BRD4780-mediated clearance of mutant alpha-1-antitrypsin involves the autophagiclysosomal pathway
Accumulation of misfolded proteins is a hallmark of several proteinopathies and represents a potential therapeutic target. In alpha-1-antitrypsin deficiency (AATD), mutant A1AT accumulates intracellularly due to protein misfolding. BRD4780 has been shown to facilitate the degradation of proteins retained within the early secretory pathway. We investigated its effect on mutant A1AT and the potential involvement of autophagy in this process.
Authors
- V. Barešová
- Šárka Veselá
- Mariia Lunová (ORCID: https://orcid.org/0000-0002-5795-7781)
- Milan Jirsa (ORCID: https://orcid.org/0000-0001-7300-6735)
- M. Zivna
- Strnad P.
- S. Kmoch
- P. Vyleťal
- D. Mušálková
Institutions
- Charles University (CZ)
- Institute of Clinical and Experimental Medicine (CZ)
- General University Hospital in Prague (CZ)
- RWTH Aachen University (DE)
Publication Details
- Journal
- Zenodo (CERN European Organization for Nuclear Research)
- Published
- 2026-09-21
- DOI
- https://doi.org/10.5281/zenodo.22870509
- Primary Topic
- Endoplasmic Reticulum Stress and Disease
- Type
- article
- Field-Weighted Citation Impact
- 0.00