Anti Schwann Cell/Peripheral Myelin mAb (Clone Schwann/2E)

Catalog No:
CAC-GU01-M01AS-A
$314.00

Catalog numbers beginning with "CAC" are antibodies from our exclusive Cosmo Bio Antibody Collection. Visit the CAC Antibody homepage to browse the collection list, organized by research topic.

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Application: IHC(p) 
Clonality: Monoclonal 
Host: Mouse 
Purification: Ascities 
Reactivity: Mouse, Rat, Human 

Myelin is a lipid-rich (fatty) substance formed in the central nervous system (CNS) by glial cells called oligodendrocytes, and in the peripheral nervous system (PNS) by Schwann cells. Myelin insulates nerve cell axons to increase the speed at which information (encoded as an electrical signal) travels from one nerve cell body to another (as in the CNS) or, for example, from a nerve cell body to a muscle (as in the PNS). The myelinated axon can be likened to an electrical wire (the axon) with insulating material (myelin) around it. However, unlike the plastic covering on an electrical wire, myelin does not form a single long sheath over the entire length of the axon. Rather, each myelin sheath insulates the axon over a single section and, in general, each axon comprises multiple long myelinated sections separated from each other by short gaps called Nodes of Ranvier. Each myelin sheath is formed by the concentric wrapping of an oligodendrocyte or Schwann cell process around the axon. More precisely, myelin speeds the transmission of electrical impulses called action potentials along myelinated axons by insulating the axon and reducing axonal membrane capacitance. On a molecular level, it increases the distance between the cations on the outside of the axon and the Na⁺ ions that move through the axoplasm during an action potential, thereby greatly reducing the magnitude of the repulsive forces (which are inversely proportional to the square of the distance, as per Coulomb's law) between them that would otherwise act to inhibit the movement of the Na⁺-ions. The discontinuous structure of the myelin sheath results in saltatory conduction[1][2] whereby the action potential "jumps" from one node of Ranvier, over a long myelinated stretch of the axon called the internode, before "recharging" at the next node of Ranvier, and so on, until it reaches the axon terminal. Nodes of Ranvier are the short (~1 micron) unmyelinated regions of the axon between adjacent long (~0.2 mm - >1 mm) myelinated internodes. Once it reaches the axon terminal, this electrical signal provokes the release of a chemical message or neurotransmitter that binds to receptors on the adjacent post-synaptic cell (e.g. nerve cell in the CNS or muscle cell in the PNS) at specialized regions called synapses. This "insulating" role for myelin is essential for normal motor function (i.e. movement such as walking), sensory function (e.g. hearing, seeing or feeling the sensation of pain) and cognition (e.g. acquiring and recalling knowledge), as demonstrated by the consequences of disorders that affect it, such as the genetically determined leukodystrophies;[3] the acquired inflammatory demyelinating disorder, multiple sclerosis;[4] and the inflammatory demyelinating peripheral neuropathies.[5] Due to its high prevalence, multiple sclerosis, which specifically affects the central nervous system (brain, spinal cord and optic nerve), is the best known disorder of myelin. [from: Wikipedia contributors. (2019, June 2). Myelin. In Wikipedia, The Free Encyclopedia. Retrieved 20:18, June 4, 2019, from https://en.wikipedia.org/w/index.php?title=Myelin&oldid=899981120]

References:
1) Nakazato Y, et al.: Monoclonal antibodies which recognize phosphorylated and nonphosphorylated epitopes of neurofilament protein. Biomed Res 1987, 8:369-376.
2) Arai H, et al. (1998) A novel marker of Schwann cells and myelin of the peripheral nervous system. Pathology Int. 48:206-214.
3) 新井華子, 他 (1998) シュワン細胞と末梢性髄鞘の新しいマーカー(Schwann/2E 抗体)によるシュワン細胞由来腫瘍の検索. Kitakanto Med. J. 48:1-8.
4) Jasmin L, et a. (2000) Schwann cells are removed from the spinal cord after effecting recovery from paraplegia. J Neurosci. 20:9215-9223.
5) Jasmin L, et al. (2002) Remyelination within the CNS: do schwann cells pave the way for oligodendrocytes? Neuroscientist

Documents & Links for Anti Schwann Cell/Peripheral Myelin mAb (Clone Schwann/2E)
Datasheet Anti Schwann Cell/Peripheral Myelin mAb (Clone Schwann/2E) Datasheet

Documents & Links for Anti Schwann Cell/Peripheral Myelin mAb (Clone Schwann/2E)
Datasheet Anti Schwann Cell/Peripheral Myelin mAb (Clone Schwann/2E) Datasheet

Citations for Anti Schwann Cell/Peripheral Myelin mAb (Clone Schwann/2E) – 5 Found
Sano et al. 2019. Subendocardial nodular proliferation of myofibroblasts in a laboratory beagle. J Tox Path. :.  Journal
Simonetti et al. 2014. Wnt-Fzd signaling sensitizes peripheral sensory neurons via distinct noncanonical pathways. Neuron. 83(1):104-21.   PubMed, Journal
Willoughby et al. 2012. Effects of the sustained release of IGF-1 on extraocular muscle of the infant non-human primate: adaptations at the effector organ level. Invest Ophthalmol Vis Sci. 53(1):68-75.   PubMed, Journal
Di Maio et al. 2011. In vivo imaging of dorsal root regeneration: rapid immobilization and presynaptic differentiation at the CNS/PNS border. J Neurosci. 31(12):4569-82.   PubMed, Journal
Jasmin et al. 2000. Schwann cells are removed from the spinal cord after effecting recovery from paraplegia. J Neurosci. 20(24):9215-23.   PubMed, Journal