetic silencing of 14-3-3sigma in cancerDmitri Lodygin
Molecular Oncology, Independent Max-Planck Research Group, Max-Planck-Institute of Biochemistry, Martinsried, Munich, Germany
Semin Cancer Biol 16:214-24. 2006..In the future the detection of CpG methylation of 14-3-3sigma may be used for diagnostic and prognostic purposes... - Prostate cancer is characterized by epigenetic silencing of 14-3-3sigma expressionDimitri Lodygin
Molecular Oncology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D 82152 Martinsried Munich, Germany
Oncogene 23:9034-41. 2004.... - Induction of cullin 7 by DNA damage attenuates p53 functionPeter Jung
Molecular Oncology, Max Planck Institute of Biochemistry, D 82152 Martinsried, Germany
Proc Natl Acad Sci U S A 104:11388-93. 2007..Pharmacological modulation of Cul7 function may allow the sensitization of cancer cells expressing wild-type p53 to genotoxic agents used in cancer therapy... - Large-scale identification of c-MYC-associated proteins using a combined TAP/MudPIT approachHeike B Koch
Molecular Oncology, Independent Max Planck Research Group, Max Planck Institute of Biochemistry, Martinsried, Germany
Cell Cycle 6:205-17. 2007..Furthermore, this first comprehensive description of the c-MYC-associated sub-proteome will facilitate further studies aimed to elucidate the biology of c-MYC... - Digital karyotyping reveals frequent inactivation of the dystrophin/DMD gene in malignant melanomaHenrike Körner
Molecular Oncology, Independent Max Planck Research Group, Max Planck Institute of Biochemistry, Martinsried, Germany
Cell Cycle 6:189-98. 2007..Therefore, loss of DMD may critically change the migratory and proliferative capacity of melanocytes. Taken together, our results suggest that inactivation of DMD is involved in the pathogenesis of malignant melanoma... - Targeted proteomic analysis of 14-3-3 sigma, a p53 effector commonly silenced in cancerAnne Benzinger
Molecular Oncology, Max-Planck-Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried/Munich, Germany
Mol Cell Proteomics 4:785-95. 2005..The data suggest that the cancer-specific loss of 14-3-3 sigma expression by epigenetic silencing or p53 mutations contributes to cancer formation by multiple routes... - Induction of the Cdk inhibitor p21 by LY83583 inhibits tumor cell proliferation in a p53-independent mannerDimitri Lodygin
Max-Planck-Institute of Biochemistry, Molecular Oncology, Munich, Germany
J Clin Invest 110:1717-27. 2002..These results suggest that LY, or derivatives, may be useful therapeutic agents for the treatment of tumors... - Characterization of epithelial senescence by serial analysis of gene expression: identification of genes potentially involved in prostate cancerGerold Untergasser
Molecular Oncology, Max-Planck-Institute of Biochemistry, Am Klopferspitz 18 A, D-82152 Martinsried/Munich, Germany
Cancer Res 62:6255-62. 2002.... - Inducible microRNA expression by an all-in-one episomal vector systemAlexey Epanchintsev
Molecular Oncology, Independent Max-Planck-Research Group, Max-Planck-Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried/Munich, Germany
Nucleic Acids Res 34:e119. 2006..Furthermore, the vector was adapted for convenient ligation-free transfer of microRNA cassettes from public libraries. This conditional knockdown-system should prove useful for many research and gene therapeutic applications... - Extracellular 14-3-3sigma protein: a potential mediator of epithelial-mesenchymal interactionsHeiko Hermeking
Molecular Oncology, Max-Planck-Institute of Biochemistry, Martinsried/Munich, Germany
J Invest Dermatol 124:ix-x. 2005 - Characterization of 14-3-3sigma dimerization determinants: requirement of homodimerization for inhibition of cell proliferationBerlinda Verdoodt
Molecular Oncology, Independent Max-Planck Research Group, Max-Planck-Institute of Biochemistry, Munich, Germany
Cell Cycle 5:2920-6. 2006..As inactivation of 14-3-3sigma sensitizes to DNA-damaging drugs, substances designed to interfere with 14-3-3sigma homodimerization may be used to inactivate 14-3-3sigma function for cancer therapeutic purposes... - Analysis of 14-3-3sigma expression in hyperproliferative skin diseases reveals selective loss associated with CpG-methylation in basal cell carcinomaDimitri Lodygin
Molecular Oncology, Max-Planck-Institute of Biochemistry, Am Klopferspitz 18a, D-82152 Martinsried near Munich, Germany
Oncogene 22:5519-24. 2003..As experimental removal of 14-3-3sigma sensitizes to DNA damage, silencing of 14-3-3sigma may explain the high efficacy of radiation therapy in the treatment of BCC... - 14-3-3 proteins and cancer biologyHeiko Hermeking
Semin Cancer Biol 16:161. 2006 - AP4 encodes a c-MYC-inducible repressor of p21Peter Jung
Molecular Tumorpathology, Institute of Pathology, Ruhr University Bochum, D 44789 Bochum, Germany
Proc Natl Acad Sci U S A 105:15046-51. 2008..Notably, AP4 is specifically expressed in colonic progenitor and colorectal carcinoma cells. In conclusion, our results indicate that c-MYC employs AP4 to maintain cells in a proliferative, progenitor-like state... - Downregulation of 14-3-3sigma in ovary, prostate and endometrial carcinomas is associated with CpG island methylationPaulette Mhawech
Department of Clinical Pathology, Geneva University Hospital, Geneva, Switzerland
Mod Pathol 18:340-8. 2005..Loss of 14-3-3sigma expression due to promoter hypermethylation may represent the most frequent molecular aberration in ovarian, endometrial and prostate adenocarcinomas... - Evidence for a cancer-specific switch at the CDK4 promoter with loss of control by both USF and c-MycSnehalata A Pawar
Department of Molecular Genetics, The University of Texas, MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA
Oncogene 23:6125-35. 2004..These results suggest that a major switch in the transcriptional control of CDK4 occurs during breast carcinogenesis, with likely alteration of cell cycle regulation... - The crystal structure of the non-liganded 14-3-3sigma protein: insights into determinants of isoform specific ligand binding and dimerizationAnne Benzinger
Molecular Oncology Group, Max-Planck-Institute for Biochemistry, Martinsried, Germany
Cell Res 15:219-27. 2005..The structural differences among the 14-3-3 isoforms described here presumably contribute to isoform-specific interactions and functions... - Human Proteinpedia enables sharing of human protein dataSuresh Mathivanan
Nat Biotechnol 26:164-7. 2008 - Functional epigenomics identifies genes frequently silenced in prostate cancerDimitri Lodygin
Molecular Oncology Group, Max-Planck-Institutes of Biochemistry, Martinsried and Institute of Pathology, Ludwig-Maximilians University, Munich, Germany
Cancer Res 65:4218-27. 2005..The high frequency of CpG methylation detected in the promoters of the identified genes suggests a potential causal involvement in prostate cancer and may prove useful for diagnostic purposes...