A new protein containing an SH2 domain that inhibits JAK kinases

@article{Endo1997ANP,
  title={A new protein containing an SH2 domain that inhibits JAK kinases},
  author={Takaho A. Endo and Masaaki Masuhara and Masahiro Yokouchi and Ritsu Suzuki and Hiroshi Sakamoto and Kaoru Mitsui and Akira Matsumoto and Shyu Tanimura and Motoaki Ohtsubo and Hiroyuki Misawa and Tadaaki Miyazaki and N. Genov{\'e}s Leonor and Tadatsugu Taniguchi and Takashi Fujita and Yuzuru Kanakura and Seturo Komiya and Akihiko Yoshimura},
  journal={Nature},
  year={1997},
  volume={387},
  pages={921-924}
}
The proliferation and differentiation of cells of many lineages are regulated by secreted proteins known as cytokines. Cytokines exert their biological effect through binding to cell-surface receptors that are associated with one or more members of the JAK family of cytoplasmic tyrosine kinases. Cytokine-induced receptor dimerization leads to the activation of JAKs, rapid tyrosine-phosphorylation of the cytoplasmic domains, and subsequent recruitment of various signalling proteins, including… 
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    Proceedings of the National Academy of Sciences of the United States of America
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TLDR
Data demonstrate that SH2-Bbeta is a potent cytoplasmic activator of JAK2 and is thereby expected to be an important cellular regulator of signaling by GH and other hormones and cytokines that activateJAK2.
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TLDR
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TLDR
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TLDR
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A family of cytokine-inducible inhibitors of signalling
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Transcription of all four SOCS genes is increased rapidly in response to interleukin-6, in vitro and in vivo, suggesting they may act in a classic negative feedback loop to regulate cytokine signal transduction.
SOCS proteins in regulation of receptor tyrosine kinase signaling
TLDR
It is evident that RTKs can sometimes bypass SOCS regulation and SOCS proteins can even potentiateRTKs-mediated mitogenic signaling, and SOCs proteins may also influence signaling in other ways.
Cytokines and STAT signaling.
Cross-regulation of JAK and Src kinases
TLDR
The recent identification of a somatic JAK2 mutation as the cause of polycythema vera, further highlights the clinical importance of these molecules.
Signal Transduction of IL-6, Leukemia-Inhibitory Factor, and Oncostatin M: Structural Receptor Requirements for Signal Attenuation1
TLDR
It is demonstrated that no further tyrosines in the cytoplasmic part of gp130 are required for the phosphorylation of SHP2, and it is shown that repression of gene induction via Y759 does not require the presence of the SHp2 and STAT recruitment sites within the same receptor subunit, but within thesame receptor complex.
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Transcription of all four SOCS genes is increased rapidly in response to interleukin-6, in vitro and in vivo, suggesting they may act in a classic negative feedback loop to regulate cytokine signal transduction.
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TLDR
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TLDR
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TLDR
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TLDR
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