Results 141 to 150 of about 1,754 (190)

Loss of oligodendrocyte transcription factor 2 protein expression in metabolically stressed oligodendrocytes. [PDF]

Acta Neuropathol
Kaddatz H, Wenzel L, Pril E, Meien S, Harz V, Burkert L, Behrangi N, Zimmermann A, Frintrop L, Amor S, Kipp M, Heinig L.   +11 more
europepmc   +1 more source

Micro-scale control of oligodendrocyte morphology and myelination by the intellectual disability-linked protein acyltransferase ZDHHC9. [PDF]

Elife
Jeong HK, Gonzalez-Fernandez E, Crawley I, Coakley JM, Hwang J, Martin DDO, Bamji SX, Kim JI, Kang SH, Thomas GM.   +9 more
europepmc   +1 more source

Metabolic coupling between glutamate and N-acetylaspartate in the human brain. [PDF]

J Cereb Blood Flow Metab
Hong S, Tomar JS, Shen J.
europepmc   +1 more source

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Purification and preliminary characterization of brain aspartoacylase

Archives of Biochemistry and Biophysics, 2003
Aspartoacylase catalyzes the deacetylation of N-acetylaspartic acid (NAA) in the brain to produce acetate and L-aspartate. An aspartoacylase deficiency, with concomitant accumulation of NAA, is responsible for Canavan disease, a lethal autosomal recessive disorder.
Ronald E Viola, Christopher R Faehnle
exaly   +5 more sources

Involvement of aspartoacylase in tremor expression in rats

Experimental Animals, 2016
Essential tremor (ET) is a common movement disorder with a poorly understood etiology. The TRM/Kyo mutant rat, showing spontaneous tremor, is an animal model of ET. Recently, we demonstrated that tremors in these rats emerge when two mutant loci, a missense mutation in the hyperpolarization-activated cyclic nucleotide-gated potassium channel 1 (Hcn1 ...
Miyuu Tanaka, Tetsushi Sakuma, Takashi Yamamoto   +2 more
exaly   +4 more sources

Aspartoacylase Supports Oxidative Energy Metabolism during Myelination [PDF]

Journal of Cerebral Blood Flow and Metabolism, 2012
The inherited leukodystrophy Canavan disease arises due to a loss of the ability to catabolize N-acetylaspartic acid (NAA) in the brain and constitutes a major point of focus for efforts to define NAA function. Accumulation of noncatabolized NAA is diagnostic for Canavan disease, but contrasts with the abnormally low NAA associated with compromised ...
Jeremy S, Francis, Louise, Strande, Vladamir, Markov, Paola, Leone   +3 more
exaly   +3 more sources

Purification, Characterization, and Localization of Aspartoacylase from Bovine Brain

Journal of Neurochemistry, 1991
Abstract: Canavan disease, an autosomal recessive disorder, is characterized biochemically by N‐acetylaspartic aciduria and aspartoacylase (N‐acyl‐L‐aspartate amidohydrolase; EC 3.5.1.15) deficiency. However, the role of aspartoacylase and N‐acetylaspartic acid in brain metabolism is unknown.
Rajinder K Kaul
exaly   +3 more sources

Expression of aspartoacylase (ASPA) and Canavan disease

Gene, 2012
Canavan disease (CD) is a neurodegenerative disorder usually presenting in the first six months of life. CD patients can be identified via elevated levels of N-acetyl-l-aspartate in the pattern of urinary organic acids assessed by gas chromatography-mass spectrometry.
Sommer, Anke, Saß, Jörn-Oliver
openaire   +4 more sources