Rabbit Anti-Human DEDAF
- Known as:
- Rabbit Antibody toHuman DEDAF
- Catalog number:
- 129-10238
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rabbit Anti-Human DEDAF
Related genes to: Rabbit Anti-Human DEDAF
- Gene:
- RYBP NIH gene
- Name:
- RING1 and YY1 binding protein
- Previous symbol:
- -
- Synonyms:
- YEAF1, AAP1, DEDAF
- Chromosome:
- 3p13
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-28
- Date modifiied:
- 2016-10-05
Related products to: Rabbit Anti-Human DEDAF
Related articles to: Rabbit Anti-Human DEDAF
- Mono-ubiquitination of histone H2A at lysine 119 (H2AK119Ub) is deposited by the Polycomb repressive complex 1 (PRC1) and represents an abundant post-translational modification (PTM) of histones. H2AK119Ub is crucially involved in the regulation of a wide range of biological processes, including organization of the genome into distinct functional domains, gene silencing, and the maintenance of cell identities during development, among others. Biochemically, the deposition and removal of H2AK119Ub are tightly controlled in cells owing to a dynamic balance between the specific "writers" (i.e., PRC1) and "erasers" (i.e., deubiquitinases (DUBs) such as BAP1 and USP16). Furthermore, the increasing evidence establishes a notion that H2AK119Ub serves as a signal for recruiting specific "readers" (such as JARID2, DNMT3A, RYBP, SSX, and RSF1), which elicit the critical downstream effects such as modulating gene transcription, maintaining genome integrity, and shaping cell identity. This H2AK119Ub-based signaling is often perturbed in human diseases, pointing to a connection between its dysregulation and pathological development. This review is aimed at providing a timely, in-depth analysis of the molecular machinery governing H2AK119Ub, its interactions with other chromatin factors, and its causal role in the onset and progression of diseases, notably cancer. - Source: PubMed
Publication date: 2026/04/01
Wu DamuZhong HaiqingCai LingWang Gang Greg - Genome sequencing (GS) was applied to 3317 individuals from 1452 Korean families with suspected rare genetic disorders to assess diagnostic yield and clinical utility. Patients were categorized into 16 clinical subgroups with curated phenotypes, and variant interpretation was refined by post-analytic phenotype matching. A molecular diagnosis was achieved in 46.2% of families, influencing clinical management in 18.5% of diagnosed cases. Family-based GS had a higher yield than singleton testing (48.5% vs. 41.5%). Neuromuscular and neurodevelopmental disorders showed the highest yields. GS-specific variant types, including deep intronic, noncoding, complex structural variants, and tandem repeat expansions, accounted for 14.6% of diagnoses. Secondary findings were identified in 4.3% of individuals. Novel disease-associated genes such as RYBP, DNAJA3, CAMK2D, and small nuclear RNA genes were also reported. These results highlight the diagnostic power of GS and support its use as a first-tier test, especially in underrepresented populations. - Source: PubMed
Publication date: 2025/12/08
Lee SeungbokSeo Go HunKim Soo YeonJang Se SongJang SeoyunChoi SongjiChin HyungjinLee Seung JaeOh Dong EonRyu Seung WooKim JihyeMoon DongseokJang SeokhuiLim Byung ChanMoon JangsupHan HeonjongLee HaneChae Jong-Hee - Adenosine-to-inosine RNA editing can affect miRNA activity, but its role in skeletal muscle development remains unclear. Here, we investigated miR-376b-3p in goat skeletal muscle satellite cells (MuSCs), which undergo adenosine deaminase acting on RNA 1-mediated editing at the sixth nucleotide of its seed sequence. Although both isoforms were detected, the unedited miR-376b-3p (miR-WT) predominated over the edited form (miR-E) during skeletal muscle development and MuSC differentiation. Functional assays revealed that miR-WT, but not the miR-E type, enhanced MuSC proliferation and differentiation by upregulating Pax7, PCNA, MyoD, MyoG, and MyHC, and promoting myotube formation. Furthermore, we identified Ring1 and YY1 binding protein (RYBP), a repressor of myogenesis, as a direct target of miR-WT. Overexpression of RYBP inhibited MuSC differentiation, whereas miR-WT relieved this repression through direct binding to the RYBP 3'UTR. In contrast, miR-E failed to target RYBP and lacked promyogenic activity. These findings demonstrate that adenosine-to-inosine editing attenuates the function of miR-376b-3p, highlighting its role as a post-transcriptional regulator of skeletal muscle development. - Source: PubMed
Publication date: 2025/12/05
Xu XiaoliWei ChengqiZeng PeijieZhan SiyuanDai DinghuiLi LiZhang Hongping - Long non-coding RNAs (lncRNAs) are emerging as key regulators of neuroblastoma (NB) progression; however, their interplay with MYCN-driven mechanisms remains to be elucidated. The present study aimed to characterize the expression profile of lncRNA RP11-196G11.6 in NB, and to further explore its functional role and mechanism in the pathogenesis of this disease. Transcriptomics data from NB and disseminated tumor cell (DTC) samples (Gene Expression Omnibus; accession no. GSE94035) were analyzed via principal component analysis (PCA), differential expression analysis and CIBERSORT immune profiling. The biological function was assessed using gain- and loss-of-function experiments in IMR-32 (MYCN) and SH-SY5Y (MYCN) cells. Dual-luciferase reporter assays were performed to identify the interaction between RP11-196G11.6, microRNA (miR)-376a-3p and RING1 and YY1-binding protein (RYBP). Rescue experiments were performed by co-transfecting RP11-196G11.6-overexpressing cells with a miR-376a-3p mimic to identify the hypothetical regulatory role of RP11-196G11.6 in NB progression . The present analysis results demonstrated that the PCA could distinguish tumor and DTC samples, with MYCN amplification driving distinct clustering in tumors but not in DTCs. Differential expression analysis based on MYCN in both tumor and DTC groups identified 161 differentially expressed lncRNAs (73 upregulated and 88 downregulated). Notably, RP11-196G11.6 was highly expressed in MYCN tumors, and silencing RP11-196G11.6 promoted the viability, migration, invasion and epithelial-mesenchymal transition in MYCN cells, whereas RP11-196G11.6 overexpression induced the opposite effects in MYCN cells. Mechanistically, RP11-196G11.6 directly inhibited miR-376a-3p, which targeted RYBP. Overexpression of miR-376a-3p reversed the tumor suppressor phenotype driven by RP11-196G11.6. In summary, the present study demonstrated that RP11-196G11.6 may inhibit NB progression by sponging miR-376a-3p, leading to the upregulation of RYBP expression and consequently inhibiting NB progression. These findings revealed a novel lncRNA-miRNA axis involved in NB pathogenesis. - Source: PubMed
Publication date: 2025/11/06
Zhang JieHuang KaiZhou JianwuLiao WengeLi FeiZhao ZhenzhenWang Shan - Ovarian cancer (OC) has the highest mortality rate among all gynecological cancers, yet its pathogenesis remains unclear. This study aims to use integrated bioinformatics methods to identify important biomarkers and subtypes closely related to tumor immunity and fatty acid synthesis in OC. - Source: PubMed
Publication date: 2025/10/22
Zhang YuxuanZhang WeiXie WenliWang XiangyuWei Ping