|Positive WB detected in||Schwann cells|
|Positive IF detected in||myelinating SCs cells|
|Western Blot (WB)||WB : 1:500-1:1000|
|Immunofluorescence (IF)||IF : 1:20-1:200|
|Sample-dependent, check data in validation data gallery|
10572-1-AP targets MPZ / P0 in WB, IHC, IF, ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||frog, human, mouse, rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||MPZ / P0 fusion protein Ag0848|
|Full Name||myelin protein zero|
|Calculated molecular weight||28 kDa|
|Observed molecular weight||30 kDa|
|GenBank accession number||BC006491|
|Gene ID (NCBI)||4359|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
MPZ (myelin protein zero), also known as P0, a transmembrane glycoprotein (~30 kDa), is a member of the immunoglobulin supergene family. Synthesized by myelin-forming Schwann cells, MPZ is the major structural protein component of myelin in the peripheral nervous system. It is involved in formation and maintenance of compact myelin, and plays a role in the creation of an extracellular membrane face which guides the wrapping process and ultimately compacts adjacent lamellae. More than 120 mutations detected in the gene of MPZ cause various forms of hereditary neuropathy, which include Charcot-Marie-Tooth disease type 1B (CMT1B), CMT2, Dejerine-Sottas syndrome (DSS), and congenital hypomyelination neuropathy (CHN). This antibody can recognize endogenous MPZ, and can be used as a marker of myelinating Schwann cells.
Oxid Med Cell Longev
Neuroprotective Effect of Salvianolic Acid A against Diabetic Peripheral Neuropathy through Modulation of Nrf2.
Phylogenetically Conserved Sequences Around Myelin P0 Stop Codon are Essential for Translational Readthrough to Produce L-MPZ.
Sensory neurons do not induce motor neuron loss in a human stem cell model of spinal muscular atrophy.
Mol Cell Neurosci
MMPs initiate Schwann cell-mediated MBP degradation and mechanical nociception after nerve damage.
Front Cell Neurosci
Schwann Cell Expressed Nogo-B Modulates Axonal Branching of Adult Sensory Neurons Through the Nogo-B Receptor NgBR.
J Neuropathol Exp Neurol
Matrix metalloproteinase inhibition enhances the rate of nerve regeneration in vivo by promoting dedifferentiation and mitosis of supporting schwann cells.