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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...
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...
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...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
TGF - β Signaling Pathway01:16

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

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Related Experiment Video

Updated: Jul 11, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Ras mediates cell survival by regulating tuberin.

A Freilinger1, M Rosner, M Hanneder

  • 1Medical Genetics, Obstetrics and Gynecology, Medical University of Vienna, Vienna, Austria.

Oncogene
|October 9, 2007
PubMed
Summary

Mutational activation of the Ras oncogene promotes cancer by affecting cell survival. Ras inactivation of tuberin, crucial for blocking apoptosis, is regulated by the MEK/ERK pathway, highlighting a key interaction in oncogenesis.

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Last Updated: Jul 11, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Mutational activation of the Ras oncogene is a key driver of oncogenesis.
  • Ras signaling pathways, including PI3K/AKT and MEK/ERK, influence cell cycle regulation and survival.
  • Tuberin, a tumor suppressor, normally inhibits mTOR and p70S6K, impacting apoptosis.

Purpose of the Study:

  • To investigate the role of Ras in regulating cell survival and apoptosis.
  • To elucidate the functional interaction between Ras and tuberin in the context of oncogenesis.
  • To determine the involvement of the MEK/ERK pathway in Ras-mediated effects on tuberin and p70S6K.

Main Methods:

  • Utilized Ras-mutated cancer models.
  • Assessed p70S6K activity and apoptosis.
  • Employed tuberin-negative fibroblasts for mechanistic studies.
  • Investigated the MEK/ERK pathway's role in Ras signaling.

Main Results:

  • Ras-induced cell survival correlates with increased p70S6K activity.
  • Ras negatively impacts tuberin-mediated apoptosis and p70S6K inactivation.
  • Ras's effects on apoptosis are dependent on the MEK/ERK pathway.
  • Functional tuberin is essential for Ras to counteract apoptosis.

Conclusions:

  • Ras inactivation of tuberin is a critical mechanism for regulating cell survival in Ras-driven oncogenesis.
  • This study reveals a novel functional interaction between the tumor suppressor tuberin and the oncogene Ras in apoptosis regulation.
  • Understanding this interaction provides insights into potential therapeutic strategies targeting Ras-driven cancers.