FOLR1 Antibody

FOLR1 Antibody Datasheet

FOLR1 Antibody Product Information

• Immunogen: Recombinant Mouse FOLR1 protein (Catalog#50573-M08H)
• Antibody Type: Rabbit Polyclonal Antibody ( Antibody Purification Platform )
• Ig Type: Rabbit IgG
• Formulation: 0.2 μm filtered solution in PBS with 5% trehalose
• Preparation: Produced in rabbits immunized with purified, recombinant Mouse FOLR1 (rM FOLR1; Catalog#50573-M08H; NP_032060.2; Met 1-Met 231). Total IgG was purified by Protein A affinity chromatography.

FOLR1 Antibody Usage Guide

• Specificity: Mouse FOLR1
• Western blot: This antibody can be used at 1-2 μg/mL with the appropriate secondary reagents to detect Mouse FOLR1 in WB.
• Direct ELISA: This antibody can be used at 0.5-1.0 μg/mL with the appropriate secondary reagents to detect Mouse FOLR1. The detection limit for Mouse FOLR1 is approximately 0.0049 ng/well.
• Storage: This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free.
  Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.

FOLR1 Antibody Background

Folate receptor alpha, also known as Adult folate-binding protein, Folate receptor 1, Ovarian tumor-associated antigen MOv18, FOLR1 and FOLR, is a cell membrane protein which belongs to thefolate receptor family. FOLR1 is exclusively expressed in tissues of epithelial origin. Expression of FOLR1 is increased in malignant tissues. It is expressed in kidney, lung and cerebellum. FOLR1 is a membrane bound receptor involved in the transport of folate as well as other regulatory cellular processes. FOLR1 binds to folate and reduced folic acid derivatives and mediates delivery of 5-methyltetrahydrofolate to the interior of cells. Defects in FOLR1 are the cause of neurodegeneration due to cerebral folate transport deficiency (NCFTD). NCFTD is an autosomal recessive disorder resulting from brain-specific folate deficiency early in life. Onset is apparent in late infancy with severe developmental regression, movement disturbances, epilepsy, and leukodystrophy.

References

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