{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"submitter":["Jan Kubovčiak"],"organism":["Mus musculus"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-14685"],"description":["Patients with myeloproliferative neoplasms (MPN), are known to be at an elevated risk for thrombosis but the mechanism for MPN-related coagulation activation is not yet fully characterized. While increased hematocrit has been re-evaluated as a contributing factor, additional mechanisms such as chronic inflammation and a pro-adhesive phenotype associated with increased endothelial P-selectin expression have been elucidated in MPN thrombogenesis. Additionally, non-myeloid inflammatory cells, red blood cells and platelets may also contribute to increased vascular resistance and promote thrombosis. However, the mechanism of thrombosis associated with JAK2 germline mutations has not been described. We performed expression gene profiling of platelets isolated from young (3 months) homozygous Jak2 R1063H mice and wild-type controls."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Sample Collection - For platelets (PLT) isolation, whole blood was collected to acid-citrate-dextrose tubes supplemented with 3 uM prostaglandin E1 (PGE), and PLT-rich plasma was collected by centrifugation. Pelleted PLTs were subjected to red cell lysis and resuspended in the presence of anti-CD45 beads (Milteney Biotec) to remove residual leukocytes.","Sequencing - Libraries were sequenced on Illumina NextSeq 2000 using P3 flowcell and 122 nt read length, single-end.","Nucleic Acid Extraction - Total RNA was isolated using RNeasy Micro Kit (Qiagen) as described in the manufacturer’s protocol.","Library Construction - Libraries were prepared with a SMARTer® Stranded Total RNA-Seq – Pico Input Mammalian library preparation kit v2 (Takara)."],"figure_sub":["Organization","MINSEQE Score","Assays and Data","Processed Data","MAGE-TAB Files"],"data_protocol":["Data Transformation - Salmon 1.9.0 was used to quantify per gene expression from reads aligned to GRCm39 assembly (Ensembl annotation version 109). Quantified per-gene expression for each sample is provided as processed data.","Sequence Alignment - Data was processed with  nf-core/rnaseq pipeline version 3.10.1 using STAR 2.7.9a and Salmon 1.9.0 to quantify per gene expression against GRCm39 assembly (Ensembl annotation version 109)."],"omics_type":["Metabolomics","Unknown","Transcriptomics","Genomics","Proteomics"],"instrument_platform":["NextSeq 2000"],"study_type":["RNA-seq of coding RNA"],"species":["Mus musculus"],"pubmed_authors":["Jan Kubovčiak","Lucie Lanikova"],"additional_accession":[]},"is_claimable":false,"name":"Expression profiling of platelets from young (3 months) homozygous Jak2 R1063H mice and wild-type controls","description":"Patients with myeloproliferative neoplasms (MPN), are known to be at an elevated risk for thrombosis but the mechanism for MPN-related coagulation activation is not yet fully characterized. While increased hematocrit has been re-evaluated as a contributing factor, additional mechanisms such as chronic inflammation and a pro-adhesive phenotype associated with increased endothelial P-selectin expression have been elucidated in MPN thrombogenesis. Additionally, non-myeloid inflammatory cells, red blood cells and platelets may also contribute to increased vascular resistance and promote thrombosis. However, the mechanism of thrombosis associated with JAK2 germline mutations has not been described. We performed expression gene profiling of platelets isolated from young (3 months) homozygous Jak2 R1063H mice and wild-type controls.","dates":{"release":"2025-08-22T00:00:00Z","modification":"2025-08-19T00:01:42.034Z","creation":"2024-12-11T00:51:19.485Z"},"accession":"E-MTAB-14685","cross_references":{"ENA":["ERP166989"],"EFO":["EFO_0002944","EFO_0004170","EFO_0004917","EFO_0005518","EFO_0003816","EFO_0003738","EFO_0004184"]}}