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Editorial
Published at www.nejm.org September 19, 2007 (10.1056/NEJMe078197)

STAT3 Signaling and the Hyper-IgE Syndrome
David E. Levy, Ph.D., and Cynthia A. Loomis, M.D., Ph.D.

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The Janus kinase (JAK)–signal transducer and activator of transcription (STAT) signaling pathway has emerged over the past decade as a major relay between cell-surface receptors and cytokine responses. The human genome encodes four JAK family members — JAK1, JAK2, JAK3, and tyrosine kinase 2 (TYK2) — and seven STAT proteins.1 JAKs are protein tyrosine kinases that interact with the intracellular domains of cytokine receptors (Figure 1) and that have enhanced catalytic activity toward substrate proteins after receptor activation. The primary JAK substrates are STAT proteins — latent transcription factors that require their tyrosine residues, and sometimes serine residues, . . . [Full Text of this Article]


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From the Department of Pathology, New York University School of Medicine, New York.

This article (10.1056/NEJMe078197) was published at www.nejm.org on September 19, 2007. It will appear in the October 18 issue of the Journal.


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