2970 results for "愛の戦士完全破壊2-re-imagination-version-鞭首絞め・電撃・ヘソか"

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• Mtb infected and uninfected neutrophils after 1 and 6 hrs

  Fastq.gz files for mRNA sequenced from Mtb infected and uninfected neutrophils after 1 and 6 hrs. Samples were sequenced in 2 batched as indicated per experiment. Batch 1 was SE unstranded, 100bp on an Illumina HiSeq4000 sequencer and batch 2 unstranded, 150bp paired-end on an Illumina NovaSeq6000 sequencer. Phenotypic data for the samples is also included.

  Dataset EGAD00001010893

• Using RNA-sequencing to characterize the resistance to lirafugratinib

  In addition to Exome-sequencing, we used RNA-sequencing to also characterize resistance to lirafugratinib with whole exome sequencing in patients with FGFR2-driven cancers, treated in the phase 1/2 ReFocus trial (NCT04526106) and enrolled in the UNLOCK program at Gustave Roussy

  Study EGAS50000001370

• Affymetrix_Exon_Array

  Affymetrix Exon Array dataset

  Dataset EGAD00010000936

• Illumina_1M_SNP_Array

  Illumina 1M SNP Array dataset

  Dataset EGAD00010000939

• CyclomicsSeq_Healthy_Flongle

  Contains Healthy samples sequenced on Flongle flowcells

  Dataset EGAD00001010150

• The Role of CTCF in the Organization of the Centromeric 11p15 Imprinted Domain Interactome

  Beckwith-Wiedemann Syndrome (BWS) is the most common human imprinting disorder and comprises a spectrum of overgrowth phenotypes. While approximately 35% of BWS cases are caused by isolated loss of methylation (LOM) at the human imprinting center 2 (IC2) on chromosome 11p15, only around 5% of patients develop BWS due to structural alterations to the IC2 domain. In this study, we identify a BWS-causing 7.6 kB familial deletion within the IC2 domain by performing Whole Genome Sequencing (WGS) on patient-derived human fibroblasts. Using a chromatin conformation capture technique, Capture C, on 3 control fibroblast samples, 3 BWS LOM fibroblast samples, and the single familial deletion sample, we investigate how the domain interactome changes in BWS patients. We find that high-strength interactions occur within the IC2 domain between the 5’ end of KCNQ1, KCNQ1 intron 2, and the 5’ end of CDKN1C in the control profile that are largely abrogated in the BWS samples, but some lower frequency contacts between the imprinting control region (ICR), KCNQ1 intron 2, and the 5’ end of CDKN1C are unaffected. We conclude that the strong KCNQ1-CDKN1C interactions are important in maintaining the domain imprint.

  Study phs002408

• Hi-C NTERA-2

  TGCT - GWAS loci Hi-C data

  Dataset EGAD00010001249

• RAGE engagement by SARS-CoV-2 enables monocyte infection and underlies COVID-19 severity

  Study EGAS00001007529

• RFX6-mediated dysregulation defines human β cell dysfunction in early type 2 diabetes

  Study EGAS00001006273

• Sequencing of rare human histiocytic tumour

  Sequencing of rare human histiocytic tumour

  Dataset EGAD00001002184