Recombinant Human Leptin Protein, N-PEG-tag (E. coli)

Cat. No.: OB0626-WX5

Species: Human

Origin: Recombinant

Conjugation: Unconjugate

Size:

INQUIRY Datasheet MSDS

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Product Overview

Description: Recombinant Human Leptin Protein is expressed in E. coli with an N-PEG tag. Produced in a cost-effective E. coli expression system. Recombinant human leptin protein with a PEG Tag is a chemically modified cytokine engineered with polyethylene glycol to resist proteolytic degradation and reduce renal clearance. Featuring a drastically extended circulating half-life, it is optimized for chronic in vivo animal model injections.

Source: Escherichia coli

Molecular Weight: 20 kDa

Bioactivity: The biological activity is <0.5% as determined by a cell proliferation assay using BaF/3 cells stably transfected with the long form of human leptin receptor.

Tag: N-terminal PEG

Purity: >99% by SDS-PAGE and gel filtration

Applications: ELISA; WB; Functional Assay; Cell Culture; Binding Assay; SPR; BLI; FACS; Positive Control

Specification

Concentration: 0.65 mg/mL

Formulation: Lyophilized from a sterile sodium bicarbonate solution.

Storage: Storage at -20°C.

Shipping Condition: Shipped with blue ice.

Handling Notes: During shipping, trace amounts of the recombinant protein may adhere to the interior surface of the vial cap. Before opening, it is highly recommended to briefly centrifuge the vial to bring all contents to the bottom. Avoid repeated freeze-thaw cycles to prevent activity loss.

Target Profile

Full Name: Leptin

Alternative Names: rHuLeptin; Obesity factor; Obesity protein; OB; Lep

Gene ID: 3952

Uniprot ID: P41159

Accession Number: NP_000221.1

Summary: Leptin (LEP) is an adipocyte-derived hormone secreted by white adipocytes into the systemic circulation, where it governs energy homeostasis. By binding its receptor in the brain, leptin activates downstream signaling that suppresses feeding and increases energy expenditure, while additionally exerting endocrine actions on immune and inflammatory responses, hematopoiesis, angiogenesis, reproduction, bone formation, and wound healing. Mutations within LEP or its regulatory regions cause severe and morbid obesity with hypogonadism in patients and contribute to the development and progression of type 2 diabetes mellitus.

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