Subarea 4: Cell Dynamics and Molecular Damages in Aging

The research focus of Subarea 4 is on studying damages of macromolecules (proteins, nucleic acids) and determining the structure-function relationship of biomolecules relevant to damage and damage repair processes and responses to molecular damage that might lead to aging and aging-associated pathologies.

The studies are focused on the following research areas: DNA replication, DNA damage responses (DDR), stress responses, metabolic stresses, protein trafficking and protein damages.

The research is defined by four focus areas:

  • DNA damage response in tissue homeostasis and neuropathies,
  • Quality control in the endoplasmic reticulum for secretory pathway in aging processes,
  • Intrinsic and extrinsic factors implicated in cellular decline during aging, and
  • DNA replication and genomic integrity preventing premature aging and diseases.

Research focus of Subarea 4.

The accumulation of damaged macromolecules or subcellular organelles is associated with dysfunction of a cell, which contributes to tissue & organ failure. DNA damage, genomic instability, protein misfolding or defects in toxic protein degradation can compromise cell functionality. Alterations of mitochondrial DNA and protein complexes affect cellular metabolism, which will have a general impact on cell integrity.

Publications

(since 2016)

2022

  • Upf3a is dispensable for nonsense-mediated mRNA decay in mouse pluripotent and somatic cells
    Chen C, Shen Y, Li L, Wang ZQ, Li T
    bioRxiv 2022, https://doi.org/10.1101/2022.07.
  • Conserved exchange of paralog proteins during neuronal differentiation.
    Di Fraia D, Anitei M, Mackmull MT, Parca L, Behrendt L, Andres-Pons A, Gilmour D, Helmer Citterich M, Kaether C, Beck M, Ori A
    Life Sci Alliance 2022, 5(6)
  • The Essential DNA Damage Response Complex MRN Is Dispensable for the Survival and Function of Purkinje Neurons.
    Ding* M, Qing* X, Zhang G, Baade-Büttner C, Gruber R, Lu H, Ferguson DO, Geis C, Wang** ZQ, Zhou** ZW
    Front Aging Neurosci 2022, 13, 786199 * equal contribution, ** co-senior authors
  • Career pathways, part 8.
    Ermolaeva M, Boyman L
    Nat Metab 2022, 4(4), 407-9
  • Tight association of autophagy and cell cycle in leukemia cells.
    Gschwind* A, Marx* C, Just MD, Severin P, Behring H, Marx-Blümel L, Becker S, Rothenburger L, Förster M, Beck JF, Sonnemann J
    Cell Mol Biol Lett 2022, 27(1), 32 * equal contribution
  • Multifaceted Microcephaly-Related Gene MCPH1
    Kristofova M, Ori A, Wang ZQ
    Cells 2022, 11(2), 275
  • Charakterisierung des potentiellen DNA-Replikationsfaktors PN70
    Kutz J
    Dissertation 2022, Jena, Germany
  • ADP-ribosyltransferases, an update on function and nomenclature.
    Lüscher B, Ahel I, Altmeyer M, Ashworth A, Bai P, Chang P, Cohen M, Corda D, Dantzer F, Daugherty MD, Dawson TM, Dawson VL, Deindl S, Fehr AR, Feijs KLH, Filippov DV, Gagné JP, Grimaldi G, Guettler S, Hoch NC, Hottiger MO, Korn P, Kraus WL, Ladurner A, Lehtiö L, Leung AKL, Lord CJ, Mangerich A, Matic I, Matthews J, Moldovan GL, Moss J, Natoli G, Nielsen ML, Niepel M, Nolte F, Pascal J, Paschal BM, Pawłowski K, Poirier GG, Smith S, Timinszky G, Wang ZQ, Yélamos J, Yu X, Zaja R, Ziegler M
    FEBS J 2022 (epub ahead of print)
  • Hanging the coat on a collar: Same function but different localization and mechanism for COPII.
    Malis Y, Hirschberg K, Kaether C
    Bioessays 2022 (epub ahead of print)
  • Meprin β knockout reduces brain Aβ levels and rescues learning and memory impairments in the APP/lon mouse model for Alzheimer's disease.
    Marengo L, Armbrust F, Schoenherr C, Storck SE, Schmitt U, Zampar S, Wirths O, Altmeppen H, Glatzel M, Kaether C, Weggen S, Becker-Pauly C, Pietrzik CU
    Cell Mol Life Sci 2022, 79(3), 168