RASSF2 antibody
- Known as:
- RASSF2 (anti-)
- Catalog number:
- orb101865
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- RASSF2 antibody
Related genes to: RASSF2 antibody
- Gene:
- RASSF2 NIH gene
- Name:
- Ras association domain family member 2
- Previous symbol:
- -
- Synonyms:
- KIAA0168, CENP-34
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2000-08-22
- Date modifiied:
- 2016-01-29
Related products to: RASSF2 antibody
Related articles to: RASSF2 antibody
- Porcine epidemic diarrhea virus (PEDV) infection leads to serious intestinal disease in piglets, often leading to high mortality rates and substantial economic losses. Understanding host-PEDV interactions is crucial for PEDV therapeutic strategies. N-methyladenosine (mA) methylation has been proven to play an important role in host antiviral immunity. However, transcriptome-wide profiling patterns and the biological functions of host mA methylation in response to PEDV infection remain incompletely understood. This study first observed significant upregulation of mA regulators (METTL3, FTO, WTAP, YTHDC1, and YTHDF2) in PEDV infection. Following transcriptome-wide mA methylation and gene expression profiling, this study identified 803 differentially methylated peaks with 674 differentially expressed mA-methylated genes and 345 differentially expressed genes (DEGs) after PEDV infection. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses indicated that these differentially methylated genes were enriched mainly in lysine degradation, histidine metabolism, and the ubiquitin-mediated proteolysis pathway, whereas these DEGs were enriched in negative regulation of viral genome replication, viral protein interaction with cytokines and cytokine receptors, nucleotide-binding oligomerization domain-like (NOD-like) receptor signaling, and immune response-related signaling pathways. Furthermore, the joint analysis of RNA sequencing (RNA-seq) and methylated RNA immunoprecipitation sequencing (MeRIP-seq) identified 16 differentially expressed genes with mA methylation ( and ), which were associated with immune response and metabolism. Taken together, the study results map the dynamic landscape of host mA methylation and demonstrate the functional enrichment of mA methylated genes during PEDV infection, thereby providing a theoretical framework for future research on the role of mA methylation in resistance to PEDV infection. - Source: PubMed
Publication date: 2026/05/18
Dong XiaZhang YueWang YingWang ChengZhou Ao - Ovarian cancer (OV) is one of the deadliest gynecological malignancies, and its high heterogeneity significantly impacts treatment efficacy. Against this background, the molecular mechanisms underlying the pathogenesis of this lethal disease have attracted extensive research attention. However, the pathogenic mechanisms of OV remain incompletely understood. Therefore, this study systematically investigates the pathogenesis of OV. This study collected 20 paired clinical samples comprising OV tissues and benign ovarian tissues to investigate RASSF2 expression. The biological effects of RASSF2 were investigated using both in vitro and in vivo models, including assessments of proliferation and migration. The impact of RASSF2 on PTEN protein stability was examined through co-immunoprecipitation and cycloheximide (CHX) chase assays. Additionally, chromatin immunoprecipitation (ChIP) was performed to investigate the SETDB1/RASSF2 interaction and H3K9me3 modifications on the chromatin of RASSF2. OV tissues exhibited significantly lower RASSF2 expression compared to normal tissues, and this reduction was associated with poorer patient survival. Overexpression of RASSF2 inhibited the proliferation and migration of OV cells. Additionally, RASSF2 inhibited OV growth in vivo. Mechanistically, RASSF2 stabilized PTEN expression to inhibit the activation of PI3K/AKT pathway. In addition, SETDB1 drove OV progression by increasing H3K9me3 enrichment at the RASSF2 promoter to negatively regulate RASSF2 expression. H3K9me3‑modified RASSF2 promotes ovarian cancer metastasis by regulating PTEN expression, which may offer a potential therapeutic target to counteract distant dissemination of OV. - Source: PubMed
Publication date: 2026/05/07
Wang JingLi XinyuChang JianmiaoHou XiaoxueSun LijiaYan YananShu LishaWu Xin - Complexity of the microenvironment of lung adenocarcinoma (LUAD) poses significant challenges in its clinical management. Systematic bioinformatic analysis of the Ras-association domain family (RASSF) identified RASSF2 as a potential tumour suppressor in LUAD. This study aims to investigate its clinical significance and functional mechanisms in LUAD. CCK-8, EdU, and colony formation assays were performed to investigate the impact of RASSF2 overexpression on the proliferative capacity of LUAD cells. Transwell and wound healing assays were performed to explore the significance of RASSF2 on LUAD cell migration and invasion. RNA sequencing analysis was conducted on three methylation-positive and three methylation-negative LUAD tissue samples to establish the underlying mechanism of RASSF2 methylation in LUAD. Functional studies indicated that RASSF2 overexpression significantly inhibited the proliferation, migration, and invasion of LUAD cells. Patients with RASSF2 promoter hypermethylation exhibited a significantly shorter overall survival than those without. RNA-seq of three pairs of LUAD tissue samples further demonstrated that RASSF2 methylation is associated with upregulation of the NF-κB signalling pathway and dysregulation of T-cell activation pathways. This study confirmed the tumour-suppressive role of RASSF2 in LUAD and suggests its potential as an immunotherapeutic target, thus providing new insights into LUAD treatment strategies. - Source: PubMed
Publication date: 2026/04/22
Han YingyingJiang WenyingChen QingningWang JunpuOu Chunlin - Increasing evidence indicates that modulating pyroptosis in endothelial cells (ECs) can alleviate atherosclerosis (AS) progression; however, despite reports that nucleolin (NCL) regulates vascular smooth muscle cell proliferation in AS, the potential mechanism by which cell surface NCL mediates pyroptosis in ECs during AS remains poorly understood. - Source: PubMed
Publication date: 2026/03/20
Fang LiShen ZhijieHuang DanLou ChenyuYu YalanLin YuliZhang Yinzhuang - The lack of reliable early markers specific to hepatocellular carcinoma (HCC) limits its effective management. While the genetic factors defining this disease are largely understood, the epigenetic mechanisms that cause HCC remain elusive. MicroRNAs (miRNAs) operate as polycistronic clusters rather than individual genes and are critical to the development and progression of multiple cancers, including HCC. In this study, we identified several miRNA clusters, including the miR-106b/25 cluster (miR-106b-5p, miR-25-3p, and miR-93-5p), that are overexpressed in HCC cells, suggesting their oncogenic function. We then performed whole-transcriptomic sequencing and identified gene targets of this cluster, namely, CAV1, DNAJB4, PTPRD, MFSD2A, TCF4, KLF6, MCC, CYB5A, ESR2, NR4A3, PRKCB, RASSF2, TXNIP, and SOD2, to be downregulated in the HCC spheroids and clinical datasets. Further, gene enrichment analysis revealed associations with critical pathways, such as Wnt signaling, TGF-beta signaling, VEGFA-VEGFR2 signaling, and EGF/R signaling pathways. Furthermore, survival analysis revealed that miR-93-5p (HR = 0.72, p = 0.0246), HCC stage (HR = 2.43, p = 0.0000113), TCF4 (HR = 0.66, p = 0.0106), DNAJB4 (HR = 1.29, p = 0.0214), MCC (HR = 1.35, p = 0.0268), and CYB5A (HR = 0.77, p = 0.0423) affect overall survival (OS). Finally, a combined prognostic model for the miRNA cluster and its target genes via the random forest approach revealed that the miR-106b/25 cluster and its interactome are significantly associated with OS (p < 0.0001), thereby providing a comprehensive understanding of the cluster and its targets in the development and progression of HCC and its use as a potential marker for HCC. - Source: PubMed
Publication date: 2025/11/06
Karunakara Shreyas HulusemaneMoorthy ManjuRamaswamy GopalakrishnaPuttamallapa Vinutha ShanubhoganahalliPrakash MaheshkumariMehtani RohitKabekkodu Shama PrasadaVishwanath Prashant MSanthekadur Prasanna Kumar