ArticleJournal of cell science2016
The membrane trafficking and functionality of the K+-Cl- co-transporter KCC2 is regulated by TGF-β2.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Neuronal KActa pharmacologica Sinica · 2024Review
- KFrontiers in cellular neuroscience · 2023Article
- TGF-β2 Regulates Transcription of the KCells · 2022Article
- Altered Development of Prefrontal GABAergic Functions and Anxiety-like Behavior in Adolescent Offspring Induced by Prenatal Stress.Brain sciences · 2022Article
- Gephyrin Interacts with the K-Cl Cotransporter KCC2 to Regulate Its Surface Expression and Function in Cortical Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- WNK3 Maintains the GABAergic Inhibitory Tone, Synaptic Excitation and Neuronal ExcitabilityFrontiers in molecular neuroscience · 2021Article
- Contribution of Smoothened Receptor Signaling in GABAergic Neurotransmission and Chloride Homeostasis in the Developing Rodent Brain.Frontiers in physiology · 2021Review
- TGF-β/Smad3 Signalling Modulates GABA Neurotransmission: Implications in Parkinson's Disease.International journal of molecular sciences · 2020Review
- Crossing the Chloride Channel: The Current and Potential Therapeutic Value of the Neuronal KBioMed research international · 2019Review
- Reciprocal Regulation of KCC2 Trafficking and Synaptic Activity.Frontiers in cellular neuroscience · 2019Review
- Neuroprotection by Propofol Post-Conditioning: Focus on PKMζ/KCC2 Pathway Activity.Cellular and molecular neurobiology · 2018Article
- Molecular architecture of potassium chloride co-transporter KCC2.Scientific reports · 2017Article
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
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Abstract
Functional activation of the neuronal K(+)-Cl(-) co-transporter KCC2 (also known as SLC12A5) is a prerequisite for shifting GABAA responses from depolarizing to hyperpolarizing during development. Here, we introduce transforming growth factor β2 (TGF-β2) as a new regulator of KCC2 membrane trafficking and functional activation. TGF-β2 controls membrane trafficking, surface expression and activity of KCC2 in developing and mature mouse primary hippocampal neurons, as determined by immunoblotting, immunofluorescence, biotinylation of surface proteins and KCC2-mediated Cl(-) extrusion. We also identify the signaling pathway from TGF-β2 to cAMP-response-element-binding protein (CREB) and Ras-associated binding protein 11b (Rab11b) as the underlying mechanism for TGF-β2-mediated KCC2 trafficking and functional activation. TGF-β2 increases colocalization and interaction of KCC2 with Rab11b, as determined by 3D stimulated emission depletion (STED) microscopy and co-immunoprecipitation, respectively, induces CREB phosphorylation, and enhances Rab11b gene expression. Loss of function of either CREB1 or Rab11b suppressed TGF-β2-dependent KCC2 trafficking, surface expression and functionality. Thus, TGF-β2 is a new regulatory factor for KCC2 functional activation and membrane trafficking, and a putative indispensable molecular determinant for the developmental shift of GABAergic transmission.
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