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)
2024
- IER3IP1-mutations cause microcephaly by selective inhibition of ER-Golgi transport
Anitei M, Bruno F, Valkova C, Dau T, Cirri E, Mestres Lascano I, Calegari F, Kaether C
bioRxiv 2024, https://doi.org/10.1101/2024.01. - Hormesis as an adaptive response to infection.
Bauer M, Ermolaeva M, Singer M, Wetzker R, Soares MP
Trends Mol Med 2024 (epub ahead of print) - PARP1 UFMylation ensures the stability of stalled replication forks.
Gong Y, Wang Z, Zong W, Shi R, Sun W, Wang S, Peng B, Takeda S, Wang ZQ, Xu X
Proc Natl Acad Sci U S A 2024, 121(18), e2322520121 - J-domain proteins: From molecular mechanisms to diseases.
Marszalek J, De Los Rios P, Cyr D, Mayer MP, Adupa V, Andréasson C, Blatch GL, Braun JEA, Brodsky JL, Bukau B, Chapple JP, Conz C, Dementin S, Genevaux P, Genest O, Goloubinoff P, Gestwicki J, Hammond CM, Hines JK, Ishikawa K, Joachimiak LA, Kirstein J, Liberek K, Mokranjac D, Nillegoda N, Ramos CHI, Rebeaud M, Ron D, Rospert S, Sahi C, Shalgi R, Tomiczek B, Ushioda R, Ustyantseva E, Ye Y, Zylicz M, Kampinga HH
Cell Stress Chaperones 2024, 29(1), 21 - Ultraviolet B acts as a dietary restriction mimetic by targeting mitochondrial bioenergetics
Martirosyan A, Li Y, Woitzat Y, Lee S, Li F, Ermolaeva MA
bioRxiv 2024, 10.1101/2024.03.05.583543 - Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging
Poliezhaieva T, Alonso Pernas P, Espada L, Bayar M, Li Y, Melike Dönertaş H, A.Ermolaeva M
bioRxiv 2024, https://doi.org/10.1101/2024.04. - DNA repair deficiencies and neurodegeneration.
Ropert B, Gallrein C, Schumacher B
DNA Repair (Amst) 2024, 138, 103679 - Reducing the metabolic burden of rRNA synthesis promotes healthy longevity in Caenorhabditis elegans.
Sharifi* S, Chaudhari* P, Martirosyan A, Eberhardt AO, Witt F, Gollowitzer A, Lange L, Woitzat Y, Okoli EM, Li H, Rahnis N, Kirkpatrick J, Werz O, Ori A, Koeberle A, Bierhoff** H, Ermolaeva** M
Nat Commun 2024, 15(1), 1702 * equal contribution, ** co-corresponding authors - Repopulated microglia after pharmacological depletion decrease dendritic spine density in adult mouse brain.
Wickel J, Chung HY, Ceanga M, von Stackelberg N, Hahn N, Candemir Ö, Baade-Büttner C, Mein N, Tomasini P, Woldeyesus DM, Andreas N, Baumgarten P, Koch P, Groth M, Wang ZQ, Geis C
Glia 2024 (epub ahead of print)
