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Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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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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Protein Kinases and Phosphatases02:54

Protein Kinases and Phosphatases

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Protein Kinases and Phosphatases02:54

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Proteins undergo chemical modifications that trigger changes in the charge, structure, and conformation of the proteins. Phosphorylation, acetylation, glycosylation, nitrosylation, ubiquitination, lipidation, methylation, and proteolysis are various protein modifications that regulate protein activity. Such modifications are usually enzyme-driven.
Protein kinases
Many proteins in the cell are regulated by phosphorylation, the addition of a phosphate group. A family of enzymes called kinases...
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Receptor Tyrosine Kinases01:26

Receptor Tyrosine Kinases

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Receptor tyrosine kinases or RTKs are membrane-bound receptors that phosphorylate specific tyrosine on protein substrates. RTKs regulate cellular growth, differentiation, survival, and migration. They contain an extracellular ligand binding domain, a transmembrane domain, and a cytosolic tail with intrinsic kinase activity. Several extracellular signaling molecules activate RTKs in one or more ways and relay the signal downstream. Ligands such as platelet-derived growth factor (PDGF) or...
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MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
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Janus Kinases in Leukemia.

Juuli Raivola1, Teemu Haikarainen1, Bobin George Abraham1

  • 1Faculty of Medicine and Health Technology, Tampere University, 33014 Tampere, Finland.

Cancers
|March 6, 2021
PubMed
Summary
This summary is machine-generated.

Janus kinase (JAK) signaling deregulation drives leukemia development. This review covers JAK mutations in leukemia and examines current and emerging JAK inhibitors for improved treatment outcomes.

Keywords:
Janus kinaseskinase inhibitorleukemia

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Area of Science:

  • Molecular Biology
  • Oncology
  • Immunology

Background:

  • Janus kinases (JAKs) are crucial for cytokine signaling, regulating cell growth, differentiation, and immune responses.
  • Dysregulated JAK/STAT signaling is implicated in various cancers, including leukemia, and autoimmune diseases.
  • Genomic alterations in JAKs (JAK1, JAK2, JAK3, TYK2) are common in leukemia, often leading to hyperactive signaling.

Purpose of the Study:

  • To review the role of JAK-STAT signaling deregulation in leukemia pathogenesis.
  • To discuss current and investigational JAK inhibitors for treating hematological malignancies.

Main Methods:

  • Literature review of JAK-STAT signaling in leukemia.
  • Analysis of genomic aberrations in JAKs associated with leukemia.
  • Overview of FDA-approved and clinical-stage JAK inhibitors.

Main Results:

  • Somatic mutations and fusion proteins in JAKs contribute to oncogenesis in leukemia.
  • Six JAK inhibitors are FDA-approved for autoimmune diseases and hematological malignancies.
  • Current JAK inhibitors show suboptimal efficacy, highlighting the need for novel therapeutic strategies.

Conclusions:

  • Targeting JAK-STAT signaling is a validated therapeutic approach for leukemia.
  • Further development of JAK inhibitors is essential to improve treatment efficacy and harness their full potential in leukemia therapy.