Anti-Myelin Protein Zero antibody (ab31851)
Key features and details
- Rabbit polyclonal to Myelin Protein Zero
- Suitable for: WB
- Reacts with: Mouse
- Isotype: IgG
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Overview
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Product name
Anti-Myelin Protein Zero antibody
See all Myelin Protein Zero primary antibodies -
Description
Rabbit polyclonal to Myelin Protein Zero -
Host species
Rabbit -
Tested applications
Suitable for: WBmore details
Unsuitable for: IHC-Fr -
Species reactivity
Reacts with: Mouse
Predicted to work with: Rat, Human -
Immunogen
Synthetic peptide conjugated to KLH derived from within residues 200 to the C-terminus of Rat Myelin Protein Zero.
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General notes
The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.
If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, along with publications, customer reviews and Q&As
Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle. -
Storage buffer
pH: 7.40
Preservative: 0.02% Sodium azide
Constituent: PBS
Batches of this product that have a concentration < 1mg/ml may have BSA added as a stabilising agent. If you would like information about the formulation of a specific lot, please contact our scientific support team who will be happy to help. -
Concentration information loading...
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Purity
Immunogen affinity purified -
Clonality
Polyclonal -
Isotype
IgG -
Research areas
Associated products
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Compatible Secondaries
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Isotype control
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Positive Controls
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Recombinant Protein
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab31851 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Application | Abreviews | Notes |
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WB | (5) |
Use a concentration of 1 µg/ml. Detects a band of approximately 25 kDa (predicted molecular weight: 27 kDa).
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Notes |
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WB
Use a concentration of 1 µg/ml. Detects a band of approximately 25 kDa (predicted molecular weight: 27 kDa). |
Target
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Function
Creation of an extracellular membrane face which guides the wrapping process and ultimately compacts adjacent lamellae. -
Tissue specificity
Found only in peripheral nervous system Schwann cells. -
Involvement in disease
Defects 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 similarities
Belongs to the myelin P0 protein family.
Contains 1 Ig-like V-type (immunoglobulin-like) domain. -
Post-translational
modificationsN-glycosylated; contains sulfate-substituted glycan. -
Cellular localization
Membrane. - Information by UniProt
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Database links
- Entrez Gene: 4359 Human
- Entrez Gene: 17528 Mouse
- Entrez Gene: 24564 Rat
- Omim: 159440 Human
- SwissProt: P25189 Human
- SwissProt: P27573 Mouse
- SwissProt: P06907 Rat
- Unigene: 591486 Human
see all -
Alternative names
- Charcot Marie Tooth neuropathy 1B antibody
- CHM antibody
- CMT1 antibody
see all
Images
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Anti-Myelin Protein Zero antibody (ab31851) at 1 µg/ml + Mouse Sciatic Nerve Whole Tissue Lysate at 20 µg
Secondary
IRDye 680 Conjugated Goat Anti-Rabbit IgG (H+L) at 1/15000 dilution
Performed under reducing conditions.
Predicted band size: 27 kDa
Observed band size: 25 kDa why is the actual band size different from the predicted?
We also see a similar banding pattern in Rat Sciatic Nerve lysate although the band is more smeared then observed in the Western Blot shown here. We believe the smearing is caused by glycosylation of the target protein.
Datasheets and documents
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SDS download
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Datasheet download
References (47)
ab31851 has been referenced in 47 publications.
- Willows JW et al. A clearing-free protocol for imaging intact whole adipose tissue innervation in mice. STAR Protoc 3:101109 (2022). PubMed: 35106499
- Huang Z et al. Mammalian Sterile 20-Like Kinase 1 Mediates Neuropathic Pain Associated with Its Effects on Regulating Mitophagy in Schwann Cells. Oxid Med Cell Longev 2022:3458283 (2022). PubMed: 35656021
- Sun Y et al. Ninj2 regulates Schwann cells development by interfering laminin-integrin signaling. Theranostics 12:7307-7318 (2022). PubMed: 36438492
- Zhou N et al. Schwann Cell-Derived Exosomes Induce the Differentiation of Human Adipose-Derived Stem Cells Into Schwann Cells. Front Mol Biosci 8:835135 (2021). PubMed: 35174212
- Tan C et al. Effect of Schwann cell transplantation combined with electroacupuncture on axonal regeneration and remyelination in rats with spinal cord injury. Anat Rec (Hoboken) 304:2506-2520 (2021). PubMed: 34319000