Recombinant Human CFHR1 protein(Met1-Arg330), His-tagged

• Cat.No.: CFHR1-8555H
• Product Overview: Recombinant Human CFHR1 (Q03591) (Met1-Arg330) was expressed in HEK293 with a polyhistidine tag at the C-terminus.

Specification

• Species: Human
• Source: HEK293
• Tag: His
• Protein Length: Met1-Arg330
• Form: Lyophilized from sterile PBS, pH 7.4. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.
• Molecular Mass: The recombinant human CFHR1 consists of 323 amino acids and predicts a molecular mass of 37.2 KDa. It migrates as an approximately 45 KDa band in SDS-PAGE under reducing conditions.
• Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method.
• Purity: > 95 % as determined by SDS-PAGE
• Storage: Samples are stable for up to twelve months from date of receipt at -20°C to -80°C. Store it under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
• Reconstitution: It is recommended that sterile water be added to the vial to prepare a stock solution of 0.2 ug/ul. Centrifuge the vial at 4°C before opening to recover the entire contents.

Gene Information

• Gene Name: CFHR1 complement factor H-related 1 [ Homo sapiens ]
• Official Symbol: CFHR1
• Synonyms: CFHR1; complement factor H-related 1; CFHL1, CFHL1P, CFHR1P, complement factor H related 1 pseudogene , H factor (complement) like 1 , H factor (complement) like 2 , HFL1, HFL2; complement factor H-related protein 1; CFHL; FHR1; H36 1; H36 2; H36; FHR-1; H-factor-like 1; h factor-like protein 1; H factor (complement)-like 1; H factor (complement)-like 2; complement factor H-related 1 pseudogene; HFL1; HFL2; CFHL1; H36-1; H36-2; CFHL1P; CFHR1P; MGC104329
• Gene ID: 3078
• mRNA Refseq: NM_002113
• Protein Refseq: NP_002104
• MIM: 134371
• UniProt ID: Q03591

Case Study

Case 1: Papp A, et al. Front Immunol. 2022

When ECM components meet body fluids, they can trigger complement activation and cause inflammation in places like the kidneys and eyes. Usually, complement inhibitors like factor H (FH) keep this in check. Proteins FHR1 and FHR5, linked to these diseases, were studied to see if they interact with ECM components. Both FH and FHRs showed varied binding to ECM, with FHR1 and FHR5 connecting to specific ECM parts like laminin and fibromodulin through distinct domains. FHR1 and FHR5 also affected FH's activity, reducing its cofactor function and enhancing complement pathway activation, leading to more C3 fragments being deposited.

Fig1. FHR1 binding to ECM ligands was analyzed by protein microarray.

Fig2. ECM protein microarray to analyze the effect of FHR1 and FHR5 on terminal complement pathway activation.

Case 2: Togarsimalemath SK, et al. Kidney Int. 2017

The complement factor H family often recombines, leading to gene deletions or abnormal proteins associated with certain kidney diseases. Researchers found a 146 Kbp deletion in some CFHR genes creating a CFHR1-R5 hybrid protein in four family members with kidney problems. They showed low C3 and factor B levels and high sC5b9 and Bb fragments, indicating an issue in the alternative pathway. The abnormal protein was tied to CFHR1 and CFHR2, affecting Factor H activity on C3 convertase decay.

Fig1. Study of multimerization.

Fig2. Pulldown experiment.

Application

Recombinant CFHR1 protein is gaining attention because it might help with certain immune-related kidney issues. Thinking about conditions like atypical Hemolytic Uremic Syndrome, where the immune system can damage the kidneys, researchers see potential in CFHR1 to calm things down. It acts like the body's natural controls, opening new possibilities for treatments. Beyond the kidneys, this protein also has potential in treating eye conditions such as age-related macular degeneration, which is a big player in vision loss. Because it's lab-made, scientists can tweak and test it to see what works best. This adaptability is exciting because it brings us closer to personalized medicine, where treatments could be tailored specifically to each person's genetic makeup.

Fig1. Complement activation pathways. (Christine Skerka, 2013)