NHLRC2 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- NHLRC2 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00374354-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- NHLRC2 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: NHLRC2 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- NHLRC2 NIH gene
- Name:
- NHL repeat containing 2
- Previous symbol:
- -
- Synonyms:
- FLJ25621, FLJ20147, FLJ33312, MGC45492, DKFZp779F115
- Chromosome:
- 10q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-27
- Date modifiied:
- 2019-02-25
Related products to: NHLRC2 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: NHLRC2 293T Cell Transient Overexpression Lysate(Denatured)
- Numerous plant and human viruses depend on arthropods for their transmission. RNA interference (RNAi) constitutes a pivotal antiviral immune system in arthropods. Component 3 promoter of RISC (C3PO) complex plays an important regulatory role in small RNA production of the RNAi pathway. However, how C3PO affects viral infection in arthropod vectors remains elusive. Here, using the system of rice stripe virus (RSV) and its insect vector small brown planthopper, we found that C3PO facilitates RSV replication in insect vectors. C3PO directly degrades precursors of miRNAs, especially miR-971-3p. The RNA-dependent RNA polymerase (RdRp) of RSV synergistically cooperates with C3PO to degrade miR-971-3p precursor. The reduction of miR-971-3p elevates the expression of target gene NHL repeat-containing protein 2 (NHLRC2), which scavenges reactive oxygen species, thereby facilitating viral replication. Similar function of C3PO is elucidated in mosquitoes during the infection of sindbis virus, indicating the conservation of insect C3PO taking part in arbovirus infection. Our study extends the understanding of C3PO in insect vectors and offers the potential of C3PO as target for reducing arbovirus transmission. - Source: PubMed
Publication date: 2025/10/31
Xiao YanGuan TianyuXia QianfengChen ChenWang QianLuo LanLu HongCui Feng - Fibrosis, neurodegeneration and cerebral angiomatosis (FINCA) is a childhood-onset neurodevelopmental disorder with multi-organ manifestations, including recurrent infections. It is caused by variants in , initiating a cascade of unknown pathological events. We investigated the FINCA disease-causing p.Asp148Tyr variant in NHLRC2 by analysing transcriptional changes in mouse embryonic stem cells (mESCs). We conducted behavioural and immunological phenotyping of FINCA mice compound heterozygous for the knockout allele and p.Asp148Tyr variant and explored their T cell populations and cytokine production in splenocytes. Additionally, we employed proximity-labelling mass spectrometry to identify changes in protein-protein interactions resulting from the p.Asp148Tyr variant in human embryonic kidney cells. We discovered significant transcriptional changes in mESCs homozygous for the p.Asp148Tyr variant or knockout allele compared to wild-type cells, with genes involved in cell metabolism, adhesion, neurodevelopment and immune response. FINCA mice exhibited hyperactivity and decreased exploration of new object in adolescence, and an altered innate immune response, particularly in interferon γ production. By comparing p.Asp148Tyr-induced changes in gene expression in mouse cells and putative interaction partners in human cells, we identified Rho GTPase signalling as a common affected pathway. Our study provides insights into the molecular pathways impacted by the p.Asp148Tyr NHLRC2. The FINCA mouse, which recapitulates several features of the human condition, particularly neurodevelopmental and immune response defects, serves as a tool for investigations on the role of environmental triggers in disease pathogenesis. Our results suggest that targeting immune pathways could offer a strategy for therapeutic intervention in FINCA disease. - Source: PubMed
Publication date: 2025/05/22
Hiltunen Anniina EKangas Salla MGondane AishwaryaKoivisto HennaSalokas KariHeikkinen AnneSalo Miia HRöning TapioTallgren AnttiGlumoff VirpiDenis Maria CKaragianni NikiMyllyharju JohannaVarjosalo MarkkuTanila HeikkiItkonen Harri MRämet MikaUusimaa JohannaHinttala Reetta - The complete array of genes required for terminal erythroid differentiation remains unknown. To address this knowledge gap, we perform a genome-scale CRISPR knock-out screen in the human erythroid progenitor cell line HUDEP-2 and validate candidate regulators of erythroid differentiation in a custom secondary screen. Comparison of sgRNA abundance in the CRISPR library, proerythroblasts, and orthochromatic erythroblasts, resulted in the identification of genes that are essential for proerythroblast survival and genes that are required for terminal erythroid differentiation. Among the top genes identified are known regulators of erythropoiesis, underscoring the validity of this screen. Notably, using a Log2 fold change of <-1 and false discovery rate of <0.01, the screen identified 277 genes that are required for terminal erythroid differentiation, including multiple genes not previously nominated through GWAS. NHLRC2, which was previously implicated in hemolytic anemia, was a highly ranked gene. We suggest that anemia due to NHLRC2 mutation results at least in part from a defect in erythroid differentiation. Another highly ranked gene in the screen is VAC14, which we validated for its requirement in erythropoiesis in vitro and in vivo. Thus, data from this CRISPR screen may help classify the underlying mechanisms that contribute to erythroid disorders. - Source: PubMed
Publication date: 2025/04/12
Myers GreggoryFriedman AnnYu LeiPourmandi NargesKerpet ClaireIto Masaki ASaba RilieTang ViOzel Ayse BilgeBergin Ingrid LJohnson Craig NKu Chia-JuiWang YuBalbin-Cuesta GinetteLim Kim-ChewLin ZesenDrysdale ClaireMcGee BethKurita RyoNakamura YukioLiu XiaofangSiemieniak DavidSingh Sharon ALyssiotis Costas AMaillard IvanWeisman Lois SEngel James DouglasKhoriaty Rami - The clearance of extravasated erythrocytes represents the most reasonable strategy against brain injury post-subarachnoid hemorrhage (SAH). There is little knowledge about the autologous clearance of extravasated erythrocytes post-SAH. The leptomeningeal lymphatic endothelial cells (LLECs) have been less studied functionally, which were firstly harvested and cultured by our group previously and are probably related to the clearance of extravasated erythrocytes post-SAH for they closely surround subarachnoid space. We established a SAH animal model, employed primary LLECs , mimicked the conditions of the SAH , performed RNA sequencing, and transfected LLECs with adenovirus and adeno-associated virus both and to reveal the molecular mechanisms of efferocytosis of erythrocytes by LLECs and its neuroprotection post-SAH. Firstly, we demonstrated the eryptosis-initiated degradation of extravasated erythrocytes . Furthermore, we found LLECs preferentially adhered and engulfed apoptotic erythrocytes and while sparing from intact erythrocytes, suggesting their novel capacity in the efferocytosis of erythrocytes. Additionally, the efferocytosis of erythrocytes by LLECs plays a role on neuroprotection via improving neurological functions, maintaining neurostructural integrity, and alleviating neuropathological consequences post-SAH. During efferocytosis, phosphatidylserine (PS) and phosphatidylserine receptor (PSR) mediated the recognition of apoptotic erythrocytes by LLECs. We also confirmed that NHL repeat-containing 2 (NHLRC2) positively regulated the efferocytosis of erythrocytes by LLECs to serve as a central regulator in it mediated neuroprotection post-SAH. This study elucidated the efferocytosis of erythrocytes by LLECs and subsequently neuroprotection post-SAH. These findings highlight a prompt, efficient, and regulable pathway for the autologous clearance of extravasated erythrocytes that performs as a sentinel against brain injury post-SAH. - Source: PubMed
Publication date: 2025/01/20
Deng Hong-JiXu Yun-HuoWu KunLi Yun-CongZhang Yong-JinYu Han-FuLi ChongXu DanWang Fei - Epidemiological and genetic studies have elucidated the effect of antihypertensive medication (AHM) on stroke subtypes varying upon drug classes, but which drug target genes, how, and where mediated this association remains unknown. We aimed to investigate the impact of AHM on stroke subtypes. - Source: PubMed
Publication date: 2025/01/16
Zheng HeWang WenbinQiu WeidaFeng Yingqing