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Validated All-in-One™ qPCR Primer for LIFR(NM_001127671.2) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes a protein that belongs to the type I cytokine receptor family. This protein combines with a high-affinity converter subunit, gp130, to form a receptor complex that mediates the action of the leukemia inhibitory factor, a polyfunctional cytokine that is involved in cellular differentiation, proliferation and survival in the adult and the embryo. Mutations in this gene cause Schwartz-Jampel syndrome type 2, a disease belonging to the group of the bent-bone dysplasias. A translocation that involves the promoter of this gene, t(5;8)(p13;q12) with the pleiomorphic adenoma gene 1, is associated with salivary gland pleiomorphic adenoma, a common type of benign epithelial tumor of the salivary gland. Multiple splice variants encoding the same protein have been found for this gene. [provided by RefSeq].
Gene References into function
- Review. The structure and function of the LIF-R gene and protein, mRNA processing, and its role in tumor cells are reviewed.
- upper cytokine-binding module and the Ig-like domain of the leukaemia inhibitory factor (LIF) receptor are sufficient for a functional LIF receptor complex
- Separate functions for the two modules of the membrane-proximal cytokine binding domain of glycoprotein 190, the leukemia inhibitory factor low affinity receptor, in ligand binding and receptor activation (gp190)
- interactions of CNTFR with LIFR and gp130 in vitro
- Leukemia inhibitory factor (LIF), cardiotrophin-1, and oncostatin M share structural binding determinants in the immunoglobulin-like domain of LIF receptor
- mutations alter the stability of LIFR messenger RNA transcripts, resulting in the absence of the LIFR protein and in the impairment of the JAK/STAT3 signaling pathway in patient cells
- immunocytochemical staining and mRNA expression of LIF and its receptor are consistent with the concept that LIF might be involved in growth initiation of human primordial follicles through its receptor
- At early human post-implantation stage, LIF is produced from decidua and chorionic villi and may exert its action on trophoblasts. Anembryonic pregnancy cannot be accounted for by defective expression of either LIF or LIF-Rbeta in most circumstances.
- In cells overexpressing a LIFR mutant with the N-terminal cytokine binding domain deleted, signaling by ciliary neurotrophic factor was abolished.
- Down-regulation of PRB in the endometrium is concomitant with the presence of glycodelin in the endometrium, suggesting interaction.
- Expression of leukemia inhibitory factor and its receptor is low in undifferentiated human embryonic stem cells but increases during differentiation.
- sOSMR is able to bind OSM and interleukin-31 when associated to soluble gp130 or soluble interleukin-31R, respectively, and to neutralize both cytokine properties
- The regulation of LIF and its receptor (LIFR) expression in pancreatic carcinoma cells were studied.
- Results present the biophysical and structural characterization of the full-length, transmembrane form of a quaternary cytokine receptor complex consisting of gp130, LIF-R, Ciliary Neurotrophic Factor (CNTF), and its alpha receptor (CNTF-Ralpha).