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Article

Loss of Socs2 improves molecular responses to IFNα in a mouse model of myeloproliferative neoplasms driven by JAK2-V617F.

Leukemia - 1 Apr 2025

Usart Marc, Kimmerlin Quentin, Stetka Jan, Stoll Cédric, Rai Shivam, Almeida Fonseca Tiago, Karjalainen Riikka, Hao-Shen Hui, Roux Julien, El Taher Athimed, Lynch Dylan, Makukhin Nikolai, Ciulli Alessio, Skoda Radek C

Abstract excerpt

Therapy with pegylated interferon alpha (pegIFNα) can induce a deep molecular response in a subset of patients with myeloproliferative neoplasms (MPN). Here we investigated the role of Socs2, a negative regulator of cytokine signaling, in modulating the response to pegIFNα in a JAK2-V617F mouse model of MPN. Deleting Socs2 in JAK2-V617F mice resulted in increased sensitivity to cytokines, without causing...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 40069287
DOI: 10.1038/s41375-025-02550-5

Genes

JAK2
SOCS2
CD34

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

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Loss of Socs2 improves molecular responses to IFNα in a mouse model of myeloproliferative neoplasms driven by JAK2-V617F.PMID 40069287Read ↗

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