David M, Zhou G, Pine R, Dixon J E, Larner A C
Division of Cytokine Biology, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA.
J Biol Chem. 1996 Jul 5;271(27):15862-5. doi: 10.1074/jbc.271.27.15862.
Interferons (IFNs) induce early response genes by stimulating Janus family (Jak) tyrosine kinases, leading to tyrosine phosphorylation of Stat (signal transducer and activator of transcription) proteins. Previous studies demonstrated that a protein-tyrosine phosphatase (PTP) is required for activation of the ISGF3 transcription complex by IFNalpha/beta, but the specific PTP responsible remained unidentified. We now show that the SH2 domain containing tyrosine phosphatase PTP1D (also designated as SHPTP2, SHPTP3, PTP2C, or Syp) is constitutively associated with the IFNalpha/beta receptor and becomes tyrosine-phosphorylated in response to ligand. Furthermore, transient expression of a phosphatase-inactive mutant or the COOH-terminal SH2 domain of PTP1D causes a dominant negative effect on IFNalpha/beta-induced early response gene expression. These results provide strong evidence that PTP1D functions as a positive regulator of the IFNalpha/beta-induced Jak/Stat signal transduction pathway.
干扰素(IFN)通过刺激Janus家族(Jak)酪氨酸激酶诱导早期反应基因,从而导致信号转导及转录激活因子(Stat)蛋白的酪氨酸磷酸化。先前的研究表明,一种蛋白酪氨酸磷酸酶(PTP)是IFNα/β激活ISGF3转录复合物所必需的,但具体负责的PTP仍未明确。我们现在发现,含SH2结构域的酪氨酸磷酸酶PTP1D(也称为SHPTP2、SHPTP3、PTP2C或Syp)与IFNα/β受体组成性结合,并在配体刺激下发生酪氨酸磷酸化。此外,磷酸酶失活突变体或PTP1D的COOH末端SH2结构域的瞬时表达对IFNα/β诱导的早期反应基因表达产生显性负效应。这些结果提供了强有力的证据,表明PTP1D作为IFNα/β诱导的Jak/Stat信号转导途径的正调控因子发挥作用。