COMPLETE UNIT FOR SAFE AND DNA DAMAGE FREE VIEWING OF ETHIDIUM BROMIDE, SYBR GREEN AND SYBR GOLD STAINED GELS _ 110V
- Known as:
- COMPLETE UNIT SAFE Desoxyribonucleic acid DAMAGE FREE VIEWING ETHIDIUM BROMIDE, SYBR GREEN SYBR GOLD STAINED GELS _ 110V
- Catalog number:
- CSL-ET/SYBRCLONER$
- Category:
- -
- Supplier:
- Cleaver
- Gene target:
- COMPLETE UNIT FOR SAFE AND DNA DAMAGE FREE VIEWING ETHIDIUM BROMIDE SYBR GREEN GOLD STAINED GELS _ 110V
Related genes to: COMPLETE UNIT FOR SAFE AND DNA DAMAGE FREE VIEWING OF ETHIDIUM BROMIDE, SYBR GREEN AND SYBR GOLD STAINED GELS _ 110V
- Gene:
- MAGEE1 NIH gene
- Name:
- MAGE family member E1
- Previous symbol:
- -
- Synonyms:
- KIAA1587, DAMAGE
- Chromosome:
- Xq13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-25
- Date modifiied:
- 2016-10-05
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- In an attempt to identify potential active anticancer agents with low cytotoxic properties and CA inhibitors, a new series of hybrid compounds incorporating imidazole ring and hydrazone moiety as part of their structure were synthesized by aza-Michael addition reaction followed by intramolecular cyclization. The structure of synthesized compounds was elucidated using various spectral techniques. Synthesized compounds were evaluated for their in vitro anticancer (prostate cell lines; PC3) and CA inhibitory (hCA I and hCA II) activity. Among them, some compound displayed remarkable anticancer activity and CA inhibitory activity with K values in range of 17.53±7.19-150.50±68.87 nM against cytosolic hCA I isoform associated with epilepsy, and 28.82±14.26-153.27±55.80 nM against dominant cytosolic hCA II isoforms associated with glaucoma. Furthermore, the theoretical parameters of the bioactive molecules were calculated to establish their drug-likeness qualities. The proteins used for the calculations are prostate cancer protein (PDB ID: 3RUK and 6XXP). ADME/T analysis was carried out to examine the drug properties of the studied molecules. - Source: PubMed
Publication date: 2023/05/23
Kekeçmuhammed HüseyinTapera MichaelAydoğdu EkremSarıpınar EminAydin Karatas ElanurMehtap Uc EdaAkyuz MesutTüzün BurakGulcin İlhamiEmin Bora RıfatÖzer İlhan İlhan - The phenotypic repercussion of ZDHHC15 haploinsufficiency is not well-known. This gene was initially suggested as a candidate for X-linked mental retardation, but such an association was later questioned. We studied a multiplex family with three members with autism spectrum disorder (ASD) by array CGH, karyotype, exome sequencing and X-chromosome inactivation patterns. Medical history interviews, cognitive and physical examinations, and sensory profiling were also assessed. The three family members with ASD (with normal cognitive abilities and an abnormal sensory profile) were the only carriers of a 1.7 Mb deletion in the long arm of chromosome X, involving: ZDHHC15, MAGEE2, PBDC1, MAGEE1, MIR384 and MIR325. The normal chromosome X was preferentially inactivated in female carriers, and the whole exome sequencing of an affected family member did not reveal any additional genetic variant that could explain the phenotype. Thus, in the present family, ASD segregates with a deletion on chromosome X that includes ZDHHC15. Considering our results together with gene data (regarding function, expression, conservation and animal/cellular models), ZDHHC15 is a candidate gene for ASD. Emerging evidence also suggests that this gene could be associated with other neurodevelopmental disorders, with incomplete penetrance and variable expressivity. - Source: PubMed
Publication date: 2022/12/23
Casellas-Vidal DolorsMademont-Soler IreneSánchez JoanaPlaja AlbertoCastells NeusCamós MariaNieto-Moragas JavierDel Mar García MariaRodriguez-Solera CeliaRivera HelenaBrunet JoanÁlvarez SaraPerapoch JosepQueralt XavierObón María - Aldosterone-producing adenomas (APAs) are a major cause of primary aldosteronism (PA) and are characterized by constitutively producing aldosterone, which leads to hypertension. Several mutations have been identified in ion channels or ion channel-associated genes that result in APAs. To date, no studies have used a genome-wide association study (GWAS) approach to search for predisposing loci for APAs. Thus, we investigated Scandinavian APA cases (n = 35) and Swedish controls (n = 60) in a GWAS and discovered a susceptibility locus on chromosome Xq13.3 (rs2224095, OR = 7.9, 95% CI = 2.8-22.4, P = 1 × 10) in a 4-Mb region that was significantly associated with APA. Direct genotyping of sentinel SNP rs2224095 in a replication cohort of APAs (n = 83) and a control group (n = 740) revealed persistently strong significance (OR = 6.1, 95% CI = 3.5-10.6, p < 0.0005). We sequenced an adjacent gene, MAGEE1, of the sentinel SNP and identified a rare variant in one APA, p.Gly327Glu, which is complementary to other mutations in our primary cohort. Expression quantitative trait loci (eQTL) were investigated on the X-chromosome, and 24 trans-eQTL were identified. Some of the genes identified by trans-eQTL point towards a novel mechanistic explanation for the association of the SNPs with APAs. In conclusion, our study provides further insights into the genetic basis of APAs. - Source: PubMed
Publication date: 2021/05/18
Dutta Ravi KumarLarsson MalinArnesen ThomasHeie AnetteWalz MartinAlesina PieroGimm OliverSöderkvist Peter - Glioblastoma is the most common primary malignancy of the brain, the prognosis of which is poor. Immunotherapy with cancer/testis (CT) antigens is a novel therapeutic approach for glioblastoma. This study aimed to investigate the expression rate of MAGE-E1, GAGE, and SOX-6 in glioblastoma tumors using the method of immunohistochemistry (IHC). - Source: PubMed
Publication date: 2020/12/20
Tabatabaei Yazdi Seyed AbbasSafaei MasoomehGholamin MehranAbdollahi AlirezaNili FatemehJabbari Nooghabi MehdiAnvari KazemMojarrad Majid - Melanoma associated antigen (MAGE) is an extensively studied family of tumor-associated genes that share a common MAGE homology domain (MHD). Based upon their expression pattern, MAGE genes have been broadly classified into type 1 MAGEs (T1Ms) and type 2 MAGEs (T2Ms) categories. Interestingly, several T2Ms are highly expressed in the brain and involved in the regulation of neuronal development, differentiation, and survival. Available literature suggests possible tumor suppressor functions of a few T2Ms, while information available about their expression, regulation, and clinical significance in glioma is scanty. This prompted us to perform a comprehensive analysis of T2M expression in glioma. Gene expression data from glioma datasets: Oncomine, TCGA, and REMBRANDT study, were used to assess the mRNA expression of T2M genes (, and ), and their association with clinical characteristics and composition of the tumor microenvironment. Further, mutation, copy number alteration, and DNA methylation data from TCGA were assessed for determining potential mechanisms of T2Ms expression in glioma. Expression analysis revealed overexpression of MAGED subfamily genes in glioma, while other genes of this family exhibited reduced expression in advanced grades of this malignancy. Further, the expression of T2Ms exhibited varying extent of positive correlations with each other. Amongst downregulated T2Ms, expression exhibited negative correlations with DNA methylation. Additionally, genes associated with were enriched in Myc and Hedgehog signaling. Furthermore, T2Ms downregulation was associated with immune infiltration in glioma tissues and poor overall survival of glioma patients. In multivariate Cox regression analysis, emerged as an independent prognosticator in lower grade glioma. Conclusively, these results suggest that expression of T2Ms is associated with important clinical and molecular features in glioma. Mechanistic studies may further provide novel insights into their role in glioma progression. - Source: PubMed
Publication date: 2020/12/23
Arora MohitKumari SaritaSingh JayChopra AnitaChauhan Shyam S