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Videos de Conceptos Relacionados

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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PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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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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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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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.
The mTOR pathway or the...
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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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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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Abnormal Proliferation02:23

Abnormal Proliferation

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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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Video Experimental Relacionado

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 se hace cargo cuando el K-Ras oncogénico duerme.

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
Resumen

La recaída del tumor después de la terapia dirigida es un gran desafío. Una nueva investigación revela que YAP1 (proteína asociada al sí 1) actúa como un impulsor clave, compensando la pérdida de la señalización K-Ras en los cánceres.

Área de la Ciencia:

  • Oncología Oncología.
  • Biología Molecular Biología Molecular
  • Genética del cáncer Genética del cáncer.

Sus antecedentes:

  • La recaída del tumor después de la terapia dirigida a oncogenes sigue siendo un desafío clínico significativo.
  • Las células cancerosas a menudo exhiben adicción a vías de señalización oncogénicas específicas, como K-Ras.

Objetivo del estudio:

  • Aclarar los mecanismos moleculares subyacentes a la recaída tumoral después del fracaso de las terapias dirigidas a la adicción oncogénica.
  • Identificar los reguladores clave que compensan la pérdida de la señalización de K-Ras en los cánceres dependientes de K-Ras.

Principales métodos:

  • Investigó el papel de los coactivadores de transcripción en la resistencia a la terapia del cáncer.
  • Utilizó enfoques genéticos y de biología molecular para estudiar la compensación de la vía de señalización.

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Principales resultados:

  • Identificó el coactivador transcripcional YAP1 (proteína asociada a sí 1) como un factor crítico en la recaída del tumor.
  • Se demostró que YAP1 impulsa mecanismos compensatorios después de la pérdida de la señalización K-Ras.
  • Destacó el papel central de YAP1 en los cánceres dependientes de K-Ras.

Conclusiones:

  • YAP1 es un objetivo terapéutico clave para superar la resistencia en los cánceres dependientes de K-Ras.
  • Comprender el papel de YAP1 en la compensación de la señalización es crucial para desarrollar estrategias efectivas contra el cáncer.