mProX™ Human FCGR2B Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Fc Receptor Cell Lines
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Published Data
Fig.1 Suppression of either CD22 or FCGR2B resulted in heightened BLNK phosphorylation following BCR stimulation, with FCGR2B depletion displaying a more pronounced impact on this signaling pathway.
P493-6 cells cultured in the presence of 1 μM doxycycline were subjected to different treatments: control, anti-CD22, or anti-FCGR2B small interfering RNA (siRNA) for 48 hours, followed by the addition of 10 μg/mL soluble anti-IgM to activate the BCR for 15 minutes. Subsequently, Western blot analysis was conducted to assess the protein levels of CD22, FCGR2B, P-BLNK, total-BLNK, and actin in the samples.
Ref: Psathas, James N., et al. "The Myc-miR-17-92 axis amplifies B-cell receptor signaling via inhibition of ITIM proteins: a novel lymphomagenic feed-forward loop." Blood, The Journal of the American Society of Hematology 122.26 (2013): 4220-4229.
Pubmed: 24169826
DOI: 10.1182/blood-2012-12-473090
Research Highlights
Gu, Xiao-Jing. et al. "Expanding causal genes for Parkinson's disease via multi-omics analysis." NPJ Parkinson's disease, 2023.
Genome-wide association studies (GWASs) have identified several loci associated with Parkinson's disease (PD). However, there is still a need to uncover potential causal/risk genes and develop etiological therapies for PD. This study aimed to address this urgent need by utilizing expression quantitative trait loci (eQTL) and protein quantitative trait loci (pQTL) data from various tissues (blood, cerebrospinal fluid, and brain) combined with GWAS summary statistics. Using a pipeline consisting of Mendelian randomization, Steiger filtering analysis, Bayesian colocalization, fine mapping, protein-protein network, and enrichment analysis, the authors identified GPNMB as a robust causal gene for PD at the protein level in all three tissues, as well as at the transcriptional level in the brain. The protective role of CD38 (in brain pQTL and eQTL) was also observed. However, inconsistent roles of DGKQ were found between protein and mRNA levels. Additional analysis also revealed 9 other proteins (CTSB, ARSA, SEC23IP, CD84, ENTPD1, FCGR2B, BAG3, SNCA, FCGR2A) associated with PD risk, although based on only a single pQTL after multiple corrections. Furthermore, interactions between these proteins and known PD causative genes and therapeutic targets were identified. Overall, this study highlights the potential roles of GPNMB, CD38, and DGKQ in the pathogenesis of PD, but further evidence is needed to confirm the involvement of other identified proteins in PD. These findings may aid in uncovering the genetic basis of PD and identifying potential drug targets for future interventions.
Gu, Xiao-Jing. et al. "Expanding causal genes for Parkinson's disease via multi-omics analysis." NPJ Parkinson's disease, 2023.
Pubmed:
37865667
DOI:
10.1038/s41531-023-00591-0
Zhao, Man. et al. "Higher expression of PLEK and LY86 as the potential biomarker of carotid atherosclerosis." Medicine, 2023.
Carotid atherosclerosis (AS) is a condition that affects the carotid artery and can result in transient ischemic attack and stroke. The relationship between pleckstrin (PLEK) and lymphocyte antigen 86 (LY86) and carotid AS is not fully understood. In order to investigate this, the authors downloaded two AS datasets, GSE43292 and GSE125771, from the gene expression omnibus database. They identified 305 differentially expressed genes (DEGs), which were mainly involved in immune system processes, extracellular regions, and cytokine binding. Further analysis revealed that the target cells were enriched in the Rap1 signal pathway, B cell receptor signal pathway, and PPAR signal pathway. In addition, metascape enrichment analysis revealed that these DEGs were associated with responses to bacteria, cell activation, and chemotaxis. Through protein-protein interaction network analysis, 10 core genes (TYROBP, FCER1G, PLEK, LY86, IL10RA, ITGB2, LCP2, FCGR2B, CD86, CCR1) were identified as highly related to carotid AS. Among these genes, PLEK, LY86, IL10RA, ITGB2, and LCP2 were found to be highly expressed in carotid AS samples and lowly expressed in normal samples. Furthermore, comparative toxicogenomics database analysis showed that five of these genes were associated with pneumonia, inflammation, necrosis, and drug allergies. In particular, the expression of PLEK and LY86 was found to be correlated with the prognosis of carotid AS, with higher expression levels being associated with poorer outcomes. Taken together, these findings suggest that PLEK and LY86 may play important roles in the development and progression of carotid AS.
Zhao, Man. et al. "Higher expression of PLEK and LY86 as the potential biomarker of carotid atherosclerosis." Medicine, 2023.
Pubmed:
37861500
DOI:
10.1097/MD.0000000000034445