STAT3 supports experimental K-RasG12D–induced murine myeloproliferative neoplasms dependent on serine phosphorylation

Author:

Gough Daniel J.1,Marié Isabelle J.1,Lobry Camille1,Aifantis Iannis1,Levy David E.1

Affiliation:

1. Department of Pathology and NYU Cancer Institute, New York University School of Medicine, New York, NY

Abstract

Key Points Absence of STAT3 serine phosphorylation restricts activated K-Ras–driven myeloproliferative disease in a mouse model. A mitochondrial function of STAT3 supports K-Ras–driven, factor-independent growth of myeloid progenitors in vitro.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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