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Home>Research>Subarea 5: Computational and Systems Biology of Aging
Research focus of Subarea 5.

Subarea 5: Computational and Systems Biology of Aging

Subarea 5 focuses on the development of methods to analyse and understand complex biological systems. This work includes the design of computer algorithms and biostatistical approaches as well as the development of novel Omic strategies (i.e. genomics/epigenomics, transcriptomics, proteomics, and metabolomics) to study aging and aging-related diseases. According to the FLI, due to the Subarea's expertise in computational data analysis, it is deeply interconnected with all other Subareas. The Subarea hosts two critical core facilities (Life Science Computing, Proteomics) and provides consulting services in statistics. Furthermore, it organizes courses on data analysis and statistics.

The research is defined by five focus areas:

  • Mapping extrinsic and intrinsic factors influencing stem cells during aging,
  • Integration of spatiotemporal proteomics and transcriptomics data,
  • Comprehensive evaluation of qualitative and quantitative expression changes,
  • Identification and analysis of epigenomic alterations during aging and age-related diseases, and
  • Network analysis of genomic, transcriptomic and epigenomic alterations during aging.

Research focus of Subarea 5.

The biology of aging can be viewed as a multilayered array of networks at the level of organs, cells, molecules, and genes. The FLI wants to meet this complexity by establishing the new Subarea on “Computational and Systems Biology of Aging”. The overall goal is to interconnect research at different scales, taking place in Subareas 1-4 of the Institute’s research program. The new group on Systems Biology will integrate data from networks at multiple scales and will thus point to mechanisms and interactions that would not be seen in unilayer approaches.

Publications

(since 2016)

2024

  • INHBA is enriched in HPV-negative oropharyngeal squamous cell carcinoma and promotes cancer progression.
    Abou Kors T, Hofmann L, Betzler A, Payer K, Bens M, Truong J, von Witzleben A, Thomas J, Kraus JM, Kalaajieh R, Huber D, Ezić J, Benckendorff J, Greve J, Schuler PJ, Ottensmeier CH, Kestler HA, Hoffmann TK, Theodoraki MN, Brunner C, Laban S
    Cancer Res Commun 2024 (epub ahead of print)
  • NRF2 activation by cysteine as a survival mechanism for triple-negative breast cancer cells.
    Bottoni L, Minetti A, Realini G, Pio E, Giustarini D, Rossi R, Rocchio C, Franci L, Salvini L, Catona O, D'Aurizio R, Rasa M, Giurisato E, Neri F, Orlandini M, Chiariello M, Galvagni F
    Oncogene 2024 (epub ahead of print)
  • Genomregulation durch Tumorsuppressoren und Onkoproteine
    Fischer M
    BIOspektrum 2024, 30, 123
  • Systematic computational hunting for small RNAs derived from ncRNAs during dengue virus infection in endothelial HMEC-1 cells.
    Gutierrez-Diaz A, Hoffmann S, Gallego-Gómez JC, Bermudez-Santana CI
    Front Bioinform 2024, 4, 1293412
  • Denervation alters the secretome of myofibers and thereby affects muscle stem cell lineage progression and functionality.
    Henze H, Hüttner SS, Koch P, Schüler SC, Groth M, von Eyss B, von Maltzahn J
    NPJ Regen Med 2024, 9(1), 10
  • Bashing irreproducibility with shournal.
    Kirchner T, Riege K, Hoffmann S
    Sci Rep 2024, 14(1), 4872
  • Glycerophosphodiesters inhibit lysosomal phospholipid catabolism in Batten disease.
    Nyame K, Hims A, Aburous A, Laqtom NN, Dong W, Medoh UN, Heiby JC, Xiong J, Ori A, Abu-Remaileh M
    Mol Cell 2024 (epub ahead of print)
  • Nonlinear DNA methylation trajectories in aging male mice.
    Olecka* M, van Bömmel* A, Best L, Haase M, Foerste S, Riege K, Dost T, Flor S, Witte OW, Franzenburg S, Groth M, von Eyss B, Kaleta C, Frahm C, Hoffmann S
    Nat Commun 2024, 15(1), 3074 * equal contribution
  • Remodelling of the cardiac extracellular matrix proteome during chronological and pathological ageing.
    Santinha D, Vilaça A, Estronca L, Schüler SC, Bartoli C, De Sandre-Giovannoli A, Figueiredo A, Quaas M, Pompe T, Ori** A, Ferreira** L
    Mol Cell Proteomics 2024, 23(1), 100706 ** co-corresponding authors
  • Mis-spliced transcripts generate de novo proteins in TDP-43-related ALS/FTD.
    Seddighi S, Qi YA, Brown AL, Wilkins OG, Bereda C, Belair C, Zhang YJ, Prudencio M, Keuss MJ, Khandeshi A, Pickles S, Kargbo-Hill SE, Hawrot J, Ramos DM, Yuan H, Roberts J, Sacramento EK, Shah SI, Nalls MA, Colón-Mercado JM, Reyes JF, Ryan VH, Nelson MP, Cook CN, Li Z, Screven L, Kwan JY, Mehta PR, Zanovello M, Hallegger M, Shantaraman A, Ping L, Koike Y, Oskarsson B, Staff NP, Duong DM, Ahmed A, Secrier M, Ule J, Jacobson S, Reich DS, Rohrer JD, Malaspina A, Dickson DW, Glass JD, Ori A, Seyfried NT, Maragkakis M, Petrucelli L, Fratta P, Ward ME
    Sci Transl Med 2024 (epub ahead of print)