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
- Preeclampsia (PE) is a severe pregnancy disorder caused by placental dysfunction. Protein O-fucosylation is a type of protein post translational modification that is catalyzed by protein O-fucosyltransferases (poFUTs). However, the role and underlying mechanisms of O-fucosylation/poFUT1 in PE remain elusive. Here, we revealed a lower level of poFUT1 in the plasma and placental tissues of PE patients than in normal pregnancy (NP) women. Moreover, poFUT1 deletion induced PE-like phenotypes in a mouse model. Mechanistically, we globally screened O-fucosylated proteins and identified EDIL3 with an O-fucosylation site at threonine 88. Furthermore, O-fucosylation-EDIL3 can directly interact with LIFR on trophoblasts, consequently activating the STAT3 signaling pathway, promoting the invasion and vascular remodeling ability of trophoblasts. Conversely, de-O-fucosylation-EDIL3 aggravated PE-like phenotypes by attenuating placental development in vitro and in vivo. Our data elucidate the function of poFUT1/O-fucosylation EDIL3/LIFR axis during placental development, providing glycol-based target for diagnostic and therapeutic of preeclampsia. - Source: PubMed
Publication date: 2026/05/13
Li YaqiWu HongpanLei YuyuBai ShuyuWang JiaoYan BinLiu YuboLiu Shuai - Liver sinusoidal endothelial cells (LSECs) play essential roles in liver regeneration after injury, but the underlying mechanisms remain incompletely defined. Here we report that leukemia inhibitory factor (LIF), which is rapidly induced after liver injury, acts as a key regulator of LSECs-driven liver regeneration through interaction with LSECs-enriched LIF receptor (LIFR). LIF directly stimulates LSECs proliferation and induces hepatocyte growth factor (HGF) release in a dose-dependent manner via LIFR signaling in LSECs, thereby indirectly promoting hepatocyte proliferation. Systemic LIF neutralization or endothelial cells (ECs)-specific loss impairs liver regeneration, whereas low-titer AAV-mediated LIF expression increases vascular density, elevates circulating HGF, and improves early liver recovery after partial hepatectomy (PHx) in mice. Together, these findings establish LIF-LIFR as a previously unrecognized endothelial axis to promote hepatocyte proliferation and suggest potential therapeutic strategies to enhance liver repair in patients. - Source: PubMed
Publication date: 2026/02/25
Zhou WenjingDiemer TanjaXin HongGinne Krishna ChaitanyaNaresh Kumar R NMori TommasoBiswas NilimaPiermarocchi CarloFerrara Napoleone - Heart failure (HF) is a critical condition characterized by the heart's inability to pump blood effectively, leading to significant morbidity and mortality. Inflammation and metabolic disturbances play key roles in its progression. This study is aimed at elucidating the causal relationships between inflammatory cytokines, metabolites, and HF using Mendelian randomization (MR). - Source: PubMed
Yao YanbingTang LinghuiZhou PeilinHuang FengZeng Zhiyu - Inflammation and immune response significantly contribute to brain injury following subarachnoid hemorrhage (SAH), a severe neurological condition. This study employed Mendelian randomization, colocalization, and multi-omics analysis to examine potential causal connections between inflammatory proteins, immune cells, and SAH, aiming to elucidate its pathogenesis. - Source: PubMed
Shi XingjieZhang ChengYang TaoSun ZhimingWang ChaoZhou LuchengHou ShiqiangLin NingZhang Lanlan - This study explores the transcriptomic, mutational, and immunogenic characteristics linked to significantly differentially expressed genes (DEGs) in colorectal (COAD), liver (LIHC), lung (LUAD), gastric (STAD), and breast (BRCA) cancers. Applying integrated bioinformatics algorithms, we discovered common upregulated and downregulated hub genes and assessed their prognostic importance, genomic modifications, copy number variations, functional enrichment, and pathway engagement. The persistent overexpression of ANLN and CTHRC1 in five cancer types, along with poor survival outcomes, underscores their suitability for multi-epitope vaccine development, emphasizing their antigenic potential and significance as universal therapeutic targets. Five genes-ABCA8, PDK4, MT1M, TMEM100, and LIFR-exhibited consistent downregulation and demonstrated tumor-suppressive characteristics. Genomic analyses demonstrated elevated mutation frequencies in ABCA8 and LIFR, predominantly C>T transitions that suggest age-related mutational signatures. Copy number alterations confirmed oncogenic amplifications (ANLN and CTHRC1) and tumor suppressor deletions (e.g., ABCA8). Functional enrichment associated differentially expressed genes with mitosis, chromosome segregation, and metabolic pathways. A multi-epitope vaccine targeting ANLN and CTHRC1 has been established leveraging predicted B-cell and T-cell epitopes, β-defensin as an adjuvant, and efficient linkers. Structural validation indicated desirable folding, stability, and solubility. The vaccine exhibited significant MHC binding, accomplishing 99% global population coverage, alongside strong immune simulation findings. Codon optimization and subsequent cloning into the pET28a(+) vector confirmed the preparation for bacterial expression. ANLN and CTHRC1 demonstrate significant targets for universal immunotherapy. The multi-epitope vaccine demonstrates significant efficacy in silico and has the potential to be widely employed as a cancer immunotherapeutic. - Source: PubMed
Publication date: 2026/04/19
Roy Suronjit KumarHasan RubaitBiswas Mohammad ShahangirPodder Munna KumarMoin Abu TayabPatil Rajesh B