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

PROVIDER: PRJEB93875 | ENA |

REPOSITORIES: ENA

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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

Project description: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.

2025-08-22 | E-MTAB-15355 | biostudies-arrayexpress

Expression profiling of hematopoietic stem cells/progenitors from young (3 months) and old (12 months) homozygous Jak2 R1063H mice and wild-type controls

Project description:While familial and sporadic forms of myeloproliferative neoplasms (MPNs) have long been recognized, emerging evidence implicates germline variations, in predisposing individuals to JAK2 V617F-positive myeloproliferative neoplasms (MPN). Understanding the role of genetic variants, such as the JAK2 germline mutations, in MPN susceptibility, along with the contribution to disease pathogenesis, is crucial for elucidating the underlying mechanisms driving MPN development and progression. To study the biology of germline JAK2 R1063H mutation in more detail, we edited the endogenous Jak2 locus by CRISPR/Cas9 technology. We performed expression gene profiling of young (3 months) and old (12 months) HSC (defined as Lin-, Sca1+/ckithigh, CD150high/CD48low) and LK cells (defined as Lin-, Sca1-/ckithigh).

2025-08-22 | E-MTAB-14686 | biostudies-arrayexpress

Expression profiling of hematopoietic stem cells/progenitors from young (3 months) and old (12 months) homozygous Jak2 R1063H mice and wild-type controls

Project description:Expression profiling of hematopoietic stem cells/progenitors from young (3 months) and old (12 months) homozygous Jak2 R1063H mice and wild-type controls

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Expression profiling of platelets from young (3 months) homozygous Jak2 R1063H mice and wild-type controls

Project 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.

2025-08-22 | E-MTAB-14685 | biostudies-arrayexpress

RNA-seq of quadriceps muscle tissues from 10 months old, 30 months old, 30 months old calorie restricted, 30 months old rapamycin treated adult mice

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Ribo-seq of quadriceps muscle tissues from 10 months old, 30 months old, 30 months old calorie restricted, 30 months old rapamycin treated adult mice

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Expression profiling of platelets from young (3 months) homozygous Jak2 R1063H mice and wild-type controls

Project description:Expression profiling of platelets from young (3 months) homozygous Jak2 R1063H mice and wild-type controls

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TEL-JAK2 dependent transcriptome

Project description:TEL-JAK2 is a fusion oncogene resulting from a t(9;12) chromosomal translocation in T-ALL, translated as a constitutively activated TEL-JAK2 tyrosine kinase. Mice carrying a TEL-JAK2 transgene develop T-ALL. Gene deregulated in TEL-JAK2 T-ALL cells as compared to mouse thymocytes were identified Leukemic cells were collected from the thymus of terminally-ill TEL-JAK2 mice; thymocytes were collected from the thymus of 2 months-old mice. All mice on C57B/6 background. RNA was extracted from each sample and processed for hybridization to Affymetrix arrays.

2013-09-28 | E-GEOD-51241 | biostudies-arrayexpress

RNA-seq of quadriceps muscle tissues from 10 months old, 30 months old, 30 months old calorie restricted, 30 months old rapamycin treated adult mice

Project description:We carried out RNA sequencing on the Quadriceps femoris muscle of 10 months old, 30 months old, 30 months old calorie restricted, 30 months old rapamycin treated. The treatments were started at the age of 15 months. The main goal of the study was to decipher the transcriptional changes in wild-type aging and upon above mentioned anti-aging treatments as well as to estimate the translation efficiency using ribo-seq and RNA-seq data.

2025-11-23 | E-MTAB-13569 | biostudies-arrayexpress

Ribo-seq of quadriceps muscle tissues from 10 months old, 30 months old, 30 months old calorie restricted, 30 months old rapamycin treated adult mice

Project description:We carried out ribosome footprinting on the Quadriceps femoris muscle of 10 months old, 30 months old, 30 months old calorie restricted, 30 months old rapamycin treated. The treatments were started at the age of 15 months. The main goal of the study was to decipher the translation changes in wild-type aging and upon above mentioned anti-aging treatments. We further investigated non-canonical targets of translational control and identify novel translational units.

2025-11-23 | E-MTAB-13568 | biostudies-arrayexpress

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