Transcriptome analysis of atad3-null zebrafish embryos elucidates possible disease mechanisms
The atad3-null zebrafish model emerges as a reliable representation of human ATAD3A-associated disorders, with similarities in differentially expressed pathways and processes. Furthermore, our study underscores mitochondrial dysfunction as the primary underlying pathogenic mechanism in ATAD3A-associated disorders and identifies potential readouts for therapeutic studies.
Authors
- Nathan Ronin (ORCID: https://orcid.org/0009-0003-2141-1079)
- Zohar Ben-Moshe
- Hadar Benyamini
- Ann Saada (ORCID: https://orcid.org/0000-0003-2951-0656)
- Yair Wexler (ORCID: https://orcid.org/0000-0002-6270-3188)
- Shira Yanovsky‐Dagan
- Inbar Plaschkes (ORCID: https://orcid.org/0000-0002-9211-1060)
- Orli Halstuk
- Shlomit Ezer (ORCID: https://orcid.org/0009-0009-0074-2980)
- Shahar Rotem‐Bamberger
- Tamar Harel (ORCID: https://orcid.org/0000-0003-3595-7075)
- Adi Inbal (ORCID: https://orcid.org/0000-0002-5666-109X)
Institutions
- Tel Aviv University (IL)
- Hebrew University of Jerusalem (IL)
- Hadassah Medical Center (IL)
- Jerusalem Institute for Israel Studies (IL)
- Jerusalem Multidisciplinary College (IL)
- Israeli Centers for Research Excellence (IL)
Publication Details
- Journal
- Orphanet Journal of Rare Diseases
- Published
- 2025-04-15
- DOI
- https://doi.org/10.1186/s13023-025-03709-0
- Primary Topic
- Autophagy in Disease and Therapy
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Israel Science Foundation