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J Biol Chem, Vol. 274, Issue 35, 24497-24502, August 27, 1999
From the INSERM U344, Faculté de Médecine Necker, 156 rue de Vaugirard, 75730 Paris Cedex 15, France
Prolactin (PRL) has been shown to activate the
cytoplasmic tyrosine kinase Janus kinase 2 (Jak2) and the subsequent
recruitment of various signaling molecules including members of the
signal transducer and activator of transcription family of
transcription factors. Recently, an expanding family of
cytokine-inducible inhibitors of signaling has been identified that
initially included four members: suppressor of cytokine signaling
(SOCS)-1, SOCS-2, SOCS-3, and cytokine-inducible src homology domain 2 (SH-2) proteins. The present study analyzes the role of these members
in PRL signaling. Constitutive expression of SOCS-1 and SOCS-3
suppressed PRL-induced signal transducer and activator of transcription
5-dependent gene transcription, and Jak2 tyrosine kinase
activity was greatly reduced in the presence of SOCS-1 or SOCS-3.
SOCS-1 was shown to associate with Jak2, whereas SOCS-2 was associated
with the prolactin receptor. Co-transfection studies were conducted to
further analyze the interactions of SOCS proteins. SOCS-2 was shown to
suppress the inhibitory effect of SOCS-1 by restoring Jak2 kinase
activity but did not affect the inhibitory effect of SOCS-3 on PRL
signaling. Northern blot analysis revealed that SOCS-3 and
SOCS-1 genes were transiently expressed in response to PRL,
both in vivo and in vitro, whereas the
expression of SOCS-2 and CIS genes was still elevated 24 h after hormonal stimulation. We thus propose that the
early expressed SOCS genes (SOCS-1 and
SOCS-3) switch off PRL signaling and that the later
expressed SOCS-2 gene can restore the sensitivity of cells
to PRL, partly by suppressing the SOCS-1 inhibitory effect.
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D. Krebs and D. Hilton SOCS: physiological suppressors of cytokine signaling J. Cell Sci., January 8, 2000; 113(16): 2813 - 2819. [Abstract] [PDF]
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 C. J. AUERNHAMMER, C. BOUSQUET, V. CHESNOKOVA, and S. MELMED SOCS Proteins: Modulators of Neuroimmunoendocrine Functions: Impact on Corticotroph LIF Signaling Ann. N.Y. Acad. Sci., January 1, 2000; 917(1): 658 - 664. [Abstract] [Full Text] [PDF]
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P. A. Ram and D. J. Waxman Role of the Cytokine-inducible SH2 Protein CIS in Desensitization of STAT5b Signaling by Continuous Growth Hormone J. Biol. Chem., December 8, 2000; 275(50): 39487 - 39496. [Abstract] [Full Text] [PDF]
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N. Aoki and T. Matsuda A Cytosolic Protein-tyrosine Phosphatase PTP1B Specifically Dephosphorylates and Deactivates Prolactin-activated STAT5a and STAT5b J. Biol. Chem., December 8, 2000; 275(50): 39718 - 39726. [Abstract] [Full Text] [PDF]
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 D. Metcalf, S. Mifsud, L. Di Rago, N. A. Nicola, D. J. Hilton, and W. S. Alexander Polycystic kidneys and chronic inflammatory lesions are the delayed consequences of loss of the suppressor of cytokine signaling-1 (SOCS-1) PNAS, January 22, 2002; 99(2): 943 - 948. [Abstract] [Full Text] [PDF]
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S. E. Nicholson, D. De Souza, L. J. Fabri, J. Corbin, T. A. Willson, J.-G. Zhang, A. Silva, M. Asimakis, A. Farley, A. D. Nash, et al. Suppressor of cytokine signaling-3 preferentially binds to the SHP-2-binding site on the shared cytokine receptor subunit gp130 PNAS, June 6, 2000; 97(12): 6493 - 6498. [Abstract] [Full Text] [PDF]
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