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Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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...
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
Protein Kinases and Phosphatases02:54

Protein Kinases and Phosphatases

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...
Protein Kinases and Phosphatases02:54

Protein Kinases and Phosphatases

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
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Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

Janus kinase mutations.

Ross L Levine1

  • 1Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. leviner@mskcc.org

Seminars in Oncology
|April 28, 2009
PubMed
Summary
This summary is machine-generated.

Janus kinase (JAK) mutations are common in myeloproliferative neoplasms (MPNs) like polycythemia vera and essential thrombocytosis. JAK inhibitors show promise, but further research is needed to identify which patients benefit most.

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Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Chronic myeloproliferative neoplasms (MPNs), including polycythemia vera (PV), essential thrombocytosis (ET), and primary myelofibrosis (MF), are often linked to Janus kinase (JAK) gene mutations.
  • These MPNs are characterized by distinct hematological abnormalities: PV by excess red blood cells, ET by excessive platelets, and MF by neutrophil/monocyte accumulation, bone marrow fibrosis, and failure.
  • Despite recent advances, the complex pathophysiology of MPNs remains incompletely understood, with some underlying mechanisms still unknown.

Purpose of the Study:

  • To summarize the current understanding of MPN pathophysiology, particularly the role of JAK mutations.
  • To highlight the potential therapeutic role of JAK inhibitors in treating MPNs and other JAK-driven malignancies.
  • To emphasize the need for further research to identify patient subsets who would most benefit from JAK kinase inhibitors.

Main Methods:

  • Review of recent scientific literature on MPNs, JAK mutations, and JAK inhibitor therapies.
  • Analysis of the genetic and functional studies related to JAK signaling pathways in MPNs.
  • Synthesis of current knowledge regarding the clinical presentation and molecular basis of PV, ET, and MF.

Main Results:

  • Mutations in the JAK2 gene are frequently observed in PV, ET, and MF, playing a key role in their pathogenesis.
  • A subset of MPN patients lack identifiable JAK2 mutations, indicating alternative or parallel signaling pathways are involved.
  • JAK inhibitors have demonstrated potential therapeutic benefits for MPN patients and may be applicable to other cancers driven by JAK signaling.

Conclusions:

  • JAK signaling is a critical pathway in the development of MPNs, and JAK inhibitors represent a promising therapeutic strategy.
  • The heterogeneity of MPNs, including the existence of JAK2-mutation-negative cases, necessitates further investigation into underlying mechanisms.
  • Identifying specific genetic markers and functional assays is crucial for personalizing JAK inhibitor therapy and maximizing treatment efficacy in MPNs and related malignancies.