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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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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...
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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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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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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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Related Experiment Video

Updated: Apr 27, 2026

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
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Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

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YAP1 takes over when oncogenic K-Ras slumbers.

Florian R Greten1

  • 1Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy, Paul-Ehrlich-Strasse 42-44, 60596 Frankfurt, Germany.

Cell
|July 5, 2014
PubMed
Summary

Tumor relapse after targeted therapy is a major challenge. New research reveals that YAP1 (Yes-associated protein 1) acts as a key driver, compensating for lost K-Ras signaling in cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Tumor relapse following oncogene-targeted therapy remains a significant clinical challenge.
  • Cancer cells often exhibit addiction to specific oncogenic signaling pathways, such as K-Ras.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying tumor relapse after the failure of therapies targeting oncogene addiction.
  • To identify key regulators that compensate for the loss of K-Ras signaling in K-Ras-dependent cancers.

Main Methods:

  • Investigated the role of transcriptional coactivators in cancer therapy resistance.
  • Utilized genetic and molecular biology approaches to study signaling pathway compensation.

Main Results:

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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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Related Experiment Videos

Last Updated: Apr 27, 2026

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  • Identified the transcriptional coactivator YAP1 (Yes-associated protein 1) as a critical factor in tumor relapse.
  • Demonstrated that YAP1 drives compensatory mechanisms following the loss of K-Ras signaling.
  • Highlighted YAP1's central role in K-Ras-dependent cancers.

Conclusions:

  • YAP1 is a key therapeutic target for overcoming resistance in K-Ras-dependent cancers.
  • Understanding YAP1's role in signaling compensation is crucial for developing effective anti-cancer strategies.