Analysis typeOther
OEZ013173
DescriptionThe superQ pipeline (https://github.com/liumz93/superQ/) was used to identify the integration events. Briefly, after the adapter and low-quality sequence trimming using cutadapt (https://cutadapt.readthedocs.io/), the remaining sequences were aligned to the hg38 genome using bowtie2 (https://bowtie-bio.sourceforge.net/bowtie2/). The PCR duplication was removed by the molecular barcode.
Analysis typeReference Alignment
OEZ014269
DescriptionThe superQ pipeline (https://github.com/liumz93/superQ/) was used to identify the integration events. Briefly, after the adapter and low-quality sequence trimming using cutadapt (https://cutadapt.readthedocs.io/), the remaining sequences were aligned to the hg38 genome using bowtie2 (https://bowtie-bio.sourceforge.net/bowtie2/). The PCR duplication was removed by the molecular barcode.
Analysis typeReference Alignment
OEZ014268
DescriptionThe superQ pipeline (https://github.com/liumz93/superQ/) was used to identify the integration events. Briefly, after the adapter and low-quality sequence trimming using cutadapt (https://cutadapt.readthedocs.io/), the remaining sequences were aligned to the hg38 genome using bowtie2 (https://bowtie-bio.sourceforge.net/bowtie2/). The PCR duplication was removed by the molecular barcode.
Analysis typeReference Alignment
OEZ014115
DescriptionMultiple genome-wide association studies (GWASs) have identified the MTMR3/HORMAD2/LIF/OSM region to be associated with IgA nephropathy (IgAN), but the causal variants, implicated genes, and altered functions are poorly understood. Here, we performed fine-mapping analyses based on the GWAS datasets consisting of 2,762 IgAN cases and 5,803 controls. We identified two variants explaining the entire GWAS signal, rs4823074 and rs16988135, both of which linked to the MTMR3 promoters in B-lymphoblastoid cells. Mendelian randomization studies suggested that the risk alleles may modulate disease susceptibility by affecting serum IgA levels through increased MTMR3 expression. Consistently, we observed elevated MTMR3 expression in PBMCs from IgAN patients. Further mechanistic studies in vitro demonstrated that MTMR3 increased IgA production dependent upon its PtdIns3P binding domain. Moreover, our study provided the in vivo functional evidence that Mtmr3−/− mice exhibited defective TLR9-induced IgA production and glomerular IgA deposition. Collectively, the present study indicated the role of MTMR3 in IgAN pathogenesis by enhancing TLR9-induced IgA immunity, and provided novel insights into using genetic data to explore a novel intervention target for IgAN.
Analysis typeOther
OEZ009584
DescriptionCryoEM
Analysis typeDe Novo Assembly
OEZ014267
DescriptionThe median fluorescence signal at each site (F635_Median) was divided by the background (B635_Median) for data analysis, that is, original signal strength (I) = F635_Median/B635_Median. The median and SD of I were calculated to obtain the corrected data Z-Score (corrected signal strength) for each site. Proteins with a Z-Score greater than 2.8 were those that bind to HDCA. The mean value (I mean) represents the mean value of the original signal strength of each protein. I Mean-Ratio is the ratio between the Biotin-HDCA group and Biotin group. To call the candidates, the cutoff was set as a P value≤0.05 and I Mean-Ratio≥1.4.
Analysis typeDe Novo Assembly
OEZ014266
Analysis typeDe Novo Assembly
OEZ014264
Analysis typeOther
OEZ013253
DescriptionViral sequences identified from metagenomes and genomes data across global acid mine drainage.
Analysis typeSequence Annotation
OEZ008166