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PLP1 encodes a transmembrane proteolipid protein that is the predominant myelin protein present in the central nervous system. Zusätzlich bieten wir Ihnen Proteolipid Protein 1 Kits (20) und Proteolipid Protein 1 Proteine (4) und viele weitere Produktgruppen zu diesem Protein an.
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Cow (Bovine) Monoclonal PLP1 Primary Antibody für IHC (fro), FACS - ABIN2475779
Ballard: Retrospective studies of left atrial thrombus: does misclassification impair their clinical utility? in Journal of general internal medicine 1991
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Mouse (Murine) Polyclonal PLP1 Primary Antibody für ICC, WB - ABIN261597
Horiuchi, Maezawa, Itoh, Wakayama, Jin, Itoh, Decarli: Amyloid β1-42 oligomer inhibits myelin sheet formation in vitro. in Neurobiology of aging 2012
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Human Polyclonal PLP1 Primary Antibody für ICC, IF - ABIN151155
Cachón-González, Wang, Ziegler, Cheng, Cox: Reversibility of neuropathology in Tay-Sachs-related diseases. in Human molecular genetics 2014
axonal mitochondria, smooth endoplasmic reticulum, and microtubules were characterized in rodent optic nerves where PLP (zeige C3 Antikörper) is replaced by the peripheral nerve myelin protein, P0.
The observations collectively support the idea that GST-pi (zeige GSTP1 Antikörper)(Nuc (zeige SREBF2 Antikörper))/DM-20 mRNA-expressing cells are the progeny of NG2 (zeige Vcan Antikörper)-positive OPCs rather than a novel type of oligodendrocyte-lineage progenitor cells and that DM-20 mRNA expression is dynamically regulated during differentiation of OPCs into oligodendrocytes.
In the absence of P0, thus, PLP (zeige C3 Antikörper) also contributes to myelination by Schwann cells and to the preservation of peripheral axons
while PLP (zeige C3 Antikörper) can co-exist with P0 in peripheral nervous system(PNS) myelin, PLP (zeige C3 Antikörper) cannot replace P0 as the major structural protein of PNS myelin.
Both extracellular and intracellular epitopes of PLP (zeige C3 Antikörper) contribute to the pathogenesis of MP4-induced experimental autoimmune encephalomyelitis already in the setting of intact myelin.
The insertion of native PLP (zeige C3 Antikörper) into Olg mitochondria of animals with PLP1/Plp1 regulates extracellular pH and adenosine triphosphate.
This study shows for the first time that Plp (zeige C3 Antikörper)-null mice exhibit severe early-onset thermal hyperalgesia that is not associated with changes in thermal allodynic behavior.
A novel mechanism sheds light on the immune regulation by which sulfatide-reactive type II natural killer (NK)T cells suppress inflammatory class II histocompatibility-restricted pathogenic CD4 (zeige CD4 Antikörper)+ T cell responses in a T cell-mediated autoimmune disease.
that an early reactive glia response occurs following mutations in the PLP (zeige C3 Antikörper) gene
Result suggest that plp1 plays a role either in the structural integrity of oligodendrocyte progenitor cell processes or in their response to extracellular cues that orient process outgrowth.
it seems that the epitopes of some microorganisms mimicking PLP such as PLP58-74 might have a potential role in the initiation of Multiple Sclerosis.
Human induced pluripotent stem cells-derived oligodendrocytes from 12 individuals with Pelizaeus-Merzbacher and identified individual and shared defects in PLP1 mRNA expression and splicing, oligodendrocyte progenitor development, and oligodendrocyte morphology and capacity for myelination.
report a novel mutation of the PLP1 gene in two siblings with Pelizaeus-Merzbacher disease associated with a rare and protean neuroimaging finding of optic nerve enlargement
Identification and functional study of novel PLP1 mutations in Chinese patients with Pelizaeus-Merzbacher disease. We identified PLP1 mutations in seven male patients with PMD.
In major depressive disorder there was a significantly reduced expression of PLP1 mRNA.
Study investigated 17 unrelated Pelizaeus-Merzbacher disease subjects with copy number gains at the PLP1 locus including triplication and quadruplication of specific genomic intervals-16/17 were found to have a duplication-inverted triplication-duplication rearrangement product.
Myelin proteolipid protein is critical to regulating oligodendrocyte progenitor cell migration.
PLP1 splicing mutations may result in a wide variety of disease phenotypes through a combination of multiple molecular pathogenic mechanisms.
this study provides new insight into the genotype-phenotype correlations of patients with PLP1 splice-site mutations.
Insertion of an extra copy of Xq22.2 into 1p36 results in functional duplication of the PLP1 gene in a girl with classical Pelizaeus-Merzbacher disease.
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.
proteolipid protein 1
, proteolipid protein 1 (Pelizaeus-Merzbacher disease, spastic paraplegia 2, uncomplicated)
, myelin proteolipid protein
, myelin synthesis deficiency
, rump shaker
, major myelin proteolipid protein
, Proteolipid protein (Pelizaeus-Merzbacher disease spastic paraplegia 2 uncomplicated)
, Proteolipid protein (Pelizaeus-Merzbacher disease, spastic paraplegia 2, uncomplicated)
, proteolipid protein (myelin) 1
, proteolipid protein, lipophilin
, myelin proteolipid protein (PLP)
, myelin proteolipid protein A
, proteolipid protein 1 a