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Related Concept Videos

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.
Ras is a...
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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.
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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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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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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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Related Experiment Video

Updated: Jan 9, 2026

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RASH3D19 mediates RAS activation through a positive feedback loop in KRAS-mutant cancer.

Warapen Treekitkarnmongkol1, Hiroshi Katayama2, Deivendran Sankaran1,3

  • 1Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Nature Cell Biology
|December 1, 2025
PubMed
Summary
This summary is machine-generated.

Researchers identified RASH3D19 as a key mediator in cancer cell growth and resistance to KRAS inhibitors. Targeting RASH3D19 may overcome resistance and shrink tumors in KRAS-mutant cancers.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Actively investigating therapeutic targets for mutant KRAS-driven cancers.
  • Identifying feedback mechanisms driving adaptive resistance to KRAS inhibitors.

Purpose of the Study:

  • To identify RASH3D19 as a mediator of RAS pathway activation.
  • To investigate the role of RASH3D19 in KRAS-mutant cancer resistance.

Main Methods:

  • Investigated the KRAS-microRNA signaling axis.
  • Examined RASH3D19's role in RAS pathway activation and feedback loops.
  • Assessed the effects of RASH3D19 genetic deletion in vitro and in vivo.

Main Results:

  • Identified RASH3D19 as a mediator in a positive feedback loop involving KRAS-microRNA signaling.
  • Demonstrated that RASH3D19 promotes RAS pathway activation via EGFR complex interactions.
  • Genetic deletion of RASH3D19 inhibited cancer cell growth and sensitized cells to KRAS inhibitors.

Conclusions:

  • RASH3D19 is a crucial mediator in RAS pathway reactivation and adaptive resistance.
  • Targeting RASH3D19 offers a potential strategy to overcome resistance to KRAS inhibitors.
  • RASH3D19 inhibition may lead to tumor debulking in KRAS-mutant cancers.