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Related Concept Videos

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

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...
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...
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
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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A complex interplay between Akt, TSC2 and the two mTOR complexes.

Jingxiang Huang1, Brendan D Manning

  • 1Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA. bmanning@hsph.harvard.edu

Biochemical Society Transactions
|January 16, 2009
PubMed
Summary
This summary is machine-generated.

The tuberous sclerosis complex (TSC) 1-TSC2 regulates Akt signaling, which impacts mTORC1 and mTORC2. Dysregulation of this pathway affects cell growth and is implicated in various human diseases.

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Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Oncology

Background:

  • The Akt/PKB pathway is intricately linked with the TSC1-TSC2 complex, influencing cell growth and metabolism.
  • PI3K-Akt signaling is crucial for cell survival and proliferation, and its dysregulation is common in cancer.

Purpose of the Study:

  • To review the complex interplay between Akt, the TSC1-TSC2 complex, and mTOR signaling.
  • To elucidate the mechanisms by which TSC1-TSC2 regulates mTORC1 and mTORC2 activity.
  • To highlight the implications of these interactions in human diseases.

Main Methods:

  • Literature review of studies investigating Akt, TSC1-TSC2, and mTOR signaling pathways.
  • Analysis of molecular mechanisms underlying the regulation of mTORC1 and mTORC2 by TSC1-TSC2.
  • Discussion of the role of these pathways in cellular processes and disease pathogenesis.

Main Results:

  • Akt phosphorylates TSC2, relieving TSC1-TSC2 inhibition of Rheb and activating mTORC1.
  • Loss of TSC1-TSC2 leads to attenuated Akt signaling due to mTORC1 activation and impaired mTORC2 activity.
  • TSC1-TSC2 complex deficiency affects mTORC2-mediated Akt hydrophobic motif phosphorylation.

Conclusions:

  • The Akt-TSC-mTOR network represents a critical signaling hub with complex regulatory feedback loops.
  • Dysregulation of this network contributes to the pathogenesis of various human diseases, including cancer.
  • Further research into this pathway could reveal novel therapeutic targets.