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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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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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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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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.
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Related Experiment Video

Updated: Apr 28, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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Oncogenic Ras pushes (and pulls) cell cycle progression through ERK activation.

Paul M Campbell1

  • 1Department of Pharmacology and Physiology, Drexel University College of Medicine, 245 N. 15th Street, MS 488, Philadelphia, PA, 19102, USA, paul.campbell@drexelmed.edu.

Methods in Molecular Biology (Clifton, N.J.)
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The Ras-Raf-MEK-ERK pathway regulates crucial cell functions. Aberrant signaling in cancer highlights its importance, revealing complex control mechanisms beyond simple on/off switches.

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Area of Science:

  • Molecular Biology
  • Cellular Signaling
  • Oncology

Background:

  • The Ras-Raf-MEK-ERK signaling cascade transmits extracellular signals influencing cell proliferation, differentiation, senescence, and death.
  • Dysregulation of this pathway is implicated in various cancers, making it a key focus in tumor biology research.

Purpose of the Study:

  • To investigate the intricate control mechanisms of the Ras-Raf-MEK-ERK pathway in cell cycle regulation.
  • To illustrate that the pathway's regulation is more complex than a simple rheostat model.

Main Methods:

  • Analysis of signaling pathway components.
  • Investigation of cell cycle regulatory mechanisms.
  • Experimental validation of pathway control dynamics.

Main Results:

  • Evidence presented on the detailed regulatory mechanisms of the Ras-Raf-MEK-ERK pathway.
  • Demonstration of sophisticated control over cell cycle progression.
  • Findings suggest a non-linear, complex regulatory model for this signaling cascade.

Conclusions:

  • The Ras-Raf-MEK-ERK pathway exhibits intricate and delicate control over cell cycle regulation.
  • Pathway regulation is not a simple rheostat but involves complex feedback and integration mechanisms.
  • Understanding these complexities is crucial for cancer biology and therapeutic development.