The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ Signal transduction

Mathias Müller; James Briscoe; Carl Laxton; Dmitry Guschin; Andrew Ziemiecki; Olli Silvennoinen; Ailsa G. Harpur; Giovanna Barbieri; Bruce A. Witthuhn; Chris Schindler; Sandra Pellegrini; Andrew F. Wilks; James N. Ihle; George R. Stark; Lan M. Kerr

doi:10.1038/366129a0

The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ Signal transduction

Mathias Müller, James Briscoe, Carl Laxton, Dmitry Guschin, Andrew Ziemiecki, Olli Silvennoinen, Ailsa G. Harpur, Giovanna Barbieri, Bruce A. Witthuhn, Chris Schindler, Sandra Pellegrini, Andrew F. Wilks, James N. Ihle, George R. Stark, Lan M. Kerr

Biochemistry, Molecular Biology, and Biophysics (CBS)

Research output: Contribution to journal › Article › peer-review

717 Scopus citations

Abstract

We have produced a cell line which lacks the protein tyrosine kinase JAK1 and is completely defective in interferon response. Complementation of this mutant with JAK1 restored the response, establishing the requirement for JAK1 in both the interferon-α/beta; and -γ signal transduction pathways. The reciprocal interdependence between JAK1 and Tyk2 activities in the interferon-α pathway, and between JAK1 and JAK2 in the interferon-γ pathway, may reflect a requirement for these kinases in the correct assembly of interferon receptor complexes.

Original language	English (US)
Pages (from-to)	129-135
Number of pages	7
Journal	Nature
Volume	366
Issue number	6451
DOIs	https://doi.org/10.1038/366129a0
State	Published - 1993

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Müller, M., Briscoe, J., Laxton, C., Guschin, D., Ziemiecki, A., Silvennoinen, O., Harpur, A. G., Barbieri, G., Witthuhn, B. A., Schindler, C., Pellegrini, S., Wilks, A. F., Ihle, J. N., Stark, G. R., & Kerr, L. M. (1993). The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ Signal transduction. Nature, 366(6451), 129-135. https://doi.org/10.1038/366129a0

Müller, M, Briscoe, J, Laxton, C, Guschin, D, Ziemiecki, A, Silvennoinen, O, Harpur, AG, Barbieri, G, Witthuhn, BA, Schindler, C, Pellegrini, S, Wilks, AF, Ihle, JN, Stark, GR & Kerr, LM 1993, 'The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ Signal transduction', Nature, vol. 366, no. 6451, pp. 129-135. https://doi.org/10.1038/366129a0

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title = "The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ Signal transduction",

abstract = "We have produced a cell line which lacks the protein tyrosine kinase JAK1 and is completely defective in interferon response. Complementation of this mutant with JAK1 restored the response, establishing the requirement for JAK1 in both the interferon-α/beta; and -γ signal transduction pathways. The reciprocal interdependence between JAK1 and Tyk2 activities in the interferon-α pathway, and between JAK1 and JAK2 in the interferon-γ pathway, may reflect a requirement for these kinases in the correct assembly of interferon receptor complexes.",

author = "Mathias M{\"u}ller and James Briscoe and Carl Laxton and Dmitry Guschin and Andrew Ziemiecki and Olli Silvennoinen and Harpur, {Ailsa G.} and Giovanna Barbieri and Witthuhn, {Bruce A.} and Chris Schindler and Sandra Pellegrini and Wilks, {Andrew F.} and Ihle, {James N.} and Stark, {George R.} and Kerr, {Lan M.}",

year = "1993",

doi = "10.1038/366129a0",

language = "English (US)",

volume = "366",

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TY - JOUR

T1 - The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ Signal transduction

AU - Müller, Mathias

AU - Briscoe, James

AU - Laxton, Carl

AU - Guschin, Dmitry

AU - Ziemiecki, Andrew

AU - Silvennoinen, Olli

AU - Harpur, Ailsa G.

AU - Barbieri, Giovanna

AU - Witthuhn, Bruce A.

AU - Schindler, Chris

AU - Pellegrini, Sandra

AU - Wilks, Andrew F.

AU - Ihle, James N.

AU - Stark, George R.

AU - Kerr, Lan M.

PY - 1993

Y1 - 1993

N2 - We have produced a cell line which lacks the protein tyrosine kinase JAK1 and is completely defective in interferon response. Complementation of this mutant with JAK1 restored the response, establishing the requirement for JAK1 in both the interferon-α/beta; and -γ signal transduction pathways. The reciprocal interdependence between JAK1 and Tyk2 activities in the interferon-α pathway, and between JAK1 and JAK2 in the interferon-γ pathway, may reflect a requirement for these kinases in the correct assembly of interferon receptor complexes.

AB - We have produced a cell line which lacks the protein tyrosine kinase JAK1 and is completely defective in interferon response. Complementation of this mutant with JAK1 restored the response, establishing the requirement for JAK1 in both the interferon-α/beta; and -γ signal transduction pathways. The reciprocal interdependence between JAK1 and Tyk2 activities in the interferon-α pathway, and between JAK1 and JAK2 in the interferon-γ pathway, may reflect a requirement for these kinases in the correct assembly of interferon receptor complexes.

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The protein tyrosine kinase JAK1 complements defects in interferon-α/β and -γ Signal transduction

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