Evidence map›Paper›PMID 41558486›Full record

ArticleNeuron2026

CLN3 mediates chloride efflux from lysosomes.

Yayu Wang, Kai Li, Wei Chen, Chao Chen, Adeline J H Yong, Xiaofan Zhang, Marena Tynan-La Fontaine, Yuh Nung Jan, Lily Yeh Jan

Abstract read
In one paragraph

Article in Neuron, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Yayu WangDepartment of Physiology, University of California at San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA 94158, USA.
Kai LiDepartment of Physiology, University of California at San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA 94158, USA.
Wei ChenDepartment of Physiology, University of California at San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA 94158, USA.
Chao ChenDepartment of Physiology, University of California at San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA 94158, USA.
Adeline J H YongDepartment of Physiology, University of California at San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA 94158, USA.
Xiaofan ZhangDepartment of Physiology, University of California at San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA 94158, USA.
Marena Tynan-La FontaineDepartment of Physiology, University of California at San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA 94158, USA.
Yuh Nung JanDepartment of Physiology, University of California at San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA 94158, USA.
Lily Yeh JanDepartment of Physiology, University of California at San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA 94158, USA. Electronic address: lily.jan@ucsf.edu.

Funding

Dendrite morphogenesis, function and regenerationR35NS097227 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JAN, YUH NUNG · 2017 to 2024
$5.1M
The TMEM16 Family of Ion Channels and Lipid ScramblasesR35NS122110 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LILY JAN · 2021 to 2026
$3.2M
Dendrite development, function, degeneration and regenerationR35NS137312 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI YUH NUNG JAN · 2025 to 2026
$1.4M
NINDS NIH HHS R35 NS097227NINDS NIH HHS R35 NS122110NINDS NIH HHS R35 NS137312
6 · The paper itself

Abstract

Neurodegenerative diseases, which pose significant challenges for effective treatment, often involve risk variants of lysosomal gene products that disrupt lysosomal function, leading to the accumulation of indigestible materials and damage to brain cells. The lysosome is a degradative organelle and a signaling hub that senses nutrient availability. How lysosomal dysfunction contributes to neurodegenerative diseases is an important open question. In this study, we identified CLN3 (ceroid lipofuscinosis, neuronal 3), an endolysosomal protein that is linked to Batten disease, as an evolutionarily conserved protein that facilitates lysosomal chloride efflux. Additionally, we report that a natural compound with anti-inflammatory properties-the curcumin analog C1, which is a TFEB (transcription factor EB) activator-could enhance CLN3 activity and improve lysosomal function. These findings provide new insight into the role of CLN3 in lysosomal ion homeostasis and raise the possibility that modulation of the TFEB-CLN3 signaling axis may hold therapeutic potential for lysosomal storage disorders.

Indexed as

Chloride ChannelsChloridesLysosomesMembrane GlycoproteinsMolecular ChaperonesAnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCurcuminHEK293 CellsHumansMiceNeuronal Ceroid-LipofuscinosesBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsChloride ChannelsChloridesCLN3 protein, humanCurcuminMembrane GlycoproteinsMolecular ChaperonesBatten diseasechloride channelCLN3lysosomeneurodegenerative disease

Identifiers

PMID41558486
PMCPMC12994750

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.