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Authors demonstrate heterozygous novel or rare LIFR mutations in 3.3% of CAKUT patients, and provide evidence that Lifr deficiency and deactivating LIFR mutations cause highly similar anomalies of the urogenital tract in mice and humans.
uterine expression of the LIFR is essential for embryo implantation; this further define the components of the LIF signaling pathway necessary for effective implantation.
OSM (mOSM) signals mainly via an OSM receptor (OSMR)-gp130 heterodimer and binds with only very low affinity to mLIFR.
The predominant role of leukemia inhibitory factor receptor in skeletal muscle regeneration appears to be in regulating the inflammatory response rather than directly effecting myogenic cells.
both LIFR and gp130 protein expression were increased in the sciatic nerve and gastrocnemius muscle of diabetic mice.
Data confirmed that LIF and the LIFR were up-regulated in intra-implantation sites compared to inter-implantation sites on Day 5 of gestation.
Data demonstrate that T cells retain responsiveness to a LIF/Nanog axis and that this axis is linked to MARCH-7, a RINGv E3 ligase that regulates the LIF-receptor.
Neuropoietin induced activation of STAT3 tyrosine phosphorylation in adipocytes is independent of LIFR phosphorylation and degradation.
Review. The structure and function of the LIF-R gene and protein and the role of its cytoplasmic domain in myeloid leukemia cells are reviewed.
directly prevents oligodendrocyte death in animal models of multiple sclerosis
LIFR plays a role in modulating fetal response to high maternal glucocorticoids in late gestation, likely mediated through the glucocorticoid receptor, with implications for adult homeostasis as a direct tie between immune, neural & hormone function.
LIFR signaling can exert negative regulatory effects on neurite extension and branching of sympathetic neurons
Although not necessary for neural stem cell self-renewal, LIFR activation enhances both the clonogenicity and expression of glial fibrillary acid protein (GFAP) by these multipotential cells.
Lifr -/- mice demonstrate elevated pituitary glucocorticoid (GR) and mineralocorticoid (MR) receptor mRNA and protein levels, indicating the importance of LIF signaling for hypothalamic-pituitary adrenal axis development.
expression and function of LIF and its receptor in the pancreas
In embryonic deficient mice, preganglionic sympathetic neurons were reduced. (Leukemia inhibitory factor receptor beta)
Data show that demyelination induces oligodendrocyte expression of SOCS3, that this induction depends on leukemia inhibitory factor (LIF) and LIF receptors, and that endogenous LIF may be a key determinant of the CNS response to oligodendrocyte loss.
s-SHIP associates with gp130, which forms a heterodimeric complex with the leukemia inhibitory factor receptor (LIFR).
provides a structural template to understand the formation and orientation of the high-affinity signaling complex between LIF, LIF receptor, and gp130
From the analysis of lifr beta mutant embryos, it was established that LIFR beta is necessary for fbm neurons' identity determination and is implicated in astrocyte and oligodendrocyte differentiation, specifically within the facial nucleus.
LIFR may be a novel negative regulator during the early stage of human bone marrow mesenchymal cell osteogenic differentiation.
Data suggest that mitogen-activated protein kinase kinase 6 (MAP2K6) might be an important regulator of leukemia inhibitory factor receptor (LIFR)-induced radioresistance in nasopharyngeal carcinoma cells (NPC).
Mechanistically, nPAK4 promoted the metastasis of ERalpha-positive breast cancer cells by targeting LIFR, a bone metastasis suppressor. Strikingly, the nuclear accumulation of PAK4 might promote aggressive phenotypes, highlighting nPAK4 as a novel predictive biomarker for ERalpha-positive breast cancer bone metastasis.
LncRNA-LOWEG is a tumor suppressor that inhibits Gastric cancer cell invasion. And LIFR gene is up-regulated by lncRNA-LOWEG.
High levels of LIFR in colorectal cancer (CRC) facilitated proliferation and migration of endothelial cells, resulting in an increase in angiogenic activity. Moreover, IL-8 was found to play a role in the LIFR induced angiogenesis. IL-8 levels were correlated with LIFR levels in CRC tissues, whereas depletion of IL-8 led to a reduced angiogenic activity of LIFR in CRC cells.
These data indicate that miR-377-3p suppressed adipogenesis of human bone marrow mesenchymal stem cells by targeting LIFR, which provides novel insights into the molecular mechanism of miRNA-mediated cellular differentiation.
High expression of LIFR is associated with preeclampsia.
LIFR attenuates tumor metastasis by suppressing YAP expression, suggesting that LIFR may serve as a potential target for clear cell renal cell carcinoma treatment.
Decreased serum LIF levels may be associated with vasculopathy in systemic sclerosis (SSc) and that Fli1 deficiency may contribute to the inhibition of LIF-dependent biological effects on SSc endothelial cells by suppressing the expression of LIF, LIF receptor, and gp130.
Data show that lncRNA-CTD-2108O9.1 represses metastasis by targeting leukemia inhibitory factor receptor (LIFR).
Significant reduction in LIFR expression and the reduced activation of subsequent signaling strongly suggest a working model of how the implantation markers, LIF, may affect the endometrium of patients with adenomyosis.
study indicated impaired LIF expression levels only in women with unexplained infertility, while LIF-R expression was impaired in all sub-groups of infertile women.
Expression of cancer-specific glycan epitopes represents an excellent opportunity for diagnostics and potentially specific detection of tumors. Here, we report four proteins (LIFR, CE350, VP13A, HPT) found in sera from pancreatic cancer patients carrying aberrant glycan structures as compared to those of controls.
Endometrial expression of LIF and LIFR is significantly reduced in the epithelial cells of infertile women.
LIFR inhibited the expression of beta-catenin.
The Leukemia Inhibitory Factor Receptor Gene Is a Direct Target of RUNX1
We report the case of a girl with Stuve-Wiedemann syndrome confirmed on molecular analysis.
The C65S mutant LIFR showed altered glycosylation and an elevated expression level that might be attributed to a slow turnover of the mutant form.
High LIFr expression stimulates melanoma cell migration and is associated with unfavorable prognosis in melanoma.
These findings expand our knowledge on the role of the LIF-LIFR signal pathway in early rabbit embryogenesis and rabbit embryonic stem cell establishment.
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.
, LIF receptor
, leukemia inhibitory factor receptor alpha chain
, soluble differentiation-stimulating factor receptor
, CD118 antigen
, leukemia inhibitory factor receptor
, leukemia inhibitor factor receptor alpha-chain
, cytokine receptor-beta