1. Measured by its ability to bind mouse LIF-Fc in a functional ELISA. 2. Measured by its ability to inhibit the recombinant human LIF mediated inhibition in the M1 mouse myeloid leukemia cells. The ED50 for this effect is typically 5-20 ng/mL in the presence of 2 ng/mL recombinant human LIF.

LIFR Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 90 kDa and the accession number is P42703-1.

Mouse

HEK293 Cells

LIF,leukemia inhibitory factor receptor α,leukemia inhibitory factor receptor alpha,AW061234,A230075M04Rik

A DNA sequence encoding the extracellular domain of mouse LIFR (NP_038612.1) (Met 1-Ser 828) was expressed, with a polyhistidine tag at the C-terminus. Predicted N terminal: Leu 44

> 95 % as determined by SDS-PAGE

A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.

It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.

LIFR (leukemia inhibitory factor receptor) belongs to the family of cytokine receptors. LIFR forms a high-affinity receptor complex with gp130, which mediates the activity of LIF (leukemia inhibitory factor) and thus affects the differentiation, proliferation, and survival of a wide variety of cells in the adult and the embryo. Besides LIF, LIFR can also bind to and activate CNTF (ciliary neurotrophic factor) and CLC (Cardiotrophin Like Cytokine). Evidence showed that in the retina, LIFR activating LIF, CT-1, and Cardiotrophin Like Cytokine (CLC) are strongly upregulated in response to preconditioning with bright cyclic light leading to robust activation of signal transducer and activator of transcription-3 (STAT3) in a time-dependent manner. Further, blocking LIFR activation during preconditioning using a LIFR antagonist (LIF05) attenuated the induced STAT3 activation and also resulted in reduced preconditioning-induced protection of the retinal photoreceptors. These data demonstrate that LIFR and its ligands play an essential role in endogenous neuroprotective mechanisms triggered by preconditioning-induced stress. LIFR was newly found to be a suppressor of hepatocellular carcinoma (HCC), one of the world's top five causes of cancer-related deaths.