Product nameAnti-Myelin Protein Zero antibody
See all Myelin Protein Zero primary antibodies
DescriptionChicken polyclonal to Myelin Protein Zero
Tested applicationsSuitable for: IHC-Fr, ICC, WBmore details
Species reactivityReacts with: Mouse, Human
Synthetic peptide; sequence common to mouse and human Myelin Protein Zero.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.02% Sodium Azide
Constituents: PBS, pH 7.2
Concentration information loading...
Purification notesIgY fractions were then affinity-purified using a peptide column.
Our Abpromise guarantee covers the use of ab39375 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-Fr||Use at an assay dependent concentration.|
|ICC||1/100 - 1/200.|
|WB||1/250 - 1/500. Predicted molecular weight: 28 kDa.|
FunctionCreation of an extracellular membrane face which guides the wrapping process and ultimately compacts adjacent lamellae.
Tissue specificityFound only in peripheral nervous system Schwann cells.
Involvement in diseaseDefects in MPZ are the cause of Charcot-Marie-Tooth disease type 1B (CMT1B) [MIM:118200]. CMT1B is a form of Charcot-Marie-Tooth disease, the most common inherited disorder of the peripheral nervous system. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathy or CMT1, and primary peripheral axonal neuropathy or CMT2. Neuropathies of the CMT1 group are characterized by severely reduced nerve conduction velocities (less than 38 m/sec), segmental demyelination and remyelination with onion bulb formations on nerve biopsy, slowly progressive distal muscle atrophy and weakness, absent deep tendon reflexes, and hollow feet.
Defects in MPZ are the cause of Charcot-Marie-Tooth disease type 2I (CMT2I) [MIM:607677]. CMT2I is a form of Charcot-Marie-Tooth disease, the most common inherited disorder of the peripheral nervous system. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathy or CMT1, and primary peripheral axonal neuropathy or CMT2. Neuropathies of the CMT2 group are characterized by signs of axonal regeneration in the absence of obvious myelin alterations, normal or slightly reduced nerve conduction velocities, and progressive distal muscle weakness and atrophy. CMT2I is characterized by late onset (range 47 to 60 years).
Defects in MPZ are the cause of Charcot-Marie-Tooth disease type 2J (CMT2J) [MIM:607736]. CMT2J is a form of Charcot-Marie-Tooth disease characterized by the association of axonal peripheral neuropathy with hearing loss and pupillary abnormalities such as Adie pupil. Inheritance is autosomal dominant.
Defects in MPZ are the cause of Adie pupil (ADIEP) [MIM:103100]. A stationary, benign disorder characterized by tonic, sluggishly reacting pupil and hypoactive or absent tendon reflexes. Adie pupil is a characteristic of Charcot-Marie-Tooth disease type 2J.
Defects in MPZ may be the cause of Charcot-Marie-Tooth disease dominant intermediate type D (CMTDID) [MIM:607791]. CMTDID is a form of Charcot-Marie-Tooth disease characterized by features intermediate between demyelinating and axonal peripheral neuropathies, and motor median nerve conduction velocities ranging from 25 to 45 m/sec.
Defects in MPZ are a cause of Dejerine-Sottas syndrome (DSS) [MIM:145900]; also known as Dejerine-Sottas neuropathy (DSN) or hereditary motor and sensory neuropathy III (HMSN3). DSS is a severe degenerating neuropathy of the demyelinating Charcot-Marie-Tooth disease category, with onset by age 2 years. DSS is characterized by motor and sensory neuropathy with very slow nerve conduction velocities, increased cerebrospinal fluid protein concentrations, hypertrophic nerve changes, delayed age of walking as well as areflexia. There are both autosomal dominant and autosomal recessive forms of Dejerine-Sottas syndrome.
Defects in MPZ are a cause of congenital hypomyelination neuropathy (CHN) [MIM:605253]. CHN is characterized clinically by early onset of hypotonia, areflexia, distal muscle weakness, and very slow nerve conduction velocities.
Defects in MPZ are a cause of Roussy-Levy syndrome (ROULS) [MIM:180800]; also known as Roussy-Levy hereditary areflexic dystasia. This autosomal dominant disorder resembles Charcot-Marie-Tooth disease type 1 in that it presents with foot deformity, weakness and atrophy of distal limb muscles, especially the peronei, and absent tendon reflexes. The phenotype differs, however, in that it includes static tremor of the upper limbs and gait ataxia.
Sequence similaritiesBelongs to the myelin P0 protein family.
Contains 1 Ig-like V-type (immunoglobulin-like) domain.
modificationsN-glycosylated; contains sulfate-substituted glycan.
- Information by UniProt
- Charcot Marie Tooth neuropathy 1B antibody
- CHM antibody
- CMT1 antibody
A tissue section through an adult sciatic nerve. Myelin Protein Zero (green staining) can be seen in the myelin and Schwann cell processes surrounding the nodes of Ranvier. In this photomicrograph, rabbit antibodies against LAMP (lysozome-associated membrane glycoprotein) (red staining) serves as the counterstain, and DAPI (blue staining) allows visualization of nuclei.
All lanes : Anti-Myelin Protein Zero antibody (ab39375) at 1 µg/ml
Lane 1 : Human spinal cord tissue lysate - total protein (ab29188)
Lane 2 : Spinal Cord (Mouse) Tissue Lysate
Lysates/proteins at 10 µg per lane.
All lanes : Goat polyclonal Secondary Antibody to Chicken IgY - H&L (HRP) at 1/3000 dilution
Developed using the ECL technique.
Performed under reducing conditions.
Predicted band size: 28 kDa
Observed band size: 25 + 28 kDa why is the actual band size different from the predicted?
Exposure time: 30 seconds
The band observed at 25 kDa could potentially be a cleaved form of Myelin Protein Zero due to the presence of a 29 amino acid signal peptide.
This product has been referenced in:
- Stierli S et al. The regulation of the homeostasis and regeneration of peripheral nerve is distinct from the CNS and independent of a stem cell population. Development 145:N/A (2018). Read more (PubMed: 30413560) »
- Ulanska-Poutanen J et al. Injury-induced perivascular niche supports alternative differentiation of adult rodent CNS progenitor cells. Elife 7:N/A (2018). Read more (PubMed: 30222103) »