Persönlicher Status und Werkzeuge

Academic Career and Research Areas

Matthias Heinig conducts research in the field of computational biology. His aim is the development and application of computational and statistical tools for the identification of molecular regulatory networks underlying common diseases and the genetic and epigenetic mechanisms controlling these networks from population level DNA and multi-omics data sets. A special focus is the molecular characterization of metabolic and cardiovascular diseases, in particular diabetes and arrhythmias like atrial or ventricular fibrillation.

 

Matthias Heinig studied Bioinformatics at the Ludwig-Maximilians-University Munich, Technical University Munich und der Freie Universität Berlin. After a short research visit at the Centre national de sequencage in Evry, France he started his PhD studies at the am Max-Delbrück-Center and at the Max Planck Institute for molecular genetics in Berlin, where he graduated in 2010. Subsequently Dr. Heinig worked as a Postdoc at the Max Planck Institute for molecular genetics in Berlin. Since 2015 he leads an independent junior research group at the Institute of Computational Biology at the Helmholtz Zentrum München.

Key Publications (all publications)

Heinig M, Colome-Tatche M, Rintisch C, Schäfer S, Pravenec M, Hubner N, Vingron M, Johannes F. histoneHMM: Differential analysis of histone modifications with broad genomic footprints. BMC Bioinformatics. 2015; 16:60 

Abstract

Rintisch C*, Heinig M*, Bauerfeind A, Schafer S, Mieth C, Patone G, Hummel O, Chen W, Cook S, Cuppen E, Colome-Tatche M, Johannes F, Jansen RC, Neil H, Werner M, Pravenec M, Vingron M, and Hubner N. Natural variation of histone modification and its impact on gene expression in the rat genome. Genome Res. 2014; 24(6):942-53

Abstract

Maatz H, Jens M, Liss M, Schafer S, Heinig M, Kirchner M, Adami E, Rintisch C, Dauksaite V, Radke MH, Selbach M, Barton PJ, Cook SA, Rajewsky N, Gotthardt M, Landthaler M, Hubner N. RNA-binding protein RBM20 represses splicing to orchestrate cardiac pre-mRNA processing. J Clin Invest. 2014; 124(8):3419-30

Abstract

Heinig M*, Petretto E*, Wallace C, Bottolo L, Rotival M, Lu H, Li Y, Sarwar R, Langley SR, Bauerfeind A, Hummel O, Lee YA, Paskas S, Rintisch C, Saar K, Cooper J, Buchan R, Gray EE, Cyster JG; Cardiogenics Consortium, Erdmann J, Hengstenberg C, Maouche S, Ouwehand WH, Rice CM, Samani NJ, Schunkert H, Goodall AH, Schulz H, Roider HG, Vingron M, Blankenberg S, Münzel T, Zeller T, Szymczak S, Ziegler A, Tiret L, Smyth DJ, Pravenec M, Aitman TJ, Cambien F, Clayton D, Todd JA, Hubner N, Cook SA. A trans-acting locus regulates an anti-viral expression network and type 1 diabetes risk. Nature. 2010; 467(7314):460-4

Abstract

Manke T*, Heinig M*, and Vingron M. Quantifying the effect of sequence variation on regulatory interactions. Hum Mutat. 2010; 31(4):477-83

Abstract