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The Ras Gene02:38

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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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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...
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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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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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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
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Analyzing Ras-associated cell proliferation signaling.

Matthew C Stout1, Edgar Asiimwe, James R Birkenstamm

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

Methods in Molecular Biology (Clifton, N.J.)
|June 8, 2014
PubMed
Summary
This summary is machine-generated.

Ras signaling pathways regulate cell cycle progression and apoptosis, with downstream effectors having dual roles. Cell culture confluency significantly impacts Ras effector activation, underscoring the need for consistent growth conditions.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Signal Transduction

Background:

  • Ras-dependent signaling pathways are critical regulators of fundamental cellular processes, including cell cycle progression, proliferation, senescence, and apoptosis.
  • Downstream effectors of Ras exhibit context-dependent functions, capable of promoting cell proliferation or inducing cell cycle arrest and apoptosis.
  • Cross-talk exists between key Ras effector pathways, notably the phosphoinositide 3-kinase-AKT (PI3K-AKT) and Raf-MEK-extracellular signal-regulated kinase (Raf-MEK-ERK) pathways.

Purpose of the Study:

  • To investigate the distinct roles of various Ras-dependent signaling pathways in regulating cell cycle progression, proliferation, senescence, and apoptosis.
  • To elucidate the complex interplay between different Ras downstream signaling cascades.
  • To emphasize the critical influence of cellular growth conditions on Ras signaling.

Main Methods:

  • Experimental dissection of Ras-dependent signaling pathways.
  • Analysis of cell cycle progression, proliferation, senescence, and apoptosis.
  • Assessment of downstream effector activation under varying cell culture confluency.

Main Results:

  • Ras-dependent signaling pathways exert differential effects on cell cycle control, proliferation, and cell death.
  • The activation status of Ras downstream effectors is sensitive to the confluency of cells in culture.
  • Specific growth conditions can alter the balance between proliferation and cell cycle arrest/apoptosis.

Conclusions:

  • Understanding Ras signaling requires careful consideration of the specific pathways involved and their interactions.
  • Cell culture confluency is a crucial variable that must be controlled for reproducible studies of Ras-dependent signaling.
  • The dual roles of Ras effectors highlight the complexity of cellular regulation and the potential for therapeutic targeting.