Raul E. Guzman
Juelich, NW 52425, Germany
Last Updated: 09/26/2026
Save publications for later
Sign Up
Not sure about your diagnosis?
Check Your Symptoms
Found 22 publications
Disruption of ClC-3-mediated 2Cl-/H+ exchange leads to behavioural deficits and thalamic atrophy.
Journal: Scientific reports
Published: March 28, 2025
Endosomal 2Cl-/H+ exchangers regulate neuronal excitability by tuning Kv7/KCNQ channel density.
Journal: Brain : a journal of neurology
Published: June 12, 2024
Expanding the genetic and phenotypic relevance of CLCN4 variants in neurodevelopmental condition: 13 new patients.
Journal: Journal of neurology
Published: February 24, 2024
Genotype-phenotype correlation in CLCN4-related developmental and epileptic encephalopathy.
Journal: Human genetics
Published: February 17, 2024
Corrigendum: ClC-3 regulates the excitability of nociceptive neurons and is involved in inflammatory processes within the spinal sensory pathway.
Journal: Frontiers in cellular neuroscience
Published: March 14, 2023
Vesicular glutamate transporters are H+-anion exchangers that operate at variable stoichiometry.
Journal: Nature communications
Published: May 16, 2022
ClC-3 regulates the excitability of nociceptive neurons and is involved in inflammatory processes within the spinal sensory pathway.
Journal: Frontiers in cellular neuroscience
Published: April 20, 2022
Functional Characterization of CLCN4 Variants Associated With X-Linked Intellectual Disability and Epilepsy.
Journal: Frontiers in molecular neuroscience
Published: February 09, 2022
CLC Anion/Proton Exchangers Regulate Secretory Vesicle Filling and Granule Exocytosis in Chromaffin Cells.
Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience
Published: December 13, 2021
The molecular and phenotypic spectrum of CLCN4-related epilepsy.
Journal: Epilepsia
Published: January 05, 2021
Metabolic energy sensing by mammalian CLC anion/proton exchangers.
Journal: EMBO reports
Published: February 04, 2019
A Tripartite Interaction Among the Calcium Channel α1- and β-Subunits and F-Actin Increases the Readily Releasable Pool of Vesicles and Its Recovery After Depletion.
Journal: Frontiers in cellular neuroscience
Published: November 13, 2018
Last Updated: 09/26/2026