Human Nr4a1 Protein, His Tag (MALS verified)

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NR1-H5144-100ug
$410.00
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NR1-H5144-1mg (200ug X 5)
$2,885.00
NR1-H5144
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Synonyms

Nuclear receptor subfamily 4 group A member 1

Source

Human Nr4a1 Protein, His Tag (NR1-H5144) is expressed from E. coli cells. It contains AA Ser 351 - Phe 598 (Accession # P22736-1).

Predicted N-terminus: Met

Molecular Characterization

This protein carries a polyhistidine tag at the N-terminus.

The protein has a calculated MW of 29.5 kDa. The protein migrates as 25 kDa and 29-30 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE).

Purity

>90% as determined by SDS-PAGE.

>90% as determined by SEC-MALS.

Formulation

Lyophilized from 0.22 μm filtered solution in PBS, 0.2 M Arginine, pH7.4 with trehalose as protectant.

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Reconstitution

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

Shipping and Storage

This product is shipped at ambient temperature.

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:
  • -20°C to -70°C for 12 months in lyophilized state;
  • -70°C for 3 months under sterile conditions after reconstitution.

Background

Orphan nuclear receptor 4A1(NR4A1) belongs to the NR4A superfamily and plays an important role in inflammation, cell metabolism, proliferation and differentiation. NR4A1 expression can be induced by various stimuli in macrophages. NR4A1 has a bidirectional effect of inhibiting or promoting the inflammatory response of atherosclerosis (AS), which may be related to the different microenvironment, cell phenotype and transfection vector. NR4A1 can promote pathological angiogenesis, which is an important factor affecting plaque instability. The role of NR4A1 in inflammation and pathological angiogenesis of AS was reviewed, in order to provide a target for the treatment of stable plaque and provide a reference for the prevention and treatment of AS.