MUSK Proteins, Antibodies, cDNA Clones Research Reagents

MUSK (Muscle Associated Receptor Tyrosine Kinase, also known as CMS9; FADS; FADS1), located on 9q31.3, is conserved in chimpanzee, Rhesus monkey, dog, cow, mouse, rat, chicken, zebrafish, fruit fly, mosquito, and frog. The gene produces a 97056 Da protein composed of 869 amino acids. This gene encodes a muscle-specific tyrosine kinase receptor. Diseases such as Fetal Akinesia Deformation Sequence 1 and Myasthenic Syndrome, Congenital, 9, Associated With Acetylcholine Receptor Deficiency are associated with MUSK. The related pathways of MUSK include Degradation of the extracellular matrix and Activation of cAMP-Dependent PKA.

MUSK Protein (1)

    MUSK Antibody (1)

      MUSK cDNA Clone (4)


      In expression vector

      In lentiviral vector


      In expression vector

      MUSK qPCR Primer (1)

      MUSK Lysate (1)

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        MUSK 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.

        MUSK References

        • Glass D, et al. (1996) Agrin acts via a MuSK receptor complex. Cell. 85 (4): 513-23.
        • DeChiara T, et al. (1996) The receptor tyrosine kinase MuSK is required for neuromuscular junction formation in vivo. Cell. 85 (4): 501-12.
        • Hoch W, et al. (2001) Auto-antibodies to the receptor tyrosine kinase MuSK in patients with myasthenia gravis without acetylcholine receptor antibodies. Nat Med. 7 (3): 365-8.

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