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Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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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When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze the...
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...
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...
mTOR Signaling and Cancer Progression03:03

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Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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Published on: July 17, 2019

Oncogenic kinase signalling.

P Blume-Jensen1, T Hunter

  • 1The Salk Institute, Molecular and Cell Biology Laboratory, 10010 North Torrey Pines Road, La Jolla, California 92037, USA. blume@salk.edu

Nature
|May 18, 2001
PubMed
Summary
This summary is machine-generated.

Protein-tyrosine kinases (PTKs) regulate cell signaling, but their deregulation drives cancer. This review details how aberrant PI(3)K/Akt and mTOR/p70S6K pathways contribute to human malignancies.

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Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Oncology

Background:

  • Protein-tyrosine kinases (PTKs) are critical for cellular communication and development.
  • PTK activity is normally tightly regulated; dysregulation leads to malignant transformation.
  • Key downstream effectors include phosphoinositide 3-OH kinase (PI(3)K) and Akt/p70S6K.

Purpose of the Study:

  • To review how oncogenic PTKs arise from disrupted autoinhibitory controls.
  • To update knowledge on deregulated PI(3)K/Akt and mTOR/p70S6K signaling in human cancers.

Main Methods:

  • Literature review of PTK signaling pathways.
  • Analysis of genetic alterations affecting kinase activity.
  • Focus on PI(3)K/Akt and mTOR/p70S6K pathways in cancer.

Main Results:

  • Oncogenic PTKs result from loss of normal autoinhibition.
  • Deregulated PI(3)K/Akt signaling is a common mechanism in cancer.
  • Aberrant mTOR/p70S6K signaling also contributes significantly to malignancies.

Conclusions:

  • Understanding PTK deregulation is crucial for cancer therapy.
  • Targeting PI(3)K/Akt and mTOR/p70S6K pathways offers therapeutic potential.
  • Further research into kinase regulation is needed for cancer treatment.