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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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cAMP-dependent Protein Kinase Pathways01:25

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

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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...
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Protein Kinases and Phosphatases02:54

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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.
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Assaying Protein Kinase Activity with Radiolabeled ATP
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Maybe we don't know JAK?

Luis J Schwarz1, Justin M Balko2

  • 1Department of Medicine, Vanderbilt-Ingram Cancer Center, Vanderbilt University , Nashville, TN, USA.

Molecular & Cellular Oncology
|September 22, 2016
PubMed
Summary
This summary is machine-generated.

Precision medicine relies on biomarkers. Janus kinase-2 (JAK2) inhibition shows promise for triple-negative breast cancers with 9p24 amplification, though targeting this amplicon presents challenges.

Keywords:
9p24JAK2PD-L1breast cancerchemotherapy

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Area of Science:

  • Oncology
  • Genetics
  • Pharmacology

Background:

  • Biomarkers are crucial for precision medicine, identifying molecular phenotypes and therapeutic vulnerabilities.
  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited targeted therapies.
  • 9p24 amplification is a genetic alteration observed in some TNBCs.

Purpose of the Study:

  • To comment on the therapeutic potential of Janus kinase-2 (JAK2)-specific inhibition in TNBC.
  • To discuss the challenges associated with targeting the 9p24 amplicon in cancer treatment.

Main Methods:

  • Review and commentary on existing research.
  • Analysis of genetic amplification patterns (9p24).
  • Discussion of JAK2-specific inhibition strategies.

Main Results:

  • Janus kinase-2 (JAK2)-specific inhibition is identified as a potential therapeutic strategy for TNBC with 9p24 amplification.
  • The 9p24 amplicon presents specific challenges for targeted therapeutic development.

Conclusions:

  • Targeting JAK2 offers a precision medicine approach for a subset of TNBC patients.
  • Overcoming challenges in targeting the 9p24 amplicon is essential for clinical translation.