MUSK Protein, Human, Recombinant (aa 433-783, His & GST)

Muscle, skeletal receptor tyrosine-protein kinase, also known as Muscle-specific tyrosine-protein kinase receptor, Muscle-specific kinase receptor, and MUSK, is a single-pass type I membrane protein that belongs to the protein kinase superfamily and tyr protein kinase family. MUSK contains one FZ (frizzled) domain, three Ig-like C2-type (immunoglobulin-like) domains, and one protein kinase domain. This protein is a muscle-specific tyrosine kinase receptor and it may play a role in clustering of the acetylcholine receptor in the postsynaptic neuromuscular junction. MUSK expression is increased in muscle cells stimulated with Wnt or at conditions when the Wnt signaling was activated. MUSK is a muscle-specific receptor tyrosine kinase that is activated by agrin. It has a critical role in neuromuscular synapse formation. MUSK is a receptor tyrosine kinase that is a key mediator of agrin's action and is involved in neuromuscular junction (NMJ) organization. Defects in the MUSK encoding gene are a cause of autosomal recessive congenital myasthenic syndrome (CMS). Congenital myasthenic syndromes are inherited disorders of neuromuscular transmission that stem from mutations in presynaptic, synaptic, or postsynaptic proteins. MUSK mutations lead to decreased agrin-dependent AChR aggregation, a critical step in the formation of the neuromuscular junction. Mutations in this receptor encoding gene also have been associated with the congenital myasthenic syndrome.

Pack Size	Availability	Price/USD	Quantity
50 μg	5 days	$ 498.00

Description

Species	Human
Expression System	Baculovirus-Insect Cells
Tag	His,GST
Accession Number	O15146-2
Synonyms	FADS, CMS9, muscle, skeletal, receptor tyrosine kinase
Construction	A DNA sequence encoding the C-terminal segment of human MUSK isoform 2 (O15146-2) (Arg 433-Val 783) was fused with the N-terminal polyhistidine-tagged GST tag at the N-terminus.
Protein Purity	> 90 % as determined by SDS-PAGE
Molecular Weight	68 kDa (predicted)

Endotoxin	< 1.0 EU per μg of the protein as determined by the LAL method
Formulation	Supplied as sterile 20mM Tris, 500mM NaCl, pH 7.4, 10mM GSHPlease contact us for any concerns or special requirements. Please refer to the specific buffer information in the hard copy of CoA.
Reconstitution	A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.
Stability & Storage	Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
Shipping	Kinases are highly recommended to be shipped at frozen temperature with blue ice or dry ice. Shipment made at ambient temperature may seriously affect the activity of the ordered products.
Research Background	Muscle, skeletal receptor tyrosine-protein kinase, also known as Muscle-specific tyrosine-protein kinase receptor, Muscle-specific kinase receptor, and MUSK, is a single-pass type I membrane protein that belongs to the protein kinase superfamily and tyr protein kinase family. MUSK contains one FZ (frizzled) domain, three Ig-like C2-type (immunoglobulin-like) domains, and one protein kinase domain. This protein is a muscle-specific tyrosine kinase receptor and it may play a role in clustering of the acetylcholine receptor in the postsynaptic neuromuscular junction. MUSK expression is increased in muscle cells stimulated with Wnt or at conditions when the Wnt signaling was activated. MUSK is a muscle-specific receptor tyrosine kinase that is activated by agrin. It has a critical role in neuromuscular synapse formation. MUSK is a receptor tyrosine kinase that is a key mediator of agrin's action and is involved in neuromuscular junction (NMJ) organization. Defects in the MUSK encoding gene are a cause of autosomal recessive congenital myasthenic syndrome (CMS). Congenital myasthenic syndromes are inherited disorders of neuromuscular transmission that stem from mutations in presynaptic, synaptic, or postsynaptic proteins. MUSK mutations lead to decreased agrin-dependent AChR aggregation, a critical step in the formation of the neuromuscular junction. Mutations in this receptor encoding gene also have been associated with the congenital myasthenic syndrome.