Recombinant Cynomolgus Monkey MuSK His-tag Protein, CF

In the presence of Recombinant Human Agrin (6624-AG), immobilized Recombinant Cynomolgus Monkey MuSK His-tag Protein (Catalog # 11153-MK) at 2 µg/mL (100 µL/well), Recombinant Human LRP-4 ( 5948-LR) binds with an ED50 of 25.0‑200 ng/mL.

2 μg/lane of Recombinant Cynomolgus Monkey MuSK His-tag Protein (Catalog # 11153-MK) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue staining, showing bands at 60-70 kDa.

• Reactivity: Pm-Cm
• Applications: Bioactivity
• Format: Carrier-Free

Recombinant Cynomolgus Monkey MuSK His-tag Protein, CF Summary

• Details of Functionality: Measured by its binding ability in a functional ELISA. In the presence of Recombinant Human Agrin (Catalog # 6624-AG), immobilized Recombinant Cynomolgus Monkey MuSK His-tag (Catalog # 11153-MK) at 2 µg/mL (100 µL/well), Recombinant Human LRP-4 (Catalog # 5948-LR) binds with an ED₅₀ of 25.0-200 ng/mL.
• Source: Chinese Hamster Ovary cell line, CHO-derived cynomolgus monkey MuSK protein
  Leu24-Thr495, with a C-terminal 6-His tag
• Accession #: XP_005581150.1
• N-terminal Sequence: Leu24
• Protein/Peptide Type: Recombinant Proteins
• Purity: >95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining
• Endotoxin Note: <0.10 EU per 1 μg of the protein by the LAL method.

Applications/Dilutions

• Dilutions:
  • Bioactivity
• Theoretical MW: 53 kDa.
  Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
• SDS-PAGE: 60-70 kDa, under reducing conditions.

Packaging, Storage & Formulations

• Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 3 months, -20 to -70 °C under sterile conditions after reconstitution.
• Buffer: Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose.
• Purity: >95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining
• Reconstitution Instructions: Reconstitute at 500 μg/mL in PBS.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for Recombinant Cynomolgus Monkey MuSK His-tag Protein, CF

• EC 2.7.10
• EC 2.7.10.1
• MGC126323
• MGC126324
• muscle, skeletal, receptor tyrosine kinase
• MuSK
• skeletal receptor tyrosine-protein kinase

Background

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).

1. Burden, S.J. et al. (2013) CSH Perspectives Bio. 5(5).
2. Hubbard, S.R. and Gnanasambandan, K. (2013) Biochem Biophys. Acta. 1834:2166.
3. Nasrin, F. et al. (2014) Sci. Rep. 4:6841.
4. Kuehn, R. et al. (2005) Gene 360:83.
5. Camurdanoglu, B.Z. et al. (2016) Sci. Rep. 6:33583.
6. Herbst, R. (2020) Neurosci. Lett. (2020) 716:134676.

Bioinformatics

• Uniprot:
  • XP_005581150.1()