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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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 superfamily...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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 rapamycin-insensitive companion...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

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:
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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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Related Experiment Video

Updated: Jun 29, 2026

Bioluminescence Resonance Energy Transfer (BRET)-Based Assay for Measuring Interactions of CRAF with 14-3-3 Proteins in Live Cells
06:44

Bioluminescence Resonance Energy Transfer (BRET)-Based Assay for Measuring Interactions of CRAF with 14-3-3 Proteins in Live Cells

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An autoregulatory loop mediated by miR-21 and PDCD4 controls the AP-1 activity in RAS transformation.

F Talotta1, A Cimmino, M R Matarazzo

  • 1Institute of Genetics and Biophysics A. Buzzati Traverso, CNR, Naples, Italy.

Oncogene
|October 14, 2008
PubMed
Summary

The transcription factor AP-1 induces the oncomir miR-21, which downregulates tumor suppressors PTEN and PDCD4. This miR-21 feedback loop is crucial for AP-1 activity in RAS-driven cancer.

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Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
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Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells

Published on: March 9, 2012

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Bioluminescence Resonance Energy Transfer (BRET)-Based Assay for Measuring Interactions of CRAF with 14-3-3 Proteins in Live Cells
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Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development
09:32

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Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
10:27

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells

Published on: March 9, 2012

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • The transcription factor AP-1 is crucial in cancer development, regulating protein-coding genes.
  • AP-1's role in regulating non-coding genes during tumorigenesis remains largely undescribed.
  • MicroRNAs (miRNAs) are key regulators in cancer, with some acting as oncogenes (oncomirs).

Purpose of the Study:

  • To investigate the role of AP-1 in regulating non-coding genes, specifically miRNAs, in tumorigenesis.
  • To elucidate the mechanism by which AP-1 and miR-21 interact in RAS-driven cancers.
  • To identify novel regulatory pathways involving AP-1 and oncomirs in cancer.

Main Methods:

  • Analysis of AP-1-induced gene expression.
  • Validation of miR-21 targets.
  • Assessment of PTEN and PDCD4 downregulation.
  • Investigation of feedback mechanisms in AP-1 activity.

Main Results:

  • AP-1 induces the expression of miR-21, a frequently upregulated oncomir in solid tumors, in response to RAS signaling.
  • RAS signaling, via AP-1 and miR-21, downregulates the tumor suppressors PTEN and PDCD4.
  • PDCD4, a negative regulator of AP-1, is downregulated by miR-21, creating a positive feedback loop essential for maximal AP-1 activation.

Conclusions:

  • A novel mechanism of AP-1 positive autoregulation in RAS transformation is identified.
  • Oncomirs, like miR-21, function as critical targets and regulators of AP-1 in tumorigenesis.
  • This study reveals a new layer of gene regulation in cancer involving AP-1 and miRNAs.