ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
ClC3 is a critical regulator of the cell cycle in normal and malignant glial cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 106 citations in OpenAlex.
- Identification of anoctamin 1 (ANO1) as a key driver of esophageal epithelial proliferation in eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2020Trial
- Hydrogel-Based Delivery of Ion Channel Modulators for Cancer Therapy: Current Advances and Future Perspectives.Gels (Basel, Switzerland) · 2026Review
- CLC3 regulates V-ATPase to enhance lysosomal degradation and cisplatin resistance in cervical cancer cells.Cell death discovery · 2025Article
- Targeting Ion Channels for Cancer Therapy: From Pathophysiological Mechanisms to Clinical Translation.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Diagnostic and Therapeutic Approaches for Glioblastoma and Neuroblastoma Cancers Using Chlorotoxin Nanoparticles.Cancers · 2023Review
- Ion Channels in Gliomas-From Molecular Basis to Treatment.International journal of molecular sciences · 2023Review
- Eosinophilic esophagitis: Immune mechanisms and therapeutic targets.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2022Review
- Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Mechanisms Underlying Influence of Bioelectricity in Development.Frontiers in cell and developmental biology · 2022Review
- Bioelectric Dysregulation in Cancer Initiation, Promotion, and Progression.Frontiers in oncology · 2022Review
- The Astrogenic Balance in the Aging Brain.Current neuropharmacology · 2021Review
- Review
- Chimera RNA interference knockdown of γ-synuclein in human cortical astrocytes results in mitotic catastrophe.Neural regeneration research · 2020Article
- Article
- Role of the CLC-3 Channel Transporter in Angiogenesis by Endothelial Progenitor Cells in Ischemia-Induced Vascular Injury: A Key Passenger or a Driver?The Canadian journal of cardiology · 2020Article
- Molecular Targets for Combined Therapeutic Strategies to Limit Glioblastoma Cell Migration and Invasion.Frontiers in pharmacology · 2020Article
- Erythrocyte plasma membrane potential: past and current methods for its measurement.Biophysical reviews · 2019Review
- Gluconate suppresses seizure activity in developing brains by inhibiting CLC-3 chloride channels.Molecular brain · 2019Article
- Bioelectric Properties of Myogenic Progenitor Cells.Bioelectricity · 2019Review
- Overexpression of chloride channel-3 (ClC-3) is associated with human cervical carcinoma development and prognosis.Cancer cell international · 2019Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Although most brain cells are postmitotic, small populations of progenitor or stem cells can divide throughout life. These cells are believed to be the most likely source for primary brain malignancies including gliomas. Such tumors share many common features with nonmalignant glial cells but, because of their insidious growth, form cancers that are typically incurable. In studying the growth regulation of these tumors, we recently discovered that glioma cell division is preceded by a cytoplasmic condensation that we called premitotic condensation (PMC). PMC represents an obligatory step in cell replication and is linked to chromatin condensation. If perturbed, the time required to complete a division is significantly prolonged. We now show that PMC is a feature shared more commonly among normal and malignant cells and that the reduction of cell volume is accomplished by Cl(-) efflux through ClC3 Cl(-) channels. Patch-clamp electrophysiology demonstrated a significant upregulation of chloride currents at M phase of the cell cycle. Colocalization studies and coimmunoprecipitation experiments showed the channel on the plasma membrane and at the mitotic spindle. To demonstrate a mechanistic role for ClC3 in PMC, we knocked down ClC3 expression using short hairpin RNA constructs. This resulted in a significant reduction of chloride currents at M phase that was associated with a decrease in the rate of PMC and a similar impairment of DNA condensation. These data suggest that PMC is an integral part of cell division and is dependent on ClC3 channel function.
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Registered trials
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.