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December 8, 2025Blood

PITPβ loss disrupts malignant pAKT activation to ameliorate Jak2 V617F-induced myeloproliferative neoplasms (MPN) in mice

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Authors

NVNikita VantsevLZLiang ZhaoCACharles Abrams

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Overview

Genetic knockout of PITPβ improves survival in malignant myeloproliferative neoplasms, indicating altered erythropoiesis and stem cell function.

Key Points

  • To investigate the role of PITPβ in Jak2 V617F-induced myeloproliferative neoplasms and its impact on survival and erythropoiesis.
  • Utilized a pan-hematopoietic vavCre knockout model to create PITPβ deficient Jak2 V617F mice.
  • Assessed survival rates and blood parameters including red blood cell count and hematocrit.
  • Employed methylcellulose colony forming assay to evaluate erythroid progenitor function.
  • 85% of PITPβ deficient Jak2 V617F mice survived beyond 50 weeks compared to 10% of control.
  • PITPβ knockout normalized erythrocyte levels and reduced splenomegaly.
  • Observed reduced number of proerythroblasts in bone marrow of PITPβ deficient mice.

Cite This Study

Vantsev et al. (2025) studied this question.

synapsesocial.com/papers/69362f7f4fa91c937236e595https://doi.org/10.1182/blood-2025-5534
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