Human LIFR _CD118 Protein Vector: HEK293
- Known as:
- Human LIFR _CD118 Protein Vector: HEK293
- Catalog number:
- 10135-H03H
- Product Quantity:
- 200μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human LIFR _CD118 Protein Vector: HEK293
Related genes to: Human LIFR _CD118 Protein Vector: HEK293
- Gene:
- LIFR NIH gene
- Name:
- LIF receptor subunit alpha
- Previous symbol:
- -
- Synonyms:
- CD118
- Chromosome:
- 5p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-08-24
- Date modifiied:
- 2019-04-10
Related products to: Human LIFR _CD118 Protein Vector: HEK293
Related articles to: Human LIFR _CD118 Protein Vector: HEK293
- Observational studies have linked the gut microbiota and inflammatory proteins to atrial fibrillation (AF), but confounding, reverse causation, and instrument validity remain concerns. - Source: PubMed
Publication date: 2026/09/25
Yi ChengchengZheng WenyuanZhao JingCai WeitingWang JunqianSong LiBai MingZhang Zheng - Osteosarcopenia, the coexistence of osteoporosis and sarcopenia, increases risks of falls, fractures, disability, and mortality in older adults. Exercise is widely recognized as the most effective non-pharmacological strategy to improve both muscle and bone health, yet the molecular mechanisms underlying coordinated musculoskeletal adaptation remain incompletely understood. Among exercise-responsive myokines, leukemia inhibitory factor (LIF), a member of the interleukin-6 cytokine family, has attracted increasing attention because it is rapidly induced by muscle contraction and mechanical loading. Upon binding to the LIF receptor (LIFR)/glycoprotein 130 (gp130) complex, LIF activates downstream Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signaling, which regulates satellite cell proliferation, muscle regeneration, osteoblast differentiation, and load-induced bone formation. Based on emerging evidence that is predominantly derived from indirect or context-specific studies, we propose that the LIF/LIFR/STAT3 signaling pathway may contribute to skeletal muscle homeostasis, bone remodeling, and mechanotransduction, and may potentially participate in muscle-bone crosstalk during exercise adaptation. In this review, we synthesize current evidence supporting this hypothesis, critically discuss its context-dependent effects, and highlight key knowledge gaps, particularly the lack of direct in vivo evidence in osteosarcopenia models. Overall, the LIF/LIFR/STAT3 signaling pathway may represent a biologically plausible candidate mechanism through which exercise may promote coordinated muscle-bone adaptation, although direct experimental validation, particularly in osteosarcopenia models, remains necessary before this pathway can be considered a therapeutic target. - Source: PubMed
Publication date: 2026/09/26
Yang ZehuiWu ChaoZou JunYuan Yu - Stuve-Wiedemann syndrome is a rare autosomal recessive bent-bone dysplasia characterized by dysautonomia and distinctive skeletal abnormalities, most commonly caused by biallelic LIFR variants. - Source: PubMed
Publication date: 2026/09/11
Ürel Demir GizemAçıkgöz Nazlı BüşraUtine Gülen EdaŞimşek Kiper Pelin Özlem - Fracture nonunion represents a biologically dysregulated repair state rather than a purely mechanical failure. This study investigated whether fibroblast- derived Leukemia Inhibitory Factor (LIF) contributes to nonunion by suppressing osteogenesis via canonical LIFR-containing STAT3 signalling. - Source: PubMed
Publication date: 2026/09/15
Lu TianchaoWang DongGong MaoqiLi ZiyiWang HanzhouZhou Junlin - Stüve-Wiedemann syndrome (SWS) is an ultra-rare autosomal recessive skeletal dysplasia caused by loss-of-function variants in the leukemia inhibitory factor receptor () gene. While characterized by bone deformities and dysautonomia, severe persistent pulmonary hypertension of the newborn (PPHN) significantly contributes to high early mortality. We report a neonate with genetically confirmed SWS who presented with severe, suprasystemic PPHN refractory to standard pulmonary vasodilators, including inhaled nitric oxide. This case provides a detailed longitudinal hemodynamic characterization of severe suprasystemic PPHN in genetically confirmed SWS, including serial assessment of pulmonary pressures, shunt direction, and right ventricular function during treatment. Rather than identifying PPHN as a novel manifestation of SWS, it extends the phenotypic and hemodynamic characterization of pulmonary vascular involvement in this rare disorder. - Source: PubMed
Publication date: 2026/08/31
Chojnacka KarolinaSibrecht GretaGruca-Stryjak KarolinaSzczapa Tomasz