Key features and details
- Chicken polyclonal to Myelin Protein Zero
- Suitable for: IHC-Fr, WB
- Reacts with: Mouse, Human
- Isotype: IgY
- 研究可靠 —— 各批次间结果一致且可重复
- 长期批量供应 —— 采用重组技术，可实现快速生产
- 首次实验即可成功 —— 经过大量验证确认了特异性
- 符合伦理标准 —— 产品不含动物成分
参阅全部 Myelin Protein Zero 一抗
经测试应用适用于: IHC-Fr, WBmore details
种属反应性与反应: Mouse, Human
Synthetic peptide; sequence common to mouse and human Myelin Protein Zero.
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存放说明Shipped at 4°C. Store at +4°C short term (1-2 weeks). Store at -20°C or -80°C. Avoid freeze / thaw cycle.
存储溶液Preservative: 0.02% Sodium azide
Concentration information loading...
纯化说明IgY fractions were then affinity-purified using a peptide column.
The Abpromise guarantee
1/100 - 1/200.
1/250 - 1/500. Predicted molecular weight: 28 kDa.
1/100 - 1/200.
1/250 - 1/500. Predicted molecular weight: 28 kDa.
功能Creation of an extracellular membrane face which guides the wrapping process and ultimately compacts adjacent lamellae.
组织特异性Found only in peripheral nervous system Schwann cells.
疾病相关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.
序列相似性Belongs to the myelin P0 protein family.
Contains 1 Ig-like V-type (immunoglobulin-like) domain.
翻译后修饰N-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.
ab39375 被引用在 14 文献中.
- Saveri P et al. DNAJB2-related Charcot-Marie-Tooth disease type 2: Pathomechanism insights and phenotypic spectrum widening. Eur J Neurol 29:2056-2065 (2022). PubMed: 35286755
- Zhang R et al. Cell populations in neonatal rat peripheral nerves identified by single-cell transcriptomics. Glia 69:765-778 (2021). PubMed: 33079428
- Bargagna-Mohan P et al. Corneal nonmyelinating Schwann cells illuminated by single-cell transcriptomics and visualized by protein biomarkers. J Neurosci Res 99:731-749 (2021). PubMed: 33197966
- Lim EF et al. Presence and activation of pro-inflammatory macrophages are associated with CRYAB expression in vitro and after peripheral nerve injury. J Neuroinflammation 18:82 (2021). PubMed: 33761953
- Donsante A et al. Controlling the Release of Neurotrophin-3 and Chondroitinase ABC Enhances the Efficacy of Nerve Guidance Conduits. Adv Healthc Mater 9:e2000200 (2020). PubMed: 32548984