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Home>Research>Subarea 4: Cell Dynamics and Molecular Damages in Aging
Research focus of Subarea 4.

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)

2016

  • The DNA damage response molecule MCPH1 in brain development and beyond.
    Liu X, Zhou ZW, Wang ZQ
    Acta Biochim Biophys Sin 2016, 48(7), 678-85
  • Conserved Senescence Associated Genes and Pathways in Primary Human Fibroblasts Detected by RNA-Seq.
    Marthandan S, Baumgart M, Priebe S, Groth M, Schaer J, Kaether C, Guthke R, Cellerino A, Platzer M, Diekmann S, Hemmerich P
    PLoS One 2016, 11(5), e0154531
  • Conserved genes and pathways in primary human fibroblast strains undergoing replicative and radiation induced senescence.
    Marthandan S, Menzel U, Priebe S, Groth M, Guthke R, Platzer M, Hemmerich P, Kaether C, Diekmann S
    Biol Res 2016, 49(1), 34
  • Heterozygous PALB2 c.1592delT mutation channels DNA double-strand break repair into error-prone pathways in breast cancer patients.
    Obermeier K, Sachsenweger J, Friedl TWP, Pospiech H, Winqvist R, Wiesmüller L
    Oncogene 2016, 35(29), 3796-806
  • TSC loss distorts DNA replication programme and sensitises cells to genotoxic stress.
    Pai GM, Zielinski A, Koalick D, Ludwig K, Wang ZQ, Borgmann K, Pospiech H, Rubio I
    Oncotarget 2016, 7(51), 85365-80
  • The Oncogenic Fusion Proteins SET-Nup214 and Sequestosome-1 (SQSTM1)-Nup214 Form Dynamic Nuclear Bodies and Differentially Affect Nuclear Protein and Poly(A)+ RNA Export.
    Port SA, Mendes A, Valkova C, Spillner C, Fahrenkrog B, Kaether C, Kehlenbach RH
    J Biol Chem 2016, 291(44), 23068-83
  • Assembly of the Cdc45-Mcm2-7-GINS Complex, the Replication Helicase
    Pospiech H, Szambowska A
    In: The Initiation of DNA Replication in Eukaryotes (edited by Daniel Kaplan) 2016, 393-409, Springer International
  • Tumor suppression in mice lacking GABARAP, an Atg8/LC3 family member implicated in autophagy, is associated with alterations in cytokine secretion and cell death.
    Salah FS, Ebbinghaus M, Muley VY, Zhou Z, Al-Saadi KRD, Pacyna-Gengelbach M, O'Sullivan GA, Betz H, König R, Wang ZQ, Bräuer R, Petersen I
    Cell Death Dis 2016, 7, e2205
  • Study of the homeostasis of Poly (ADP-ribose) in response to genotoxic stress
    Schuhwerk H
    Dissertation 2016, Jena, Germany
  • Analyse des Aufbaus und der Struktur des CENP-A-Nukleosoms sowie des Mis12-Komplexes
    Weber C
    Dissertation 2016, Jena, Germany