Recombinant Cynomolgus Monkey MuSK His-tag Protein, CF

Recombinant Cynomolgus Monkey MuSK His-tag Protein, CF Summary

Product Specifications

Product Datasheets

Carrier Free

CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.

In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.

Background: MuSK

Muscle-specific kinase (MuSK), also known as muscle skeletal receptor tyrosine-protein kinase, is a single-pass transmembrane protein belonging to the protein kinase superfamily (1). Cynomolgus MuSK consists of an extracellular domain (ECD) with 3 immunoglobulin-like domains and a cysteine-rich domain (CRD), a transmembrane domain, and a cytoplasmic domain with a tyrosine kinase domain (2). Within the mature ECD, cynomolgus MuSK shares 99% and 91% amino acid sequence identity with human and mouse MuSK, respectively. Alternative splicing of MuSK results in multiple isoforms which could result in altered properties and functions (3,4). MuSK is expressed by skeletal muscle cells and excitatory neurons in the central nervous system (CNS) (1, 2). MuSK is essential for neuromuscular synapse formation and activation of the MuSK signaling cascade is critical for proper signaling between motor neurons and skeletal muscle (1-4). Once activated, MuSK stimulates the pathways that facilitate transcription of genes which encode synaptic proteins in muscle, activate retrograde signaling which promotes presynaptic differentiation, and cluster and anchor acetylcholine receptors (AChRs) (1, 5). Low-density lipoprotein receptor-related protein-4 (Lrp4), is the ligand for MuSK, and its binding affinity is potentiated by agrin (3). Mutant mice lacking agrin, MuSK, and Lrp4 fail to form neuromuscular junctions (NMJ) and subsequently died at birth due to respiratory failure (2, 3). In the presence of mutations which impair MuSK kinase activity or downstream signaling from MuSK, synapses become both structurally and functionally defective, leading to congenital myasthenia (6). The autoimmune disease myasthenia gravis is another neuromuscular disease caused by autoantibodies to AChRs, MuSK or Lrp4 (6).

Related Research Areas

• Receptor Tyrosine Kinases (RTKs)
• Synaptic Proteins
• Wnt Receptors