Human FOLR2 _ FBP Protein Vector: HEK294
- Known as:
- Human FOLR2 _ FBP Protein Vector: HEK294
- Catalog number:
- 10039-H01H
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human FOLR2 _ FBP Protein Vector: HEK294
Related genes to: Human FOLR2 _ FBP Protein Vector: HEK294
- Gene:
- FOLR2 NIH gene
- Name:
- folate receptor beta
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 1992-04-16
- Date modifiied:
- 2016-04-26
Related products to: Human FOLR2 _ FBP Protein Vector: HEK294
Related articles to: Human FOLR2 _ FBP Protein Vector: HEK294
- - Source: PubMed
Publication date: 2026/09/09
Wen JingjingChen WeiyuLi JunZhang YaminTao Juan - Obesity is a known risk factor for diseases of the pancreas, including diabetes, pancreatic cancer and pancreatitis, but mechanisms remain unclear. Here we show by spatial, transcriptomic and functional profiling of human pancreatic immune cells from obese and non-obese organ donors that obesity profoundly impacts pancreatic immune homeostasis. Obesity is associated with higher density of tissue resident memory T-cells (TRM) in the exocrine pancreas which are characterized by high cytotoxic functions, and aggregate around macrophages. Single cell sequencing of pancreatic macrophages distinguishes two main subsets - FOLR2 + CD11c- foetal-derived macrophages with pro-repair and immunoregulatory function and FOLR2- CD11c+ lipid-associated macrophages with greater T-cell interactions and pro-inflammatory function. In obesity, the pancreatic macrophage landscape shifts to lower predominance of FOLR2 + CD11c- macrophages and expansion of FOLR2- CD11c+ macrophages, which interact selectively with the TRM and inflamed exocrine epithelium. Together, these results identify macrophage-T cell circuits and immune epithelial interactions that might lead to chronic pancreatic inflammation in obesity and might contribute to obesity-related pancreatic diseases. - Source: PubMed
Publication date: 2026/07/28
Koshkin AlexeyTanagala Kranthi Kiran KishoreEichinger AnnaChait MichaelYoung AoifeShakil ShanilaYoshikawa JunichiSakamoto YosukeWells Steven BFazlollahi LadanChen XiaojuanReizis BorisFarber Donna LWeisberg Stuart P - : Heart failure (HF) arises from multiple interrelated pathological processes. Among these, lysosomal impairment and loss of autophagic homeostasis are increasingly recognized as important contributors to myocardial damage and ventricular remodeling. This study sought to identify lysophagy-associated signature genes in HF and to define their biological roles, cellular origins, and potential diagnostic relevance. : Bulk myocardial transcriptome datasets, including GSE16499, GSE57338, and GSE76701, were integrated with the human cardiac single-cell dataset GSE145154. Differential expression analysis was first performed to identify lysophagy-related differentially expressed genes (DEGs). Candidate hub genes were then screened using support vector machine-recursive feature elimination (SVM-RFE) and least absolute shrinkage and selection operator (LASSO) regression. Functional enrichment analysis, Gene Set Enrichment Analysis (GSEA), immune infiltration assessment, single-cell transcriptomic mapping, and regulatory network analysis were subsequently conducted. The expression profiles of the selected genes were validated in a murine HF model, and VAMP8 overexpression assays were performed in H9c2 cells. : Five hub genes, namely , , , , and , were consistently and markedly decreased in failing myocardial tissue. These genes were mainly linked to SNARE-dependent vesicle trafficking and lysophagy regulation. A diagnostic model incorporating these hub genes demonstrated good discriminatory performance in both the training dataset and a small independent validation cohort, supporting further evaluation of their potential diagnostic value. Single-cell analysis further indicated that these genes were primarily enriched in cardiac FOLR2 tissue-resident macrophages (TRMs). Pseudotime and cell-cell communication analyses associated this module with FOLR2 TRM cell states and predicted interactions with cardiac stromal cells. In the HF mouse model, the mRNA levels of all five hub genes were decreased, with concurrent reductions in VAMP8, MCOLN1 and DERL1 protein expression. In Ang II/LLOMe-induced H9c2 cells, VAMP8 overexpression was associated with reduced cardiomyocyte injury, attenuation of changes in the abundance of lysosome- and autophagy-related proteins, and fewer ultrastructural abnormalities, suggesting a potential cardioprotective effect. : , , , , and were identified as candidate molecular markers of HF that reflect alterations in a lysophagy- and vesicular-transport-related program associated with FOLR2 tissue-resident macrophages. These findings provide new insights into immune-microenvironment remodeling in HF and suggest potential directions for mechanistic and therapeutic investigations. - Source: PubMed
Publication date: 2026/08/15
Cheng QiWang YanliWang DeqiangWu GuoxingLiu BiyunYuan QienZhu Fen - Myelodysplastic neoplasms (MDS) are a group of heterogeneous clonal hematopoietic disorders with a high risk of progression to acute myeloid leukemia. Despite folic acid being an essential vitamin for human development that can be harmful at high levels, it is still unclear how its excess precisely impacts erythropoiesis in MDS patients. Based on non-targeted metabolomics, we identified significantly elevated folic acid levels in both MDS mice and MDS patients. Functional studies revealed that an excess folic acid diet exacerbated anemia in MDS mice, while restricted folic acid intake alleviated disease phenotypes. Mechanistically, excess folic acid promotes the nuclear translocation of FOLR2, which functions as a transcription factor to bind the promoter of IRF2BP2 and drive its expression. Upregulated IRF2BP2 subsequently represses key erythroid transcription factors GATA1 and KLF1, leading to erythroid differentiation arrest. The folic acid-FOLR2-IRF2BP2 axis is upregulated, and high IRF2BP2 expression correlates with poor prognosis in MDS patients. Our study unveils a novel pathological role of folic acid in promoting MDS progression by disrupting hematopoietic stem/progenitor cells and impairing erythropoiesis, suggesting dietary folic acid restriction and targeting FOLR2-IRF2BP2 axis as potential therapeutic strategies. The FOLR2-IRF2BP2 Axis Mediates Erythropoiesis Impairment by Excess Folic Acid in Myelodysplastic Syndromes. In NUP98-HOXD13 transgenic/MDS mice, folic acid content was significantly increased. Excess folic acid diet exacerbated disease symptoms in MDS mice. Reducing folic acid intake significantly alleviated MDS symptoms. Mechanistically, excess folic acid not only promoted the expansion of hematopoietic stem progenitor cells but also disrupted erythropoiesis involving the FOLR2-IRF2BP2 pathway. - Source: PubMed
Publication date: 2026/08/10
Yang ChaoyingWang YanpengPeng YuanliangWang ZeyuanGuo ZhimingXiao XiaojuanLi HaoboGong HanHu BinLiu LiFu MinCao PengfeiYang XiongbingLiu JingNie LingHan XuZhang Ji - Hepatic stellate cells (HSCs) and macrophages are key regulators of liver fibrosis, yet their direct communication during fibrogenesis remains incompletely characterized. We showed that genetic deletion of folate receptor beta (Folr2) significantly attenuated experimental liver fibrosis in mice. In both human and murine fibrotic livers, FOLR2 macrophages are frequently juxtaposed with activated HSCs. Functionally, FOLR2 expressed by reparative, but not M1 or scar-associated, macrophages promotes HSC activation in a contact-dependent manner. Mechanistically, FOLR2 binds to transforming growth factor beta receptor II (TGFβRII) on HSCs, sustaining transforming growth factor beta 1 (TGF-β1) signaling and driving fibrogenesis. Finally, the natural compound fraxinellone targets FOLR2, disrupts its interaction with TGFβRII, and attenuates HSC activation and liver fibrosis. These findings identify the FOLR2-TGFβRII intercellular interaction as a critical mediator of macrophage-HSC crosstalk and highlight its disruption as a promising therapeutic strategy against liver fibrosis. - Source: PubMed
Publication date: 2026/07/30
Yuan Man-ManZheng Bing-FengWang Jing-LinXu Shuai-QiWang Sheng-LanTan YangFeng YongDong Xian-ChiZhu Qi-HuaYan JieXu QiangWu Xing-Xin