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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

PITPβ loss improves survival in Jak2 V617F mice, suggesting a new therapeutic target for myeloproliferative neoplasms.

Key Points

  • PITPβ deficiency improved survival, with 85% of mice living beyond 50 weeks compared to only 10% in Jak2 V617F controls.
  • PITPβ KO normalized red blood cell counts and reduced splenomegaly, highlighting its significant role in MPN.
  • Analysis focused on pAKT signaling, revealing that PITPβ loss selectively reduces pAKT levels without impacting pSTAT5 or pERK.
  • These findings indicate PITPβ as a novel therapeutic target, with ongoing research into pharmacological AKT inhibition in MPN models.

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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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Interleukin-12 and TNFα signaling drives parallel evolution of independent leukemic clones in JAK2V617F mutant myeloproliferative neoplasms2025
  2. 2Platelet priming in MPN triggers pro-thrombotic intermediate affinity state in αIIbβ3 integrin2025 · 1 citations
  3. 3Disrupting a new NFkB-IL-6-JAK2-STAT cascade with novel NFkB inhibitors reduces primary myelofibrosis growth2025
  4. 4Therapeutic targeting of focal adhesion kinase (FAK) modulates oncogenic and immune pathways in myeloid progenitor cells expressing oncogenic Janus kinase 2-V617F.2025
  5. 5Discovery of JAK2V617F mutant specific allosteric inhibitors for the treatment of myeloproliferative neoplasms2025 · 2 citations