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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression profiling of endothelial cells from old (12 months) and very old (18 months) homozygous Jak2 R1063H mice and wild-type controls

ABSTRACT: To investigate the biological role of the germline JAK2-R1063H mutation, which may contribute to susceptibility and pathogenesis of myeloproliferative neoplasms, we generated a mouse model by introducing the R1063H variant into the endogenous Jak2 locus using CRISPR/Cas9 genome editing. This model allowed us to explore not only hematopoietic but also non-hematopoietic compartments potentially affected by the mutation. Given the ongoing debate regarding the presence and functional impact of somatic JAK2-V617F in endothelial cells — and their possible involvement in thrombotic complications — we specifically examined whether Jak2-R1063H in endothelial cells drives similar pathogenic phenotype. Therefore, we isolated lung endothelial cells (CD45⁻/CD31⁺) from 12- and 18-month-old Jak2-R1063H and wild-type mice and conducted gene expression profiling.

INSTRUMENT(S): NextSeq 2000

ORGANISM(S): Mus musculus

SUBMITTER: Jan Kubovčiak

PROVIDER: E-MTAB-15355 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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