Ask about this productRelated genes to: FOLR4 antibody
- Gene:
- IZUMO1R NIH gene
- Name:
- IZUMO1 receptor, JUNO
- Previous symbol:
- FOLR4
- Synonyms:
- Folbp3, JUNO
- Chromosome:
- 11q21
- Locus Type:
- gene with protein product
- Date approved:
- 2008-12-08
- Date modifiied:
- 2016-10-11
Related products to: FOLR4 antibody
Related articles to: FOLR4 antibody
- Tibetan sheep () have evolved remarkable adaptations to the extreme high-altitude environment of the Qinghai-Tibet Plateau. While previous studies have identified some genetic features underlying these adaptations, a comprehensive understanding of their population genetics and selection signatures remains incomplete. We hypothesized that Tibetan sheep harbor unique genetic diversity and population structure distinct from low-altitude sheep (Hu sheep and Small Tail Han sheep), and that whole-genome resequencing could identify key positively selected genes driving their high-altitude adaptation and economic trait variation. Thus, this study aimed to characterize the population structure and genetic diversity of Tibetan sheep via whole-genome resequencing and identify genomic regions and candidate genes under positive selection related to high-altitude adaptation and important economic traits (growth, meat quality, wool, reproduction). - Source: PubMed
Publication date: 2025/10/18
Zhang JunxiaZhang LitanZhang YuxiangDeng YutingWen Xiaocheng - The final step of the fertilization process involves gametes adhesion and fusion. JUNO is an essential folate receptor 4 protein present in the ooplasm of oocytes, which binds to IZUMO1, its receptor on the sperm surface. Both proteins are indispensable for the sperm-oocyte interaction, and their absence results in infertility. Despite the importance of JUNO in reproduction, there is still controversy about how different factors affect the functionality of JUNO. Therefore, the goal of this study was to provide a comprehensive overview of what we know so far about the presence and functionality of JUNO. - Source: PubMed
Publication date: 2025/04/01
Díaz-Fuster LucíaSáez-Espinosa PaulaMoya IsabelPeinado IreneGómez-Torres María José - The development of pathogenic autoreactive CD4+ T cells, particularly in the context of impaired signaling, remains poorly understood. Unraveling how defective signaling pathways contribute to their activation and persistence is crucial for identifying new therapeutic targets. We performed bulk and single-cell RNA-Seq (scRNA-Seq) and single-cell T cell receptor sequencing (scTCR-Seq) to profile a highly arthritogenic subset of naive CD4+ T cells from BALB/c-Zap70*W163C (SKG) mice, which develop CD4+ T cell-mediated autoimmune arthritis driven by a hypomorphic mutation in Zap70 - a key TCR signaling kinase. Despite impaired signaling, these cells exhibited heightened expression of T cell activation and cytokine signaling genes but diminished expression of a subset of tolerogenic markers (Izumo1r, Tnfrsf9, Cd5, S100a11) compared with WT cells. The arthritogenic cells showed an enrichment for TCR variable β (Vβ) chains targeting superantigens (Sags) from the endogenous mouse mammary tumor virus (MMTV) but exhibited diminished induction of tolerogenic markers following peripheral antigen encounter, contrasting with the robust induction of the negative regulators seen in WT cells. In arthritic joints, cells expressing Sag-reactive Vβs expanded alongside detectable MMTV proviruses. Antiretroviral treatment and Sag-reactive T cell depletion curtailed SKG arthritis, suggesting that endogenous retroviruses disrupted peripheral tolerance and promoted the activation and differentiation of autoreactive CD4+ T cells into pathogenic effector cells. - Source: PubMed
Publication date: 2024/11/26
McCarthy Elizabeth EYu StevenPerlmutter NoahNakao YukaNaito RyotaLin CharlesRiekher VivienneDeRisi JoeYe Chun JimmieWeiss ArthurAshouri Judith F - Fertilization is a complex process that depends on the fusion of the cell membrane of sperm with that of oocyte, and it involves sperm-oocyte recognition, binding, and fusion, which are mediated by multiple proteins. Among those proteins, IZUMO1 and its receptor JUNO have been identified as essential factors for sperm-oocyte recognition and fusion. However, the interaction between IZUMO1 and JUNO alone does not lead to cell membrane fusion, suggesting the involvement of additional proteins in sperm-oocyte membrane fusion. In this study, we have discovered that a protein called WDR54, which consists of WD-repeat modules, is located on the cell membrane of sperm, as well as on the cell membrane and in the cytoplasm of the oocyte. We have found that WDR54 is involved in sperm-oocyte fertilization. When sperm and oocyte were treated with anti-WDR54 ascites, the in vitro fertilization (IVF) rate significantly decreased. Furthermore, our research has shown that WDR54 interacts with both IZUMO1 and JUNO, and it colocalizes with IZUMO1 on the surface of the sperm head and with JUNO on the oocyte surface. Through structural analysis of the putative complexes of WDR54-IZUMO1 and WDR54-JUNO, we infer that these three proteins could form a complex of JUNO-WDR54-IZUMO1-JUNO (referred to as the "JWIJ complex") on the oocyte surface. Our findings suggest that WDR54 is an important factor involved in sperm-oocyte adhesion and fusion. This discovery provides new insight into the mechanisms of mammalian sperm-oocyte adhesion and fusion. - Source: PubMed
Publication date: 2023/11/07
Lai XiongLiu RuizhuoLi MengyuFan YaochunLi HongxiaHan GuotaoGuo RuijieMa HairuiSu HuiminXing Wanjin - Izumo1R is a pseudo-folate receptor with an essential role in mediating tight oocyte/spermatozoa contacts during fertilization. Intriguingly, it is also expressed in CD4 T lymphocytes, in particular Treg cells under the control of Foxp3. To understand Izumo1R function in Treg cells, we analyzed mice with Treg-specific deficiency (Iz1rTrKO). Treg differentiation and homeostasis were largely normal, with no overt autoimmunity and only marginal increases in PD1 and CD44 Treg phenotypes. pTreg differentiation was also unaffected. Iz1rTrKO mice proved uniquely susceptible to imiquimod-induced, γδT cell-dependent, skin disease, contrasting with normal responses to several inflammatory or tumor challenges, including other models of skin inflammation. Analysis of Iz1rTrKO skin revealed a subclinical inflammation that presaged IMQ-induced changes, with an imbalance of Rorγ+ γδT cells. Immunostaining of normal mouse skin revealed the expression of Izumo1, the ligand for Izumo1R, electively in dermal γδT cells. We propose that Izumo1R on Tregs enables tight contacts with γδT cells, thereby controlling a particular path of skin inflammation. - Source: PubMed
Publication date: 2023/03/27
Zarin PayamShwartz YuliaOrtiz-Lopez AdrianaHanna Bola SSassone-Corsi MartinaHsu Ya-ChiehMathis DianeBenoist Christophe