MYLK{myosin light chain kinase}rabbit.pAb
- Known as:
- MYLK{myosin light epitope phosphorylation catalyst}host: rabbit.pAb
- Catalog number:
- 201-20-3590
- Product Quantity:
- 0.2ml
- Category:
- -
- Supplier:
- Shanghai Sunred
- Gene target:
- MYLK{myosin light chain kinase}rabbit.pAb
Related genes to: MYLK{myosin light chain kinase}rabbit.pAb
- Gene:
- FCGRT NIH gene
- Name:
- Fc fragment of IgG receptor and transporter
- Previous symbol:
- -
- Synonyms:
- FCRN, alpha-chain
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-23
- Date modifiied:
- 2016-10-05
Related products to: MYLK{myosin light chain kinase}rabbit.pAb
Related articles to: MYLK{myosin light chain kinase}rabbit.pAb
- The neonatal fc receptor (FcRn) is indispensable in sustaining IgG homeostasis. Recently, the potential role of FcRn in infectious diseases has attracted more attention. However, the function of FcRn in tuberculosis is unclear. The present study aimed to investigate the role of FcRn in regulating BCG infection-induced autophagy in vitro and vivo. FCGRT knockout mice and FcRn knockdown cells were constructed by CRISPR/Cas9 and small interfering RNA. The related indicators of autophagy were detected by transmission electron microscopy, flow cytometry, and western blot. The proteins interacting with FcRn were screened by immunoprecipitation (IP) and mass spectrometry (MS). The results showed more lung injury and less autophagy marker expression in the KO-FcRn mice lungs than wild type (WT) mice after BCG infection (p < 0.01). Meanwhile, si-FcRn restrained BCG-induced macrophage autophagy by activating the PI3K/AKT/m-TOR pathway. Furthermore, FcRn was confirmed to interact with the Y-box binding protein 1 (YBX1) and promote its nuclear translocation. Hence, the current study proved that FcRn protects against BCG-induced lung injury by triggering YBX1-mediated autophagy and suppressing the PI3K /AKT/mTOR signaling pathway. These findings present a novel understanding of the immune role of FcRn in treating and preventing tuberculosis. - Source: PubMed
Publication date: 2026/02/02
Xu YananGong ZhaoqianYu JialinZhang JiameiDeng GuangcunWu Xiaoling - Colorectal cancer (CRC) is a global health issue influenced by both genetic and environmental factors. Identifying key genes closely associated with CRC is crucial for understanding its pathological mechanisms and discovering therapeutic targets. This study aimed to integrate multi-omics datasets and Mendelian randomization (MR) approaches to identify CRC-related genes and to clarify their roles in tumor immunity and therapeutic potential. - Source: PubMed
Publication date: 2025/11/26
Zhou ShengyiZhang XinyiWang ShiwenZhou YunfanSun Yizhou - Identifying biomarkers that predict social and cognitive outcomes in individuals at ultra-high risk (UHR) for psychosis remains a key challenge in preventive psychiatry. While genetic factors contribute to psychosis vulnerability, specific markers that predict individual trajectories of functional decline or resilience are still unclear. - Source: PubMed
Publication date: 2025/10/27
Doborjeh ZohrehSumich AlexanderMedvedev Oleg NBuchwald KhanDoborjeh MaryamSingh BalkaranBudhraja SugamMerkin AlexanderLam MaxYee Jie YinLee Tih-ShihGoh WilsonLee JimmyWilliams MargaretLai Edmund M-KKasabov Nikola K - IgG-based therapeutic antibodies are increasingly adopted for diverse human diseases, such as cancer and autoimmune disorders displaying remarkable therapeutic performance. A key factor in their success lies in the extended half-life of IgG molecules, which is regulated by the pH-dependent interaction between IgG and neonatal Fc receptor (FcRn). This interaction prevents lysosomal degradation of IgG. Despite the frequent use of humanized rodent models expressing human FcRn (hFcRn) in preclinical studies, these models often fail to accurately replicate human antibody pharmacokinetics (PK) due to the use of non-native promoters that influence FcRn expression. To overcome this limitation, we developed an innovative humanized FcRn knock-in (hiFcRn) mouse model using CRISPR/Cas9 technology. This model integrates hFcRn cDNA into the endogenous locus of the mouse Fcgrt gene, completely replacing native mouse FcRn (mFcRn) expression. The hiFcRn mouse model offers a more human-relevant platform for the preclinical evaluation of therapeutic antibodies and Fc-fusion proteins. - Source: PubMed
Publication date: 2025/07/26
Lee SuBinKyung MunsuPark MiyeonPark SunhaLee JaeHoonKim SuyeonLee SeunghyeonJo MigyeongJung Sang TaekLee Han-Woong - Hyperlipidemia and chronic kidney disease (CKD) are well-established risk factors for cardiovascular disease and act synergistically to promote vascular inflammation and disease progression. However, the mechanisms underlying this synergetic effect remain largely unknown. Using a mouse model combining hyperlipidemia (via high-fat diet feeding, HFD) with 5/6 nephrectomy-induced CKD, we made the following significant findings: 1) HFD + CKD upregulated 1179 genes in mouse aortas and induced prominent reactive oxygen species (ROS), far more than either HFD or CKD alone. 2) HFD + CKD upregulated 86 CRISPRi-identified mitochondrial ROS regulators, 36 CRISPRi-identified cellular ROS regulators, and 19 GSEA-collected ROS regulators. These changes were associated with the upregulations of 48 cytokines, 7 highest toxicity uremic toxin receptors-including CD1D, FCGRT, AHR, IL6RA AGER, NR1H3 and NPY5R-in aortas. 3) These uremic toxin receptors emerged as novel promoters of inflammation and trained immunity. Deficiencies in CD1D, AHR, AGER, and the trained immunity promoter SET7 each downregulated up to 5.5 % of the genes upregulated by HFD + CKD. Conversely, activation of NR1H3 using an agonist upregulated up to 12.2 % of these genes. 4) The expression of 46 cytokine genes was strongly associated with NR1H3 upregulation. 5) The NR1H3 agonist also induced the expression of 28 ROS regulators, including YBX2, a novel anti-ROS transcription factor and RNA-binding protein, suggesting a potential negative feedback mechanism. YBX2 deficiency increased the cellular ROS level, while YBX2 overexpression suppressed 27 proinflammatory genes induced by HFD + CKD. Our findings provide novel insights into the role of the NR1H3-YBX2 axis in regulating inflammation accelerated by hyperlipidemia and CKD. - Source: PubMed
Publication date: 2025/06/09
Lu YifanSun YuSaaoud FatmaXu KemanShao YingHan BaoshengJiang XiaohuaMartinez LaiselVazquez-Padron Roberto IMohsin SadiaZhao HuaqingWang HongYang Xiaofeng