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Corrigendum Open Access | 10.1172/JCI195974

Corrigendum to STAT1 promotes megakaryopoiesis downstream of GATA-1 in mice

Zan Huang, Terri D. Richmond, Andrew G. Muntean, Dwayne L. Barber, Mitchell J. Weiss, and John D. Crispino

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Published July 15, 2025 - More info

Published in Volume 135, Issue 14 on July 15, 2025
J Clin Invest. 2025;135(14):e195974. https://doi.org/10.1172/JCI195974.
© 2025 Huang et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Published July 15, 2025 - Version history
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Related article:

STAT1 promotes megakaryopoiesis downstream of GATA-1 in mice
Zan Huang, … , Mitchell J. Weiss, John D. Crispino
Zan Huang, … , Mitchell J. Weiss, John D. Crispino
Research Article Hematology

STAT1 promotes megakaryopoiesis downstream of GATA-1 in mice

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Abstract

Thrombocytosis is associated with inflammation, and certain inflammatory cytokines, including IFN-γ, stimulate megakaryocyte and platelet production. However, the roles of IFN-γ and its downstream effector STAT1 in megakaryocyte development are poorly understood. We previously reported that STAT1 expression was significantly downregulated in Gata1-knockdown murine megakaryocytes, which also have impaired terminal maturation. Here, we show that ectopic expression of STAT1, or its target effector IRF-1, rescued multiple defects in Gata1-deficient megakaryopoiesis in mice, inducing polyploidization and expression of a subset of platelet-expressing genes. Enforced expression of STAT1, IRF-1, or GATA-1 enhanced phosphorylation of STAT1, STAT3, and STAT5 in cultured Gata1-deficient murine megakaryocytes, with concomitant megakaryocyte maturation. In contrast, enhanced thrombopoietin signaling, conferred by enforced expression of constitutively active JAK2 or c-MPL, induced phosphorylation of STAT3 and STAT5, but not STAT1, and failed to rescue megakaryocyte maturation. Finally, megakaryocytes from Stat1–/– mice were defective in polyploidization. Together, these findings reveal a unique role for STAT1 in megakaryopoiesis and provide new insights into how GATA-1 regulates this process. Our studies elucidate potential mechanisms by which various inflammatory disorders can cause elevated platelet counts.

Authors

Zan Huang, Terri D. Richmond, Andrew G. Muntean, Dwayne L. Barber, Mitchell J. Weiss, John D. Crispino

×

Original citation: J Clin Invest. 2007;117(12):3890–3899. https://doi.org/10.1172/JCI33010

Citation for this corrigendum: J Clin Invest. 2025;135(14):e195974. https://doi.org/10.1172/JCI195974

The authors recently became aware that Figure 6G in the original article was an inadvertent duplication of 6K. The correct Figure 6, D–K, provided from the original source data, is shown below. In addition, the authors were unable to retrieve the original source data for the STAT1 immunoblot in Figure 4C. An updated figure panel, derived from original source data from a replicate experiment, is provided below.

Figure 6, D-K

Figure 4C

The authors regret the errors.

Footnotes

See the related article at STAT1 promotes megakaryopoiesis downstream of GATA-1 in mice.

Version history
  • Version 1 (July 15, 2025): Electronic publication

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