Evidence map›Paper›PMID 37142673›Full record

ArticleCell research2023

Disruption of ER ion homeostasis maintained by an ER anion channel CLCC1 contributes to ALS-like pathologies.

Liang Guo, Qionglei Mao, Ji He, Xiaoling Liu, Xuejiao Piao, Li Luo, Xiaoxu Hao, Hanzhi Yu, Qiang Song, Bailong Xiao and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cell research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
7.0field-weighted citation impact, top 2% of its field
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

20 citing papers in PubMed, 34 citations in OpenAlex.

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  9. Scalable and comprehensive mosaic variant calling using DRAGEN.medRxiv : the preprint server for health sciences · 2026
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  18. The ion channels of endomembranes.Physiological reviews · 2024
    Review
  19. Review
  20. 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

13 authors at 5 institutions in 2 countries.

Liang Guo *Tsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing, China.
Qionglei Mao *CAS Key Laboratory of Receptor Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia and Medica, Chinese Academy of Sciences, Shanghai, China.
Ji He *Department of Neurology, Peking University Third Hospital, Beijing, China.
Xiaoling LiuIDG/McGovern Institute for Brain Research, Tsinghua University, Beijing, China.
Xuejiao PiaoTsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing, China.
Li LuoSchool of Medicine, Tsinghua University, Beijing, China.
Xiaoxu HaoCAS Key Laboratory of Receptor Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia and Medica, Chinese Academy of Sciences, Shanghai, China.
Hanzhi YuSchool of Life Sciences, Tsinghua University, Beijing, China.
Qiang SongSchool of Medicine, Tsinghua University, Beijing, China.
Bailong XiaoTsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing, China.
Dongsheng FanDepartment of Neurology, Peking University Third Hospital, Beijing, China. dsfan2010@aliyun.com.
Zhaobing GaoCAS Key Laboratory of Receptor Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia and Medica, Chinese Academy of Sciences, Shanghai, China. zbgao@simm.ac.cn.
Yichang JiaTsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing, China. yichangjia@tsinghua.edu.cn.ORCID 0000-0002-7767-5714
Chinese Institute for Brain Research · CNChinese Academy of Sciences · CNTsinghua University · CNPeking University · CNMcGovern Institute for Brain Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although anion channel activities have been demonstrated in sarcoplasmic reticulum/endoplasmic reticulum (SR/ER), their molecular identities and functions remain unclear. Here, we link rare variants of Chloride Channel CLIC Like 1 (CLCC1) to amyotrophic lateral sclerosis (ALS)-like pathologies. We demonstrate that CLCC1 is a pore-forming component of an ER anion channel and that ALS-associated mutations impair channel conductance. CLCC1 forms homomultimers and its channel activity is inhibited by luminal Ca

Indexed as

Amyotrophic Lateral SclerosisAnimalsBiological TransportChloride ChannelsDisease Models, AnimalEndoplasmic ReticulumHomeostasisMiceMitochondrial ProteinsMutationChloride ChannelsClcc1 protein, mouseMitochondrial Proteins

Identifiers

PMID37142673
PMCPMC10313822
OpenAlexW4368365196

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.