Anti-LIFR/CD118 antibody

Anti-LIFR/CD118 antibody

• DataSheet
• Material Safety Data Sheets (MSDS)

Mouse monoclonal to LIFR/CD118

ELISA, IHC-P

Human LIFR / CD118
No cross-reactivity with Human cell lysate (293 cell line) in WB and ELISA.

SWS antibody; SJS2 antibody; STWS antibody; CD118 antibody; LIF-R antibody; LIF antibody; AW061234 antibody; A230075M04Rik antibody; CD118 antibody; FLJ98106 antibody; FLJ99923 antibody; LIFR antibody; LIF-R antibody; SJS2 antibody; STWS antibody; SWS antibody

Mouse IgG1

This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human LIFR / CD118 (rh LIFR; NP_001121143.1; Met 1-Ser 833). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.

Monoclonal

0.2 μm filtered solution in PBS with 5% trehalose

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 -80℃. 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.

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.

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