ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/068/SRR13911968/SRR13911968.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/060/SRR13911960/SRR13911960.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/054/SRR13911954/SRR13911954.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/057/SRR13911957/SRR13911957.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/065/SRR13911965/SRR13911965.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/063/SRR13911963/SRR13911963.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/051/SRR13911951/SRR13911951_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/059/SRR13911959/SRR13911959.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/052/SRR13911952/SRR13911952.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/066/SRR13911966/SRR13911966.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/055/SRR13911955/SRR13911955.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/064/SRR13911964/SRR13911964.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/053/SRR13911953/SRR13911953.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/058/SRR13911958/SRR13911958.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/061/SRR13911961/SRR13911961.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/062/SRR13911962/SRR13911962.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/069/SRR13911969/SRR13911969.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/067/SRR13911967/SRR13911967.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/056/SRR13911956/SRR13911956.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR139/051/SRR13911951/SRR13911951_2.fastq.gzprimaryOK200GenomicsCOB, Lindsley F. Kimball Research Institute (LFKRI), New York Blood Centerhttps://www.ebi.ac.uk/ena/browser/view/PRJNA708217Homo sapiensPatients with sickle cell disease (SCD) suffer from intravascular hemolysis associated vascular injury and tissue damage. Classical monocytes (CMo), which comprise most blood circulating monocytes. are activated in SCD, but the cause and consequences of activation is less clear. Using transcriptome analysis, we found upregulation of the type I Interferon (IFN) pathway in sort-purified SCD CMo. Overall design: CD14+CD16- classical monocyte were purifed with CD14 microbeads and sorted with flow cytometerxref:PubMed:34166491ENADisease, Hemoglobin SS disease, Drepanocythemia, determination, sickle cell Anemia-related, HB-S DIS W/O CRISIS NEC, HB-SS DIS NEC W CRISIS, Sickle cell anemia NOS (disorder), Hb S disease, sickle cell disease, Sickle cell anaemia NOS, Sickle Cell Anemia, RNA-seq, RNA-seq., Haemoglobin S-S disease, Sickle-cell disease, Cell Disorders, Sickle Cell, Sickle cell anaemia of unspecified type, Hemoglobin S-S disease, unspecified, HbS Disease, chemical analysis, Cell Disease, HbS disease, beta-globin-related, Hemoglobin S disease, Whole Transcriptome Shotgun Sequencing, Other sickle-cell disease with crisis, Sickle cell anemia NOS, Hb SS disease, Sickle cell anemia of unspecified type, Other sickle-cell disease without crisis, Sickle Cell Disorders, HPA1, Hereditary hemoglobinopathy disorder homozygous for hemoglobin S (disorder), Sickle Cell Disorder, Sickle Cell Anemias, Sickle cell anemia, Drepanocythaemia, inflammatory monocyte, Cell Disorder, Sickle, restriction fragment length polymorphism, Hemoglobin S, Sickling Disorder Due to Hemoglobin S, Haemoglobin S disease, Sickle Cell Disease, Hemoglobin S Disease, HPA 1 recognition polymorphism, Sickle Cell Diseases, Hemoglobin S Diseases, Hb-SS disease without crisis, Hemoglobin S disease without crisis (disorder), Sickle cell syndrome, Sickle cell anemia of unspecified type (disorder), Hereditary hemoglobinopathy disorder homozygous for hemoglobin S, Anemias, Cell Diseases, Sickle cell anaemia, SICKLE CELL DISEASE NOS, assay, Hemoglobin SS disease without crisis (disorder)Disease, Hemoglobin SS disease, Drepanocythemia, determination, sickle cell Anemia-related, HB-S DIS W/O CRISIS NEC, HB-SS DIS NEC W CRISIS, Sickle cell anemia NOS (disorder), Hb S disease, sickle cell disease, Sickle cell anaemia NOS, Sickle Cell Anemia, RNA-seq, RNA-seq., Haemoglobin S-S disease, Sickle-cell disease, Cell Disorders, Sickle Cell, Sickle cell anaemia of unspecified type, Hemoglobin S-S disease, unspecified, HbS Disease, chemical analysis, Cell Disease, HbS disease, beta-globin-related, Hemoglobin S disease, Whole Transcriptome Shotgun Sequencing, Other sickle-cell disease with crisis, Sickle cell anemia NOS, Hb SS disease, Sickle cell anemia of unspecified type, Other sickle-cell disease without crisis, Sickle Cell Disorders, HPA1, Hereditary hemoglobinopathy disorder homozygous for hemoglobin S (disorder), Sickle Cell Disorder, Sickle Cell Anemias, Sickle cell anemia, Drepanocythaemia, inflammatory monocyte, Cell Disorder, Sickle, restriction fragment length polymorphism, Hemoglobin S, Sickling Disorder Due to Hemoglobin S, Haemoglobin S disease, Sickle Cell Disease, Hemoglobin S Disease, HPA 1 recognition polymorphism, Sickle Cell Diseases, Hemoglobin S Diseases, Hb-SS disease without crisis, Hemoglobin S disease without crisis (disorder), Sickle cell syndrome, Sickle cell anemia of unspecified type (disorder), Hereditary hemoglobinopathy disorder homozygous for hemoglobin S, Anemias, Cell Diseases, Sickle cell anaemia, SICKLE CELL DISEASE NOS, assay, Hemoglobin SS disease without crisis (disorder)falseRNA-Seq analysis of classical monocyte in pateints with sickle cell disease [RNA-Seq]RNA-Seq analysis of classical monocyte in pateints with sickle cell disease [RNA-Seq]2025-09-242021-11-13PRJNA708217GSE168532960634166491