rM RANK-L
- Known as:
- rM RANK-L
- Catalog number:
- AK8239-0002
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Akro
- Gene target:
- RANK-
Related genes to: rM RANK-L
- Gene:
- ANKFY1 NIH gene
- Name:
- ankyrin repeat and FYVE domain containing 1
- Previous symbol:
- -
- Synonyms:
- ANKHZN, KIAA1255, ZFYVE14, BTBD23, RANK-5
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-29
- Date modifiied:
- 2018-05-03
- Gene:
- LRRN2 NIH gene
- Name:
- leucine rich repeat neuronal 2
- Previous symbol:
- LRRN5
- Synonyms:
- GAC1, LRANK1, FIGLER7
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-05
- Date modifiied:
- 2014-11-19
- Gene:
- TNFRSF11A NIH gene
- Name:
- TNF receptor superfamily member 11a
- Previous symbol:
- PDB2, LOH18CR1
- Synonyms:
- RANK, CD265, FEO
- Chromosome:
- 18q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2019-04-23
- Gene:
- TNFSF11 NIH gene
- Name:
- TNF superfamily member 11
- Previous symbol:
- -
- Synonyms:
- TRANCE, RANKL, OPGL, ODF, CD254
- Chromosome:
- 13q14
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2017-03-02
Related products to: rM RANK-L
9A725 RANK, HumanAnti-Human CD254 (RANK Ligand) Biotin 100 ugAnti-Human CD254 (RANK Ligand) Biotin 25 ugAnti-Human CD254 (RANK Ligand) PE 100 ugAnti-Human CD254 (RANK Ligand) PE 25 ugAnti-Human CD254 (RANK Ligand) Purified 100 ugAnti-Human CD254 (RANK Ligand) Purified 100 ugAnti-Human CD254 (RANK Ligand) Purified 25 ugAnti-Human CD254 (RANK Ligand) Purified 25 ugAnti-human RANK-Ligand, soluble (MAB), Source: Monoclonal Murine, MABAnti-human RANK-Ligand, soluble, bt, Source: Polyclonal bt. Goat, PABAnti-human RANK-Ligand, soluble, bt, Source: Polyclonal bt. Goat, PABAnti-human RANK-Ligand, soluble, bt, Source: Polyclonal bt. Goat, PABAnti-human RANK-Ligand, soluble, bt, Source: Polyclonal bt. Rabbit, PABAnti-human RANK-Ligand, soluble, bt, Source: Polyclonal bt. Rabbit, PAB Related articles to: rM RANK-L
- Porcine deltacoronavirus (PDCoV) is an emerging enteric pathogen that causes severe gastrointestinal disease in neonatal piglets and poses a potential risk of cross-species transmission. Although viral strategies that counteract host immune responses have been widely studied, host factors that restrict PDCoV replication remain poorly characterized. In this study, we identify ANKFY1 as a previously unrecognized host factor that restricts PDCoV replication. PDCoV infection markedly upregulated ANKFY1 expression in LLC-PK1 cells. Using gain- and loss-of-function approaches, we demonstrated that ANKFY1 significantly suppresses PDCoV replication, whereas depletion of ANKFY1 restored both viral RNA synthesis and progeny virus production. Mechanistically, ANKFY1 specifically interacts with the viral nonstructural protein nsp8 and promoted its degradation. We further show that ANKFY1 recruits the E3 ubiquitin ligase Cullin 3 to catalyze K63/K33-linked ubiquitination of nsp8, primarily at lysine 58. The ubiquitinated nsp8 is subsequently recognized by the selective autophagy receptor p62 and delivered to autolysosomes for degradation. Disruption of p62 or autophagy flux abolished ANKFY1-mediated nsp8 degradation and antiviral activity, underscoring the essential role of the ANKFY1-Cullin3-p62 axis. Collectively, our results reveal a novel host defense mechanism in which ANKFY1 mediates selective autophagic degradation of PDCoV nsp8 to restrict viral replication. This study not only advances our understanding of PDCoV-host interactions but also identifies the ANKFY1-Cullin3-p62 pathway as a potential target for developing of broad-spectrum antiviral strategies. - Source: PubMed
Publication date: 2026/02/03
Xu YufanZhang YangyangZhu HuixinYu XiaomengLou JinxiuLiu MingyuLiu GongguanBai JuanJiang PingYang ZhenWang Xianwei - This study integrates transcriptomic, proteomic, and immunoinformatic analyses to identify peptide-based and repurposed drug candidates for Breast cancer therapy. Differential gene expression profiling across four independent datasets (GSE134938, GSE213481, GSE214054, and GSE148657) identified 455 significantly upregulated and 439 downregulated genes out of 6,124, with ANKFY1 (GSE134938) and ATE1 (GSE148657) emerging as robust markers. Functional clustering highlighted consistent upregulation of genes involved in extracellular matrix (ECM) remodeling, tumor invasion, and metabolic reprogramming (COL1A1, FN1, SPP1, MMPs, SCD), alongside downregulation of adhesion and mitochondrial genes, suggesting epithelial-mesenchymal transition (EMT) and metabolic vulnerabilities. Protein-protein interaction network analysis revealed ANKFY1, STARD4/5, and CADM1 as central hubs enriched in lipid metabolism, ECM regulation, and cytoskeletal signaling. Functional enrichment underscored cholesterol transport, steroid biosynthesis, and PPAR/AMPK signaling as key pathways in BC pathogenesis. Proteomic profiling of 21 breast cancer-associated proteins generated 28,732 human-specific peptides, prioritized using a composite scoring system integrating immunogenicity, physicochemical traits, and safety. Top peptides, including SCAMP2, CADM1, and FNBP1, exhibited high MHC binding affinity (IC50 < 30 nM), non-allergenic and non-toxic profiles, and favorable solubility, with motif analysis identifying conserved functional patterns across SCAMP2, CADM1, and FNBP1. Structural modeling and virtual screening validated these proteins as tractable targets, with nilotinib and tucatinib emerging as promising multitarget repurposed drug candidates. At the same time, terfenadine displayed strong binding but cardiotoxic potential. Collectively, these results highlight lipid-driven oncogenesis and ECM remodeling as central to BC biology and provide a translational framework for peptide-based immunotherapy and drug repurposing. - Source: PubMed
Publication date: 2026/01/03
Kamli HossamShubaili AishaYousif Adil AAndarawi Mohamed OSalih Magdi MOtifi Hassan MAl-Qahtani Saleh MKhan Najeeb Ullah - Photoresponsive molecular tools have become powerful platforms for manipulating biological functions with high spatiotemporal precision. In this review, we highlight recent advances in the development of light-activated compounds that interact with key signaling molecules and microenvironments. Inspired by various chemical reactions triggered by light-matter interactions, this review covers three representative systems: photoactivatable peroxynitrite (ONOO) generators, visible-light-driven nitric oxide (NO) releasers, and optochemical oxygen (O) scavengers. ONOO, a reactive nitrogen species formed from NO and superoxide (O), plays a critical role in protein nitration and cellular oxidative stress. By designing molecules that generate both NO and O upon light exposure, efficient ONOO release was achieved and used to induce nitration reactions. For NO manipulation, the authors developed a class of photoresponsive releasers that utilize photoinduced electron transfer (PeT) to enable blue-to-red light-triggered NO release. These photoresponsive releasers allowed optical control of vasodilation both ex vivo and in vivo, which forms the basis of a minimally invasive approach to modulate blood flow. In addition, a light-responsive O scavenger was developed to induce localized hypoxia in cell cultures. The light-responsive O scavenger enabled optical regulation of the hypoxia-responsive pathway and activation of the transient receptor potential ankyrin 1 (TRPA1) calcium channel, which underscores the utility of this approach. Together, these studies illustrate how rational molecular design, combined with precise photochemical control, can create innovative systems for probing and directing biological events. These technologies are valuable as both a basic research tool and for potential future therapeutic applications. - Source: PubMed
Ieda Naoya - While cryoablation demonstrates therapeutic potential for lung adenocarcinoma, the precise molecular mechanisms underlying its antitumor effects require further elucidation. We conducted the first transcriptome-based investigation of cryoablation's anti-tumor mechanisms using the Lewis lung carcinoma (LLC) model. Subcutaneous LLC tumors were established in C57BL/6 mice, with subsequent randomization into the model, cryoablation, and cisplatin control groups (DDP). Systematic evaluations included the tumor volume and weight, histopathology (H&E staining), Ki-67 proliferative index (IHC). RNA sequencing identified differentially expressed genes (DEGs), and bioinformatics analysis constructed lncRNA/miRNA-mRNA regulatory networks, with key targets validated by RT-qPCR and Western blotting. Our findings revealed that cryoablation significantly inhibited tumor growth (volume/weight reduction) and downregulated the Ki-67 proliferative index. Transcriptomic profiling identified 1136 mRNA, 215 lncRNA, and 39 miRNA DEGs, unveiling critical PDK1-VEGFA axis regulation and mmu-miR-210-5p-ANKFY1 targeting. Western blot analysis confirmed that cryoablation blocked the HIF-1 signaling pathway by inhibiting HIF-1α and VEGF protein expression. This study elucidates that cryoablation exerts anti-tumor effects via HIF-1 pathway blockade and non-coding RNA network remodeling, providing a theoretical foundation for optimizing cryotherapeutic strategies. - Source: PubMed
Publication date: 2025/08/05
Wang XiaofanZhang MohanLiu DiannaLin ShichengZhang YuxinLi Quanwang - Ankyrin repeat and FYVE domain containing 1 (ANKFY1) is an indispensable protein in the development of cerebellar Purkinje cells. Our preliminary study revealed that its absence caused progressive spastic ataxia, accompanied by the loss of Purkinje cells in mice. Here, we generated Ankfy1-floxed (Ankfy1) mice, in which conditional inactivation of the Ankfy1 gene was achieved specifically in cerebellar Purkinje cells via crossing with a transgenic mouse strain expressing Cre recombinase under the regulatory control of the Purkinje cell protein 2 (PCP2) promoter. We employed data-independent acquisition (DIA) mass spectrometry to compare the protein expression profiles in cerebellar samples. The samples were obtained from two groups of male mice. The first group consisted of three Pcp2-Cre; Ankfy1 male mice, where the Ankfy1 gene was conditionally knocked out in Purkinje cells, and these mice were designated as the conditional knockout (CKO) group. The second group included three Cre-negative; Ankfy1 littermate male mice served as the wild-type (WT) control group. The results identified 69 (45 upregulated and 24 downregulated) differentially expressed proteins (DEPs) in CKO vs. WT male mice with a 1.5-fold change. Enrichment analyses of these DEPs based on the Gene Ontology (GO), Orthologous Groups of Proteins (COG), and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases revealed functional clusters associated with neuronal cell morphogenesis, extracellular structures, regulation of Rho-GTPase, calcium signaling pathway, etc. Itgb2, which was upregulated in CKO mice, was the top hub gene according to protein-protein interaction (PPI) analysis. We selected seven interesting differentially expressed genes (Arhgdib, Impa2, Pcp2, Pcp4, Ppp1r17, Rhobtb2, and Cdc123) for further validation. Arhgdib and Imp2a expression was increased in the cerebellum of CKO male and female mice, and Pcp2 and Pcp4 expression was decreased. Western blotting and immunofluorescence verified the upregulation of ARHGDIB and the downregulation of PCP2 in the cerebellum. Our proteomic analysis of conditional Ankfy1 knockout mice may guide future research to help develop treatments for progressive spastic ataxia. - Source: PubMed
Publication date: 2025/07/01
Fu RongDing ManYin TongZheng LinlinLiu YueYu HangZhou RumengLu Zuneng