ArticleGlia2007
Role of Kir4.1 channels in growth control of glia.
Article in Glia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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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.
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.
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Who cites it
63 citing papers in PubMed, 97 citations in OpenAlex.
- Hydrogel-Based Delivery of Ion Channel Modulators for Cancer Therapy: Current Advances and Future Perspectives.Gels (Basel, Switzerland) · 2026Review
- Article
- Special characteristics of human astrocytes and their roles in brain homeostasis.Neuroscience applied · 2026Review
- Activation of Kir4.1 Channels by 2-D08 Promotes Myelin Repair in Multiple Sclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Preclinical Insights into the Role of Kir4.1 in Chronic Pain and Depression: Mechanisms and Therapeutic Potential.Biomolecules · 2025Review
- Roles of TRPM channels in glioma.Cancer biology & therapy · 2024Review
- Heterogeneity in oligodendrocyte precursor cell proliferation is dynamic and driven by passive bioelectrical properties.Cell reports · 2024Article
- KCNK1 promotes proliferation and metastasis of breast cancer cells by activating lactate dehydrogenase A (LDHA) and up-regulating H3K18 lactylation.PLoS biology · 2024Article
- Biophysical control of plasticity and patterning in regeneration and cancer.Cellular and molecular life sciences : CMLS · 2023Review
- Ion Channels in Gliomas-From Molecular Basis to Treatment.International journal of molecular sciences · 2023Review
- Kir4.1 is coexpressed with stemness markers in activated astrocytes in the injured brain and a Kir4.1 inhibitor BaClThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- Olfactory bulb astrocytes mediate sensory circuit processing through Sox9 in the mouse brain.Nature communications · 2021Article
- TRP Channels in Brain Tumors.Frontiers in cell and developmental biology · 2021Review
- Neurovascular Coupling in Development and Disease: Focus on Astrocytes.Frontiers in cell and developmental biology · 2021Review
- Wnt/β-Catenin Signaling Promotes Differentiation of Ischemia-Activated Adult Neural Stem/Progenitor Cells to Neuronal Precursors.Frontiers in neuroscience · 2021Article
- Review
- pH-Channeling in Cancer: How pH-Dependence of Cation Channels Shapes Cancer Pathophysiology.Cancers · 2020Review
- Parallel astrocyte calcium signaling modulates olfactory bulb responses.Journal of neuroscience research · 2020Article
- Squaring the Circle: A New Study of Inward and Outward-Rectifying Potassium Currents in U251 GBM Cells.Cellular and molecular neurobiology · 2020Article
- Astrocytogenesis: where, when, and how.F1000Research · 2020Review
3 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
2 authors at 1 institution in 1 country.
Funding
Abstract
The inwardly rectifying potassium channel Kir4.1 is widely expressed by astrocytes throughout the brain. Kir4.1 channels are absent in immature, proliferating glial cells. The progressive expression of Kir4.1 correlates with astrocyte differentiation and is characterized by the establishment of a negative membrane potential (> -70 mV) and an exit from the cell cycle. Despite some correlative evidence, a mechanistic interdependence between Kir4.1 expression, membrane hyperpolarization, and control of cell proliferation has not been demonstrated. To address this question, we used astrocyte-derived tumors (glioma) that lack functional Kir4.1 channels, and generated two glioma cell lines that stably express either AcGFP-tagged Kir4.1 channels or AcGFP vectors only. Kir4.1 expression confers the same K+ conductance to glioma membranes and a similar responsiveness to changes in [K+]o that characterizes differentiated astrocytes. Kir4.1 expression was sufficient to move the resting potential of gliomas from -50 to -80 mV. Importantly, Kir4.1 expression impaired cell growth by shifting a significant number of cells from the G2/M phase into the quiescent G0/G1 stage of the cell cycle. Furthermore, these effects could be nullified entirely if Kir4.1 channels were either pharmacologically inhibited by 100 microM BaCl2 or if cells were chronically depolarized by 20 mM KCl to the membrane voltage of growth competent glioma cells. These studies therefore demonstrate directly that Kir4.1 causes a membrane hyperpolarization that is sufficient to account for the growth attenuation, which in turn induces cell maturation characterized by a shift of the cells from G2/M into G0/G1.
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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.