Anti-Human HHR23B (RAD23B) Antibody
- Known as:
- Antibody toHuman HHR23B (RAD23B) Antibody
- Catalog number:
- Y050396
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Anti-Human HHR23B (RAD23B) Antibody
Related genes to: Anti-Human HHR23B (RAD23B) Antibody
- Gene:
- RAD23B NIH gene
- Name:
- RAD23 homolog B, nucleotide excision repair protein
- Previous symbol:
- -
- Synonyms:
- HHR23B, P58, HR23B
- Chromosome:
- 9q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-20
- Date modifiied:
- 2015-07-09
- Gene:
- RAD23BP3 NIH gene
- Name:
- RAD23B pseudogene 3
- Previous symbol:
- RAD23BLP
- Synonyms:
- -
- Chromosome:
- 21q21.1
- Locus Type:
- pseudogene
- Date approved:
- 2000-05-23
- Date modifiied:
- 2019-01-21
Related products to: Anti-Human HHR23B (RAD23B) Antibody
Related articles to: Anti-Human HHR23B (RAD23B) Antibody
- Myopia, particularly high myopia (HM), represents a critical global public health issue due to its strong association with irreversible visual impairment. While past genetic studies have identified numerous myopia-associated loci, they explain only a modest proportion of its heritability. To address this gap, we established the Myopia Associated Genetics and Intervention Consortium (MAGIC) cohort, the first large-scale whole-exome sequencing (WES) cohort dedicated to the Chinese myopia population, which has already unveiled HM-associated genes, novel rare-variant mechanisms, and open-access analytic tools. The cohort was established in Wenzhou, China, in May 2019 and comprises three phases. Phase I (n = 9696) enrolled extreme, early-onset HM adolescents; Phases II (n = 9368) and III (n = 3544; ongoing recruitment) include young adults and elders, enabling comparison and replication of genetic findings. Longitudinal data from electronic medical records (EMRs) for 2566 individuals further support progression analysis. Here, we extend the MAGIC resource to dissect the genetic basis of myopia-related anisometropia. We discovered novel association signals for spherical-equivalent anisometropia in HM adolescents, including SNP rs61758755 in RAD23B (β = 0.72, P = 1.50 × 10-9) and SNP rs59002125 in ABCC6 (β = 0.69, P = 8.86 × 10-8). We also identified 26 suggestive variants linked to anisometropia and its progression. Together, these findings underscore the value of large-scale WES in detecting functional risk alleles and provide foundational insights into the genetic architecture of myopia and its relevant refractive error. The MAGIC cohort serves as a valuable foundation for future mechanistic studies. - Source: PubMed
Publication date: 2026/05/28
Chen Zhen JiZhang RiyanWu HuiminFang Ji YuanXue ZhengboFeng LinyiZhang YueDeng YaoJiang XinyanBai QingshiChen YuDing HuaiyuanLiang JiachengDai WeiXing ShilaiYao YinghaoYu Xiaoguang Chen JieYuan JianQu JiaSu Jianzhong - Spinocerebellar ataxia type 3 (SCA3) is the most common autosomal dominant ataxia globally, caused by expanded CAG repeats in the ATXN3 gene and consequent pathogenic accumulation of mutant ATXN3 (mATXN3) aggregates. The formation of these aggregates perturbs neuronal functions and leads to progressive neurodegeneration, yet the molecular mechanisms controlling mATXN3 proteostasis remain incompletely understood. Here, we identify RAD23 homolog B (Rad23b), a ubiquitin-binding shuttle factor, as a potential regulator of mATXN3 aggregates and toxicity upon high throughput proteomic analysis. Functional assays reveal that Rad23b overexpression enhances, while Rad23b knockdown or knockout reduces, mATXN3 aggregates and neuronal cell death. Mechanistically, Rad23b directly interacts with mATXN3, promotes its ubiquitination, and facilitates its delivery to the proteasome. Paradoxically, Rad23b disrupts proteasome catalytic activity, preventing mATXN3 degradation and exacerbating aggregate formation. Immunohistochemical analysis in SCA3 transgenic mice confirms colocalization of Rad23b with mATXN3 aggregates in cerebellar neurons. These findings highlight Rad23b as a crucial modulator of mATXN3 proteostasis, and imply Rad23b as a potential therapeutic target in SCA3. - Source: PubMed
Publication date: 2026/05/22
Chen Yi-ChingTung Chih-WeiChan Siew ChinWu Po-MingCheng Pei-HsunChen Chuan-MuYang Shang-Hsun - Cardiovascular disease (CVD) is a major cause of morbidity/mortality in juvenile-onset systemic lupus erythematosus (JSLE), yet no reliable tools exist to stratify CVD-risk. - Source: PubMed
Publication date: 2026/03/26
Peng JunjieDönnes PierreMcDonnell ThomasArdoin Stacy PSchanberg Laura ELewandowski Laura BJury Elizabeth CRobinson George ACiurtin Coziana - Inactivating mutations in BAP1 (BRCA1-associated protein 1) are prevalent in many aggressive cancers of high global concern, including cholangiocarcinoma, mesothelioma, uveal melanoma, and renal cell carcinoma. However, research on BAP1 has been predominantly focused on single cancer types, lacking comprehensive pancancer studies that could uncover universal molecular mechanisms and therapeutic vulnerabilities. Our pancancer study uses K-ε-GG ubiquitin remnant motif pulldown coupled with mass spectrometry to comprehensively map the landscape of proteins deubiquitinated by BAP1. Combined with transcriptomics and functional assays, we uncover previously unrecognized roles of BAP1 in enhancing global genome nucleotide excision repair (GG-NER) by modulating the deubiquitination dynamics of three GG-NER DNA damage recognition proteins, DDB1, RAD23B, and COPS7B. We also identify LSD1 (lysine-specific histone demethylase 1) and PARP1 [poly(ADP-ribose) polymerase 1] as synthetic lethal partners of BAP1 through high-throughput drug inhibitor screening. Integrative analysis using ChIP sequencing, ATAC sequencing, and transcriptomics demonstrates the colocalization of BAP1, LSD1, and PARP1 on chromatin loci, with LSD1 promoting chromatin relaxation to facilitate efficient transcription-coupled NER (TC-NER) in addition to GG-NER, whereas PARP1 facilitates lesion recognition of both TC-NER and GG-NER. Combined inhibition of LSD1 and PARP1, using SP2509/SP2577 and olaparib, respectively, synergistically hinders NER, induces apoptosis, reduces tumor burden, and prolongs the survival of multiple BAP1-deficient pancancer in vitro models and in vivo xenografts. In conclusion, our results provide a deubiquitination landscape of BAP1; elucidate the mechanisms of action of BAP1, LSD1, and PARP1 in pancancers; and describe a promising combination therapeutic strategy applicable across multiple cancers with BAP1 mutations. - Source: PubMed
Publication date: 2026/04/01
Hong Jing HanYong Chern HanHeng Hong LeeYao XiaosaiLi ZhimeiSun YichenWang PeiliXiao RongWang Loo ChienChen JianfengGuan PeiyongChu Pek LimHagihara TakeshiNg Sheng RongJusakul ApinyaKongpetch SarinyaNargund Amrita MChu Wern CuiNg Clara Shi YaSugiura MasahiroKwek Xiu YiPham Nhu-AnLin ZihaoNg Cedric Chuan YoungLim Abner HerbertLee Jing YiChan Jason YongshengLim Kah SuanLiu WeiTeh Bin SingIqbal JabedKlanrit PoramateLoilome WatcharinWai Meng Tai DavidBrugarolas JamesLi ShangSobota Radoslaw MikolajTan PatrickJha SudhakarTan JingTeh Bin Tean - Understanding the factors involved in chromatin dynamics is crucial for the study of biochemical processes in which distant genomic regions need to come in close proximity. Previous single locus tracking studies suggest that chromatin dynamics are linked to active transcription, but studies which compare the chromatin dynamics between different locations within a defined chromatin domain are still very limited. Here we used the ANCHOR3 DNA labeling system to track multiple cis-regulatory elements and non-regulatory control regions at different positions in the mouse Klf4 locus. We observe homogeneous chromatin motion of cis-regulatory elements and non-regulatory control regions in Klf4 transcribing mESCs and their non-transcribing EpiLCs daughter cells. These observations challenge the notion that active transcription has a major effect on the locus dynamics of mammalian genes. - Source: PubMed
Publication date: 2026/03/27
van Staalduinen JenteKabbech HélèneYavuz SelçukCetin RidvanLoda Agnesevan Cappellen WiggertHoutsmuller AdriaanWendt KerstinSmal IhorGrosveld Frank