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Proteolipid protein 1

PLP, Myelin Proteolipid Protein, PLP1
This gene encodes a transmembrane proteolipid protein that is the predominant myelin protein present in the central nervous system. It may play a role in the compaction, stabilization, and maintenance of myelin sheaths, as well as in oligodendrocyte development and axonal survival. Mutations in this gene cause X-linked Pelizaeus-Merzbacher disease and spastic paraplegia type 2. Alternatively spliced transcript variants encoding distinct isoforms or having different 5' UTRs, have been identified for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, ACID, HAD, V1a, MBP
Papers using PLP antibodies
Hippocampal CA1 atrophy and synaptic loss during experimental autoimmune encephalomyelitis, EAE
Tiwari-Woodruff Seema K. et al., In Brain, 2009
... Breeding pairs of proteolipid protein-enhanced green fluorescent protein (PLP-EGFP) transgenic mice in the C57BL/6J ...
Palmitoylation is a sorting determinant for transport to the myelin membrane.
Dryer Stuart E., In PLoS ONE, 2004
... Anti-PLP goat polyclonal antibody sc-18529 was from Santa Cruz Biotechnology (California, USA) ...
Hypotension, autonomic failure, and cardiac hypertrophy in transgenic mice overexpressing the alpha 1B-adrenergic receptor
Stefanova Nadia et al., In Experimental Neurology, 2000
... (PLP)-α-SYN transgenic mice were bred at ...
Papers on PLP
Time-course of myelination and atrophy on cerebral imaging in 35 patients with PLP1-related disorders.
Boespflug-Tanguy et al., Clermont-Ferrand, France. In Dev Med Child Neurol, Feb 2016
AIM: Brain magnetic resonance imaging (MRI) motor development score (MDS) correlations were used to analyze the natural time-course of hypomyelinating PLP1-related disorders (Pelizaeus-Merzbacher disease [PMD] and spastic paraplegia type 2).
Myelin in Cartilaginous Fish.
de Bellard, Canada. In Brain Res, Feb 2016
And while they lack true proteolipid protein (PLP) like tetrapods, they express a DM-like protein in their myelin.
The magnetic resonance imaging spectrum of Pelizaeus-Merzbacher disease: A multicenter study of 19 patients.
Sato et al., Kodaira, Japan. In Brain Dev, Feb 2016
The clinical severity and genetic abnormalities (causal mutations of the proteolipid protein gene PLP1) were analyzed together with the imaging findings.
Clinical, biochemical and genetic spectrum of low alkaline phosphatase levels in adults.
Riancho et al., Santander, Spain. In Eur J Intern Med, Feb 2016
p=0.012), pyridoxal phosphate (PLP; r=-0.51,
Evolution of myelin ultrastructure and the major structural myelin proteins.
Kirschner et al., Boston, United States. In Brain Res, Nov 2015
Proteolipid protein (PLP) is a major component only in the CNS myelin of terrestrial species and is involved in compaction of the extracellular apposition.
Genes of the de novo and Salvage Biosynthesis Pathways of Vitamin B6 are Regulated under Oxidative Stress in the Plant Pathogen Rhizoctonia solani.
Jabaji et al., Canada. In Front Microbiol, 2014
Exogenous addition of the vitamers PN or PLP in culture medium significantly induced the transcription of the vitamin B6 de novo encoding genes as early as 0.5 hour post treatment (HPT).
Molecular Genetics of Hypophosphatasia and Phenotype-Genotype Correlations.
Mornet, Le Chesnay, France. In Subcell Biochem, 2014
This enzyme cleaves extracellular substrates inorganic pyrophosphates (PPi), pyridoxal-5'-phosphate (PLP), phosphoethanolamine (PEA) and nucleotides, and probably other substrates not yet identified.
Clinical Forms and Animal Models of Hypophosphatasia.
Salles, Toulouse, France. In Subcell Biochem, 2014
TNAP substrates include inorganic pyrophosphate cleaved into inorganic phosphate (Pi) in bone, pyridoxal-5'-phosphate (PLP), the circulating form of vitamin B6, and phosphoethanolamine (PEA).
Neurochemistry of Hypomyelination Investigated with MR Spectroscopy.
Takanashi, In Magn Reson Med Sci, 2014
MRS in the thalamus of a hypomyelinating mouse model, a myelin synthesis-deficient (msd) mouse, a model of connatal PMD with mutation of the Plp1 gene, revealed increased tNAA and Cr and decreased Cho.
The influence of glutamatergic receptor antagonists on biochemical and ultrastructural changes in myelin membranes of rats subjected to experimental autoimmune encephalomyelitis.
Sulkowski et al., Warsaw, Poland. In Folia Neuropathol, 2014
The aim of the study was to test the effects of the glutamatergic receptor antagonists amantadine and memantine (antagonists of NMDA receptors), LY 367384 (an antagonist of mGluR1), and MPEP (an mGluR5 antagonist) on the development of neurological symptoms in immunized animals, morphological changes in cerebral myelin, and expression of mRNA of the principal myelin proteins PLP, MBP, MOG, MAG, and CNPase.
Travels with carbon-centered radicals. 5'-deoxyadenosine and 5'-deoxyadenosine-5'-yl in radical enzymology.
Frey, Madison, United States. In Acc Chem Res, 2014
In 1986, my colleagues and I took up the problem of the mechanism by which lysine 2,3-aminomutase (LAM) catalyzes S-adenosylmethionine (SAM) and pyridoxal-5'-phosphate (PLP)-dependent interconversion of l-lysine and l-β-lysine.
Subdiffraction-resolution fluorescence microscopy reveals a domain of the centrosome critical for pericentriolar material organization.
Agard et al., San Francisco, United States. In Nat Cell Biol, 2012
Analysis of Pericentrin-like protein (PLP) reveals that its carboxy terminus is positioned at the centriole wall, it radiates outwards into the matrix and is organized in clusters having quasi-nine-fold symmetry.
Pelizaeus-Merzbacher disease-associated proteolipid protein 1 inhibits oligodendrocyte precursor cell differentiation via extracellular-signal regulated kinase signaling.
Yamauchi et al., Tokyo, Japan. In Biochem Biophys Res Commun, 2012
expression of PLP1 in oligodendrocytes markedly inhibits their differentiation, and that this inhibitory effect is effectively improved by inhibition of extracellular signal-regulated kinase activity.
Therapy of Pelizaeus-Merzbacher disease in mice by feeding a cholesterol-enriched diet.
Nave et al., Göttingen, Germany. In Nat Med, 2012
Duplication of PLP1 (proteolipid protein gene 1) and the subsequent overexpression of the myelin protein PLP (also known as DM20) in oligodendrocytes is the most frequent cause of Pelizaeus-Merzbacher disease (PMD), a fatal leukodystrophy without therapeutic options.
A novel PLP1 mutation further expands the clinical heterogeneity at the locus.
Rouleau et al., Cork, Ireland. In Can J Neurol Sci, 2012
A novel PLP1 mutation was found in a family presenting with X-linked recessive Hereditary Spastic Paraplegia.
Inverted genomic segments and complex triplication rearrangements are mediated by inverted repeats in the human genome.
Lupski et al., Houston, United States. In Nat Genet, 2011
We identified complex genomic rearrangements consisting of intermixed duplications and triplications of genomic segments at the MECP2 and PLP1 loci.
A novel proteolipid protein 1 gene mutation causing classical type Pelizaeus-Merzbacher disease.
Tsutsumi et al., Sapporo, Japan. In Brain Dev, 2011
Data suggest that a defective disulfide bond in proteolipid protein 1 could be important in the pathogenesis of Pelizaeus-Merzbacher disease.
Interaction of PLP with GFP-MAL2 in the human oligodendroglial cell line HOG.
López-Guerrero et al., Madrid, Spain. In Plos One, 2010
Results prove for the first time the interaction of PLP and MAL2 in oligodendrocytic cells, supporting the transcytotic model of PLP transport previously suggested.
Molecular genetic analysis of the PLP1 gene in 38 families with PLP1-related disorders: identification and functional characterization of 11 novel PLP1 mutations.
Filocamo et al., Genova, Italy. In Orphanet J Rare Dis, 2010
study of patients with PLP1-related disorders; PLP1 gene duplications were identified in 24 of unrelated patients whereas a variety of intragenic PLP1 mutations were found in the remaining 14 patients; of the 14 different intragenic lesions, 11 were novel
Axon-glial signaling and the glial support of axon function.
Trapp et al., Göttingen, Germany. In Annu Rev Neurosci, 2007
The underlying mechanisms are still poorly understood; we do know that to maintain axonal integrity, mammalian myelin-forming cells require the expression of some glia-specific proteins, including CNP, PLP, and MAG, as well as intact peroxisomes, none of which is necessary for myelin assembly.
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