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
- Recent studies in mouse models have demonstrated that macrophages in adult tissues are maintained not only by the differentiation of bone marrow-derived monocytes but also by the proliferation of macrophages originating from the yolk sac or fetal liver. However, the extent to which this paradigm shift occurs in human tissues is not fully understood. In this study, we detected a human peritoneal macrophage subset that exhibited embryonic origin-like phenotypes. Macrophages in the ascites of patients with gastric cancer were divided into CCR2 and CCR2 subsets, the ratios of which varied among donors. The gene expression profiles of these subsets were similar to those of the macrophage subsets in the heart. CRIg was recently reported as a marker for distinguishing between two macrophage subsets in the ascites of patients with cirrhosis. CCR2 and CCR2 subsets expressed high and low levels of CRIg, respectively. Importantly, the CCR2CRIg subset expressed the cell proliferation marker Ki67 and the recently proposed core markers (TIMD4, LYVE1, and FOLR2) of embryo-derived macrophages at higher levels than the CCR2CRIg subset. Moreover, many other markers shared by TIMD4LYVE1FOLR2 macrophages in heart, lung, kidney, and liver exhibited similar expression patterns in the peritoneal CCR2CRIg subset. These results suggest that the CCR2CRIg subset in the peritoneal cavity contains macrophages with embryonic origin. - Source: PubMed
Publication date: 2026/04/16
Takahashi NaofumiHabash Sara AKomohara YoshihiroUsuki ShingoYasunaga Kei-IchiroHino ShinjiroAbdelnaser Randa AEinarsdottir ThorbjorgNomura TakushiYonemura AtsukoIshimoto TakatsuguSuzu Shinya - Per- and polyfluoroalkyl substances (PFAS) are a class of long-lasting chemicals with widespread use and environmental persistence that have been increasingly studied for their detrimental impacts on human and animal health. Several major PFAS species are linked to neurodevelopmental toxicity. For example, epidemiological studies have associated prenatal exposure to perfluorooctanoate (PFOA) and perfluorononanoate (PFNA) with autism risk. However, the neurodevelopmental toxicities of major PFAS species have not been systematically evaluated in an animal model, and the molecular mechanisms underlying these toxicities have remained elusive. Using a high-throughput zebrafish social behavioral model, we screened six major PFAS species currently under regulation by the Environmental Protection Agency (EPA), including PFOA, PFNA, perfluorooctane sulfonate (PFOS), perfluorohexanesulfonic acid (PFHxS), perfluorobutane sulfonate (PFBS), and hexafluoropropylene oxide dimer acid ammonium salt (GenX). We found that embryonic exposure to PFNA, PFOA, and PFOS induced social deficits in zebrafish, recapitulating one of the hallmark behavioral deficits in autistic individuals. To systematically identify potential molecular targets of PFAS, we applied a proteome-wide reverse molecular docking strategy that screens small molecules against predicted binding pockets across the human structural proteome. Using this approach, we screened a virtual library containing predicted binding pockets of over 80% of the 3D human proteome. The screen predicts that folate receptor beta (FR-β, encoded by the gene FOLR2) interacts strongly with PFNA, PFOA, and PFOS but to a lesser degree with PFHxS, PFBS, and GenX, correlating positively with their in vivo toxicity. These predictions were validated through in silico molecular docking, in vitro protein binding analysis, and in vivo targeted metabolomics and loss-of-function verifications. Furthermore, embryonic co-exposure to folic acid effectively rescued social deficits induced by PFAS. Together, these results demonstrate the utility of proteome-wide reverse docking as a powerful strategy for discovering molecular targets of environmental toxicants and identify the folate pathway as a potential mechanism underlying PFAS-induced neurodevelopmental toxicity. - Source: PubMed
Publication date: 2026/04/12
Kong Ally XinyiJohnson MajaChi JinhuaEno Aiden FPham KhoaZhang PingGu HaiweiGeng Yijie - Folate receptor beta (FRβ), encoded by FOLR2, is selectively expressed in monocytes and macrophages, yet its function in innate immune signaling remains poorly defined. Here, we identify FRβ as a novel regulator of NLRP3 inflammasome activation and pyroptosis in human THP-1 macrophages. Using CRISPR/Cas9-mediated gene deletion, we show that loss of FOLR2 severely impaired caspase-1 activation, gasdermin D cleavage, and IL-1β release in response to multiple NLRP3 stimuli, without altering pro-IL-1β induction. These defects were not rescued by exogenous folate and were independent of extracellular folate concentrations. Mechanistically, FOLR2/FRβ appears to potentiate potassium efflux and the expression of multiple potassium channel-encoding genes. Single-cell RNA sequencing revealed broad transcriptional repression in FRβ-deficient macrophages, including genes involved in inflammasome signaling and ion transport. Genome-wide methylation profiling showed increased CpG hypermethylation in FOLR2-deficient cells, consistent with reduced transcriptional activity. Our findings indicate that FRβ promotes NLRP3 activation in a folate-independent manner potentially by regulating DNA methylation, gene transcription, and K+ efflux in macrophages. These findings uncover a previously unrecognized immunoregulatory function for FRβ, positioning it as a potential modulator of macrophage-driven inflammation in contexts such as host defense, autoimmunity, and tissue-specific immune responses at the tumor and maternal-fetal interface. - Source: PubMed
Rogers Lisa MFirestone KyleChinni RiyaBranco Anna CWrobleski KaylaChou TeresaGoldstein Jeffery AGu XiaopingMason EmilyChu Shaoyouder Lohe Michael Rubart-vonLow PhilipAronoff David M - PD-1/L1 inhibitors improve the prognosis of patients with advanced bladder cancer, but the clinical remission rate remains below 25%. Tumor-associated macrophages (TAMs) and chemokines are critical in the tumor microenvironment (TME), affecting tumor progression, immunotherapeutic efficacy, and patient prognosis; however, their underlying mechanisms remain unclear. This study exhibits innovation by adopting a tumor microenvironment perspective to investigate the interaction mechanism between bladder cancer cells and tumor-associated macrophages, as well as factors affecting the efficacy of immunotherapy. - Source: PubMed
Publication date: 2026/03/11
Jiang YunzhongLi JianpengYang ZezhongMa MinghaiWang LuZhang LuJing MinxuanZhang YaodongPu YuanchunChen YutongHe JialeLiu HangQu XiaoweiZhang MengzhaoFan Jinhai - The normal developmental and homeostatic roles of tissue resident macrophages are subverted in tumor-associated macrophages to promote tumor progression. Pro-tumoral macrophage activities include immune suppression and promotion of invasion and metastasis. While the myeloid Src family kinase HCK is known to regulate immune evasion, here we show that HCK promotes growth of an aggressively invasive mammary tumor through activation of macrophage motility and invasive capacity. - Source: PubMed
Publication date: 2026/02/18
Murrey Michael WPoh Ashleigh RSteer James HRinaldi CatherineMouchemore Kellie ADwyer Amy RDenisenko ElenaKuznetsova IrinaYeow YenJones Matthew EHmon Khaing P WMuirí Dáithí ÓLiu Ya-YuLin WeitaoForrest Alistair R REllies Lesley GJoyce David AErnst MatthiasPixley Fiona J