Biotinylated Human Prolactin / PRL Protein, Fc,Avitag™
Proteins and Peptides
- 貨號 Cat. No.
- PRN-H82F7
- 規格 Size
- 200ug
- 品牌 Brand
- ACROBiosystems
- Species
- Human
- Conjugate
- Precision Avi
- Expression System
- HEK293
- Tag
- Avi Tag 、 Fc Tag
Description
Source :
Biotinylated Human Prolactin, Fc,Avitag (PRN-H82F7) is expressed from human 293 cells (HEK293). It contains AA Leu 29 - Cys 227 (Accession # Q5THQ0-1).
Molecule : Prolactin
Synonyms : PRL,Prolactin
Format : Powder
Category : MABSol® Biotin Labeled Proteins
Accession : NP_000939.1
Storage : -20℃
Shipping condition : Powder,RT
Molecular Weight : 51.2 kDa
Characteristics :
This protein carries a human IgG1 Fc tag at the C-terminus, followed by a Avi tag (Avitag™). The protein has a calculated MW of 51.2 kDa. The protein migrates as 57-66 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
Endotoxin Level : Less than 1.0 EU per μg by the LAL method.
Buffer : Tris with Glycine, Arginine and NaCl, pH7.5
Description :
Prolactin (gene name PRL) is a secreted neuroendocrine pituitary hormone that acts primarily on the mammary gland to promote lactation, but has pleiotropic effects in both males and females. Prolactin is synthesized as a prohormone. Following cleavage of the signal peptide, the length of the mature hormone is between 194 and 199 amino acids, depending on species. Hormone structure is stabilized by three intramolecular disulfide bonds. Excessive secretion of prolactin - hyperprolactinemia - is a relative common disorder in humans. This condition has numerous causes, including prolactin-secreting tumors and therapy with certain drugs. The prolactin receptor (gene name PRLR) is a transmembrane type I glycoprotein that belongs to the cytokine hematopoietic receptor family. Expression of the prolactin receptor is widespread. Each prolactin molecule is thought to bind two receptor molecules
References :
(1) Farfel A., et al. 2018, Pediatr Endocrinol Rev.,15(3), 216-222. (2) De Mello-Coelho V., et al. 1998, Dev Immunol., 6(3-4), 317-23. (3) Wennbo H., et al. 2000, Oncogene., 19(8),1072-6.

