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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.
Ras is a...
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The Ras Gene02:38

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Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

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Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).
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Small GTPases - Ras and Rho01:24

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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
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Mutations in Microorganisms01:18

Mutations in Microorganisms

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Mutations are heritable changes in an organism’s genome involving alterations in the base sequence of DNA or RNA. These changes can influence cellular processes and phenotypic traits, potentially transforming the unaltered wild type into a mutant form. Such changes, termed forward mutations, are pivotal in shaping the genetic diversity of organisms.RNA viruses exhibit the highest mutation rates due to the absence of robust proofreading mechanisms during genome replication. In contrast,...
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Mutations01:35

Mutations

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Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
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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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Direct Attack on RAS: Intramolecular Communication and Mutation-Specific Effects.

Kendra Marcus1, Carla Mattos2

  • 1Department of Chemistry and Chemical Biology, Northeastern University, Boston, Massachusetts.

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|April 17, 2015
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This summary is machine-generated.

Targeting RAS proteins, key drivers of cancer, remains challenging. New research reveals how oncogenic mutations disrupt structural networks, offering novel strategies for developing cancer drugs.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Structural Biology

Background:

  • RAS proteins are critical drivers of human cancers, yet direct targeting drugs are unavailable despite decades of research.
  • Recent advances in understanding RAS structure and function offer new opportunities for therapeutic intervention.
  • Overcoming challenges in RAS-targeted therapy requires a high-resolution understanding of oncogenic mutations.

Discussion:

  • Oncogenic RAS mutants disrupt intramolecular communication networks between the active site and membrane-binding regions.
  • These disrupted networks involve conserved structural elements but exhibit isoform-specific amino acid variations.
  • Such variations may influence the stabilization of signaling-attenuating conformational states.

Key Insights:

  • Structural networks critical for RAS signaling are altered in oncogenic mutants.
  • Isoform-specific differences in these networks present potential targets for selective drug development.
  • Understanding these molecular details is crucial for designing effective RAS-targeted therapies.

Outlook:

  • Developing strategies to target novel sites within RAS structural networks offers a promising new direction.
  • Conquering RAS-driven cancers may be achievable through innovative therapeutic approaches.
  • Further research into RAS structural dynamics and mutant functions is essential.