RAG2{recombination activating gene 2}rabbit.pAb
- Known as:
- RAG2{recombination activating gene 2}host: rabbit.pAb
- Catalog number:
- 201-20-4734
- Product Quantity:
- 0.2ml
- Category:
- -
- Supplier:
- Shanghai Sunred
- Gene target:
- RAG2{recombination activating gene 2}rabbit.pAb
Related genes to: RAG2{recombination activating gene 2}rabbit.pAb
- Gene:
- DMWD NIH gene
- Name:
- DM1 locus, WD repeat containing
- Previous symbol:
- -
- Synonyms:
- DMR-N9, gene59, D19S593E
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-10
- Date modifiied:
- 2017-06-01
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- Genome-wide studies in late-onset Alzheimer's disease (LOAD) have uncovered many risk loci, yet identifying the causal genes and clarifying how these genetic signals connect to molecular and cellular mechanisms relevant to AD pathogenesis remains challenging. - Source: PubMed
Publication date: 2026/03/30
Waghmare Swapnil GKrishna Meera MMaccoux Emily CFranitza Ariel LLink Brian AE Lezi - Genome-wide association studies (GWASs) in Alzheimer disease (AD) have uncovered over 70 loci significantly associated with AD risk, but identifying the true causal gene(s) at these loci requires systematic functional validation that is rarely performed due to limitations of time and cost. Here, we integrate transcriptome-wide association study (TWAS) with colocalization analysis, fine-mapping, and additional annotation of AD GWAS variants to identify 123 genes at known and suggestive AD risk loci. A comparison with human AD brain transcriptome data confirmed that many of these candidate genes are dysregulated in human AD and correlate with neuropathology. We then tested all available orthologs in two well-established Drosophila AD models that express either wild-type tau or secreted β-amyloid (β42). Experimental perturbation of the 60 available candidates pinpointed 46 that modulated neuronal dysfunction in one or both fly models. The effects of 18 of these genes were concordant with the TWAS prediction, such that the direction of misexpression predicted to increase AD risk in humans exacerbated behavioral impairments in the AD fly models. Reversing the aberrant down- or upregulation of 11 of these genes (MTCH2, ELL, TAP2, HDC, DMWD, MYCL, SLC4A9, ABCA7, CSTF1, PTK2B, and CD2AP) proved neuroprotective in vivo. We further studied MTCH2 and found that it regulates steady-state tau protein levels in the Drosophila brain and reduces tau accumulation in human neural progenitor cells. This systematic, integrative approach effectively prioritizes genes at GWAS loci and reveals promising AD-relevant candidates for further investigation as risk factors or targets for therapeutic intervention. - Source: PubMed
Publication date: 2025/04/10
Stephens Morgan CLi JiayangMair MeganMoore JustinZhu KatyTarkunde AkashAmoh BismarkPerez Alma MBhakare AryaGuo FangfeiShulman Joshua MAl-Ramahi IsmaelBotas Juan - Despite its potential clinical relevance, the product of the DMWD (dystrophia myotonica, WD repeat containing) gene is a largely uncharacterized protein. The DMWD amino acid sequence is similar to that of WDR20, a known regulator of the USP12 and USP46 deubiquitinases (DUBs). Here, we apply a combination of in silico and experimental methods to investigate several aspects of DMWD biology. Molecular evolution and phylogenetic analyses reveal that WDR20 and DMWD, similar to USP12 and USP46, arose by duplication of a common ancestor during the whole genome duplication event in the vertebrate ancestor lineage. The analysis of public human gene expression datasets suggests that DMWD expression is positively correlated with USP12 expression in normal tissues and negatively correlated with WDR20 expression in tumors. Strikingly, a survey of the annotated interactome for DMWD and WDR20 reveals a largely nonoverlapping set of interactors for these proteins. Experimentally, we first confirmed that DMWD binds both USP12 and USP46 through direct coimmunoprecipitation of epitope-tagged proteins. We found that DMWD and WDR20 share the same binding interface in USP12, suggesting that their interaction with the DUB may be mutually exclusive. Finally, we show that both DMWD and WDR20 promote USP12 enzymatic activity, but they differentially modulate the subcellular localization of the DUB. Altogether, our findings suggest a model whereby mutually exclusive binding of DMWD and WDR20 to USP12 may lead to formation of deubiquitinase complexes with distinct subcellular localization, potentially targeting different substrate repertoires. - Source: PubMed
Publication date: 2021/04/28
Olazabal-Herrero AnneBilbao-Arribas MartinCarlevaris OnintzaSendino MariaVarela-Martinez EndikaJugo Begoña MBerra EdurneRodriguez Jose Antonio - An incubated study was conducted to explore the effect of different manure application dosages (0%, 1%, 2%, and 4%, referred to as T0, T1, T2, and T4, respectively) on dynamic changes in the organic carbon fraction and aggregate stability of soil under different incubation times (120, 180, 240, 300, and 360 days). Soil organic carbon (SOC) and its fractions, such as light fraction organic carbon (LFOC), and polysaccharides, cellulose, water-soluble substance (WSS), fulvic acid carbon (FAC), humic acid carbon (HAC) content, and aggregate stability were measured. The results showed that SOC and its fractions were increased with increasing manure application rates. The SOC, LFOC, polysaccharides, cellulose, WSS, FAC, HAC contents and the HAC/FAC ratio increased by 15.3%-83.2%, 6.8-15.9 times, 8.5%-46.4%, 39.3%-122.6%, 35.7%-112.9%, 3.3%-46.9%, 42.5%-88.3%, and 28.5%-38.6% under T1-T4 treatments, respectively, compared to the T0 treatment at the end of the incubation period. With a longer period of incubation, the contents of SOC and HAC showed a decreasing trend, the LFOC increased first and decreased. The FAC content and the HAC/FAC ratio showed a fluctuation trend, but the content of polysaccharides showed an increasing trend. The application of manure decreased the content of >2 mm mechanically stable aggregates but increased the content of > 0.25 mm water stable aggregates in the soil. The mean weight diameter of water stable aggregate (WMWD) increased by 58.6%, while by the end of the incubation period, the percentage aggregate destruction rate (PAD) decreased by 22.2% under the T4 treatment compared to the T0 treatment. Correlation analysis showed that there was a significant correlation between SOC and its fractions, and between organic carbon fractions (except polysaccharides) and aggregate stability. Path analysis showed that the content of HAC and > 2 mm mechanically stable aggregate had a significant direct impact on the mean weight diameter of mechanically stable aggregate (DMWD) (<0.05). Furthermore, the content of > 2 mm and < 0.25 mm water stable aggregates had a significant direct impact on the WMWD (<0.01). The content of<0.25 mm water stable aggregates had a significant direct impact on the PAD (<0.01), while the content of SOC and WSS had a significant indirect impact on the PAD via a direct effect on the content of<0.25 mm water stable aggregate (<0.05). - Source: PubMed
Shao Hui-YunLi Zi-YueLiu DanLi Yi-FanLu LuWang Xu-DongZhang A-FengWang Yan-Li - Multisystem manifestations in myotonic dystrophy type 1 (DM1) may be due to dosage reduction in multiple genes induced by aberrant expansion of CTG repeats in DMPK, including DMPK, its neighboring genes (SIX5 or DMWD) and downstream MBNL1. However, direct evidence is lacking. Here, we develop a new strategy to generate mice carrying multigene heterozygous mutations to mimic dosage reduction in one step by injection of haploid embryonic stem cells with mutant Dmpk, Six5 and Mbnl1 into oocytes. The triple heterozygous mutant mice exhibit adult-onset DM1 phenotypes. With the additional mutation in Dmwd, the quadruple heterozygous mutant mice recapitulate many major manifestations in congenital DM1. Moreover, muscle stem cells in both models display reduced stemness, providing a unique model for screening small molecules for treatment of DM1. Our results suggest that the complex symptoms of DM1 result from the reduced dosage of multiple genes. - Source: PubMed
Publication date: 2019/12/18
Yin QiWang HongyeLi NaDing YifuXie ZhenfeiJin LifangLi YanWang QiongLiu XinyiXu LiuqingLi QingMa YongjianCheng YanboWang KaiZhong CuiqingYu QianTang WeiChen WanjinYang WenjunZhang FanDing ChenBao LanZhou BinHu PingLi Jinsong