TRPML1 activation ameliorates lysosomal phenotypes in CLN3 deficient retinal pigment epithelial cells-Reference-Cited by-同舟云学术

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TRPML1 activation ameliorates lysosomal phenotypes in CLN3 deficient retinal pigment epithelial cells

Published:2024-07-29 Issue:1 Volume:14 Page:
ISSN:2045-2322
Container-title:Scientific Reports
language:en
Short-container-title:Sci Rep

Author:

Wünkhaus D.,Tang R.,Nyame K.,Laqtom N. N.,Schweizer M.,Scotto Rosato A.,Krogsæter E. K.,Wollnik C.,Abu-Remaileh M.,Grimm C.,Hermey G.,Kuhn R.,Gruber-Schoffnegger D.,Markmann S.

Funder

NCL foundation

Sarafan ChEM-H Chemistry/Biology Interface Program

Deutsche Forschungsgemeinschaft

Publisher

Springer Science and Business Media LLC

Link

https://www.nature.com/articles/s41598-024-67479-8.pdf

Reference59 articles.

1. Cotman, S. L. & Staropoli, J. F. The juvenile Batten disease protein, CLN3, and its role in regulating anterograde and retrograde post-Golgi trafficking. Clin. Lipidol. 7, 79–91 (2012).

2. Lerner, T. J. et al. Isolation of a novel gene underlying batten disease, CLN3. Cell 82, 949–957 (1995).

3. Cárcel-Trullols, J., Kovács, A. D. & Pearce, D. A. Cell biology of the NCL proteins: What they do and don’t do. Biochim. Biophys. Acta Mol. Basis Dis. 1852, 2242–2255 (2015).

4. Mirza, M. et al. The CLN3 gene and protein: What we know. Mol. Genet. Genomic Med. 7, 1–41 (2019).

5. Luiro, K., Yliannala, K., Ahtiainen, L., Maunu, H. & Ja, I. Interconnections of CLN3, Hook1 and Rab proteins link Batten disease to defects in the endocytic pathway. Hum. Mol. Genet. 13, 3017–3027 (2004).

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