Proteins CD32b_Fc γ RIIB , Human
- Known as:
- Proteins CD32b_Fc γ RIIB , Human
- Catalog number:
- C444
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins CD32b_Fc γ RIIB Human
Related genes to: Proteins CD32b_Fc γ RIIB , Human
- Gene:
- RXRB NIH gene
- Name:
- retinoid X receptor beta
- Previous symbol:
- -
- Synonyms:
- NR2B2, H-2RIIBP, RCoR-1
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-14
- Date modifiied:
- 2016-10-05
Related products to: Proteins CD32b_Fc γ RIIB , Human
Related articles to: Proteins CD32b_Fc γ RIIB , Human
- BH3 mimetics are a promising class of drugs in hematologic malignancies, but their efficacy in peripheral T-cell lymphoma (PTCL) remains poorly understood. To identify genetic determinants of BH3 mimetic response, we performed a genome-wide CRISPR-Cas9 knockout screen in PTCL cell lines and identified MYLIP, an E3 ubiquitin ligase targeting the LDL receptor (LDLR), as a novel sensitizer to navitoclax. MYLIP deletion enhanced the cytotoxicity of navitoclax, venetoclax, and the BCL-XL-selective degrader DT2216 across multiple PTCL models. Mechanistically, MYLIP loss increased LDLR expression, promoted cholesterol uptake, and elevated apoptotic priming. Recombinant PCSK9, which facilitates LDLR degradation, reversed MYLIP knockout-induced sensitization, establishing a functional role for LDLR in BH3 mimetic response. We also identified the nuclear receptor RXRB as an upstream regulator of MYLIP; dual RXRA/RXRB depletion more effectively suppressed MYLIP, upregulated LDLR, and potentiated navitoclax cytotoxicity. In vivo, MYLIP-deficient xenografts showed enhanced tumor suppression with navitoclax treatment. Transcriptomic analyses of primary PTCL samples revealed reduced MYLIP expression in ALK-positive anaplastic large cell lymphoma and genetically defined subsets of nodal T follicular helper cell lymphomas. These findings uncover an RXR-MYLIP-LDLR axis that links cholesterol metabolism to apoptotic susceptibility, offering mechanistic insight into BH3 mimetic sensitivity in PTCL. - Source: PubMed
Publication date: 2026/08/25
Yokoyama KeitoChiba MasahiroTakei NorioSuto KeitoIshio TakashiGoto HidekiEndo TomoyukiKadin Marshall EMaeda MichiyukiWatanabe MasashiHatakeyama ShigetsuguTeshima TakanoriYang YibinNakagawa Masao - Diabetic osteoporosis (DO) is a chronic consequence of diabetes mellitus marked by disrupted bone metabolism and elevated fracture risk, with no effective strategies currently available. Betulinic acid (BA) is a natural pentacyclic triterpenoid demonstrating anti-diabetic, anti-inflammatory, and osteoprotective effects. This research aimed to clarify the molecular mechanisms of BA in DO using network pharmacology, molecular docking, and molecular dynamics simulations. - Source: PubMed
Publication date: 2026/08/06
Sharma SheenamChaudhary RishabhSharma ChiragDabral SwarnaBansal SeemaSharma NeelamGupta Sumeet - Aflatoxin B1 (AFB1) is a highly toxic mycotoxin that causes severe renal injury, yet the molecular basis of its nephrotoxicity remains poorly defined. Here, we integrated multi-omics data with computational modeling to elucidate the mechanisms of AFB1-induced kidney damage. Three human renal transplant biopsy microarray datasets (GSE1563, GSE30718, and GSE61739), comprising 121 injury samples and 84 control samples and representing distinct forms of transplant-associated renal injury, including acute rejection and ischemic kidney injury, were analyzed using differential expression and weighted gene co-expression network analyses, which identified 174 injury-related genes. A total of 145 AFB1-associated targets were obtained from multiple public datasets. Intersection analysis between these two gene sets identified RXRB and F11 as core hub genes potentially involved in AFB1-induced renal injury. Immune infiltration and gene set enrichment analyses suggested their involvement in immune regulation and toxicity-related signaling pathways. Molecular docking demonstrated favorable binding of AFB1 to RXRB and F11, with binding energies of -9.9 and -7.4 kcal/mol, respectively, while molecular dynamics simulations further confirmed the stability of these complexes. Together, this integrative multi-omics and modeling approach reveals key molecular determinants of AFB1-induced renal toxicity and offers a theoretical foundation for developing targeted interventions against AFB1-related kidney disorders. - Source: PubMed
Publication date: 2026/08/07
Chen YihuangZhang YuanqunLiu GuohaoLiu Huan - Fat deposition determines beef marbling grade and meat quality, but the underlying molecular mechanisms remain unclear. This study aimed to investigate the role of bovine PPARD in lipid deposition, especially its effect on the expression of fatty acid transport genes (, , and ) and the lipid droplet-associated gene () in liver tissues from cattle with different marbling grades. The mRNA abundance and protein levels in liver tissues from thirty-one Wagyu × Angus crossbred beef cattle (25-26 months old) with different marbling grades (according to GB/T 29392-2022, based on the marbling richness of the longissimus dorsi muscle at the 12th-13th rib interface) were analyzed by RT-qPCR and Western blot, respectively. Additionally, was knocked down and overexpressed in bovine mammary epithelial cells to validate its effects on lipid-metabolism-related genes. The results showed that the mRNA levels of , , , , , and were significantly higher ( < 0.01) in livers tissues from the A3 and A4 groups (high marbling) than in those from the A1 and A2 groups (low to moderate marbling). Western blot analysis revealed significantly higher PPARD protein expression in the A3 and A4 groups (high marbling) than that in the A1 and A2 groups (low to moderate marbling) ( < 0.05). It should be noted that the sample size of Group A4 is only 2, and the results of this group should be considered as a preliminary trend that needs to be validated with larger sample sizes. Cellular experiments confirmed that knockdown significantly decreased mRNA expressions of , , and ( < 0.01), while overexpression significantly increased their mRNA levels ( < 0.05). These results indicate a positive correlation between PPARD expression and the transcriptional levels of genes involved in fatty acid transport and lipid droplet storage, suggesting that PPARD may be associated with hepatic lipid metabolism and potentially contribute to marbling development. These findings suggest that the PPARD signaling pathway contributes to hepatic lipid deposition and may play a role in marbling formation in beef cattle. - Source: PubMed
Publication date: 2026/07/06
Wang KaiyouWang QiWang QinyuTian ShuaiyingQi YingZhang LinXing BaokuiTuliguer Li Qiuling - Frailty is a multidimensional geriatric syndrome that lacks a consistent definition, complicating its clinical management. Epigenetic data suggest that frailty involves altered CpG sites, potentially driven by environmental epigenetic factors (the exposome) that influence aging. Systematically reviewing studies from 2009 to 2025, we quantified frailty prevalence, pooled weighted methylation beta values for associated CpG sites, performed enrichment analysis, and conducted structural network analysis to evaluate chemical interactions, following the PRISMA 2020 guidelines and with the study prospectively registered in PROSPERO (ID 1159037). Results showed a pooled frailty prevalence of 17.4% with extreme heterogeneity (I = 98.88%), and a combined methylated beta effect of -0.1378 (CI: -0.4156, 0.1400) with high heterogeneity (I = 100%), highlighting sources of variability. Interestingly, we found a CpG site (cg04772644) shared between Chinese and German cohorts, and, upon mapping, four frailty-related genes (CDC42BPB, SLC1A5, RXRB, and SLC22A18AS) were shared across cohorts. Indeed, these genes are significantly enriched in pathways including thrombin signaling, G protein-coupled receptor signaling, and immune cell differentiation signaling. Finally, our system toxicology analysis demonstrated that arsenite, bisphenol A, benzamide, dorsomorphin, and trichostatin A directly interact with the four shared genes, suggesting that the chemical exposome contributes to the observed epigenetic heterogeneity of frailty and the concomitant clinical manifestations. - Source: PubMed
Publication date: 2026/07/03
Cedillo-Rivero Alejandro EliuRodriguez-Cuartas Julian DanielGomez-Zapata ValentinaFlores-Soto EdgarGomez-Verjan Juan CarlosRivero-Segura Nadia Alejandra