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Inhibition of Cdk Activity02:34

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Related Experiment Video

Updated: Mar 17, 2026

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia
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RIPK3 Slams the Brake on Leukemogenesis.

Francis Ka-Ming Chan1

  • 1Department of Pathology, Immunology and Microbiology Program, University of Massachusetts Medical School, 368 Plantation Street, Worcester, MA 01605, USA.

Cancer Cell
|July 15, 2016
PubMed
Summary

Cancer cells evade death, but RIPK3, a necroptosis kinase, plays a key role in preventing acute myeloid leukemia development, according to new research.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Cancer cells exhibit a key characteristic of evading cell death pathways.
  • Necroptosis is a regulated form of inflammatory cell death.
  • Acute myeloid leukemia (AML) is a cancer of the blood and bone marrow.

Purpose of the Study:

  • To investigate the role of receptor-interacting protein kinase 3 (RIPK3) in the development of acute myeloid leukemia.
  • To understand how RIPK3 influences cancer cell death evasion.

Main Methods:

  • The study identified RIPK3 as a crucial kinase involved in necroptosis.
  • Researchers examined the function of RIPK3 in the context of acute myeloid leukemia development.

Main Results:

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  • RIPK3 was found to be essential in inhibiting the development of acute myeloid leukemia.
  • The kinase activity of RIPK3 is critical for its tumor-suppressive function in AML.

Conclusions:

  • RIPK3 plays a significant role in preventing the initiation and progression of acute myeloid leukemia.
  • Targeting RIPK3 or modulating necroptosis pathways may offer novel therapeutic strategies for AML.