Processing mechanism of guanidinoacetate in choroid plexus epithelial cells: conversion of guanidinoacetate to creatine via guanidinoacetate N-methyltransferase and monocarboxylate transporter 12-mediated creatine release into the CSF

Processing mechanism of guanidinoacetate in choroid plexus epithelial cells: conversion of guanidinoacetate to creatine via guanidinoacetate N-methyltransferase and monocarboxylate transporter 12-mediated creatine release into the CSF

Abstract Background Guanidinoacetate (GAA) induces epileptogenesis and neurotoxicity in the brain. As epileptic animal models have been reported to show elevated cerebral GAA levels, the processing mechanism of GAA in the brain is important for maintaining brain homeostasis. We have revealed that GA...

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Bibliographic Details
Main Authors: Ryuta Jomura, Shin-ichi Akanuma, Yoshiyuki Kubo, Masanori Tachikawa, Ken-ichi Hosoya
Format: Article
Language:English
Published: BMC 2022-06-01
Series:Fluids and Barriers of the CNS
Subjects:
Creatine
Guanidinoacetate (GAA)
Monocarboxylate transporter (MCT/SLC16A)
MCT12 (SLC16A12)
Choroid plexus epithelial cells
Blood-cerebrospinal fluid barrier (BCSFB)
Online Access:https://doi.org/10.1186/s12987-022-00328-w

Internet

https://doi.org/10.1186/s12987-022-00328-w

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