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Recombinant Mouse MSR1 protein (rFc Tag)

Species

Mouse

Purity

>90 %, SDS-PAGE

Tag

N-rFc

Activity

not tested

Cat no : Eg4727



Product Information

Purity >90 %, SDS-PAGE
Endotoxin <0.1 EU/μg protein, LAL method
Activity
Not tested
Expression HEK293-derived Mouse MSR1 protein Gln79-Ser458 (Accession# P30204-1) with a rabbit IgG Fc tag at the N-terminus.
GeneID 20288
Accession P30204-1
PredictedSize 68.8 kDa
SDS-PAGE 75-100 kDa, reducing (R) condition
Formulation Lyophilized from 0.22 μm filtered solution in PBS, pH 7.4. Normally 5% trehalose and 5% mannitol are added as protectants before lyophilization.
Reconstitution Briefly centrifuge the tube before opening. Reconstitute at 0.1-0.5 mg/mL in sterile water.
Storage Conditions
It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
  • Until expiry date, -20℃ to -80℃ as lyophilized proteins.
  • 3 months, -20℃ to -80℃ under sterile conditions after reconstitution.
Shipping The product is shipped at ambient temperature. Upon receipt, store it immediately at the recommended temperature.

Background

Macrophage scavenger receptor 1 (MSR1), also known as Scara1, is a type II transmembrane glycoprotein primarily expressed by microglia in the central nervous system (CNS) of mice. MSR1 plays a significant role in host defense against bacterial infections and has been implicated in the control of viral infections through autophagy. As an important phagocytic receptor, MSR1 can mediate the uptake of a wide range of ligands, including low-density lipoproteins, bacterial pathogens, and dead cells. This function is crucial for the clearance of misfolded protein aggregates, which may include prions, similar to its role in AD with Aβ. MSR1 contributes to inflammatory disorders and cancer. It has been shown to facilitate cellular entry of vesicular stomatitis virus (VSV) in an LDLR family-dependent manner and interacts with VSV glycoprotein G via its extracellular domains. Additionally, MSR1-mediated uptake of saturated fatty acids can activate JNK signaling and induce Tnf-α and Il-6 expression, leading to a phenotype switch from anti-inflammatory to pro-inflammatory.

References:

1. Jack Gudgeon. et al. (2022). Front Immunol. 13:1012002. 2. Long Yang. et al. (2020). Commun Biol. 3(1):556. 3. Bei Li. et al. (2021). J Mol Med (Berl). 99(6):877-887. 4. Duomeng Yang. et al. (2021). iScience. 24(6):102678.

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