Cynomolgus monkey CXCL12_SDF1b full length cDNA gene Clone _ ORF gene clone
- Known as:
- Cynomolgus monkey CXCL12_SDF1b length complementary Desoxyribonucleic acid gene Clone _ ORF gene clonality
- Catalog number:
- KG90009-M
- Product Quantity:
- 10
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- Cynomolgus monkey CXCL12_SDF1b full length cDNA gene Clone _ ORF clone
Related genes to: Cynomolgus monkey CXCL12_SDF1b full length cDNA gene Clone _ ORF gene clone
- 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
Related products to: Cynomolgus monkey CXCL12_SDF1b full length cDNA gene Clone _ ORF gene clone
Related articles to: Cynomolgus monkey CXCL12_SDF1b full length cDNA gene Clone _ ORF gene clone
- 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 - Hereditary Parkinson's disease can be triggered by an autosomal dominant overdose of alpha-Synuclein (SNCA) or the autosomal recessive deficiency of PINK1. We recently showed that the combination of PINK1-knockout with overexpression of A53T-SNCA in double mutant (DM) mice potentiates phenotypes and reduces survival. Now we studied brain hemispheres of DM mice at age of 18 months in a hypothesis-free approach, employing a quantitative label-free global proteomic mass spectrometry scan of posttranslational modifications focusing on methyl-arginine. The strongest effects were documented for the adhesion modulator CMAS, the mRNA decapping/deadenylation factor PATL1, and the synaptic plasticity mediator CRTC1/TORC1. In addition, an intriguing effect was observed for the splicing factor PSF/SFPQ, known to interact with the dopaminergic differentiation factor NURR1 as well as with DJ-1, the protein responsible for the autosomal recessive PARK7 variant of PD. CRTC1, PSF, and DJ-1 are modulators of PGC1alpha and of mitochondrial biogenesis. This pathway was further stressed by dysregulations of oxygen sensor EGLN3 and of nuclear TMPO. PSF and TMPO cooperate with dopaminergic differentiation factors LMX1B and NURR1. Further dysregulations concerned PRR18, TRIO, HNRNPA1, DMWD, WAVE1, ILDR2, DBNDD1, and NFM. Thus, we report selective novel endogenous stress responses in brain, which highlight early dysregulations of mitochondrial homeostasis and midbrain vulnerability. - Source: PubMed
Publication date: 2016/03/01
Auburger GeorgGispert SuzanaBrehm Nadine - Identify epigenetic marks in the vicinity of DMPK (linked to myotonic dystrophy, DM1) that help explain tissue-specific differences in its expression. - Source: PubMed
Publication date: 2016/01/12
Buckley LaurenLacey MichelleEhrlich Melanie