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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...
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...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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...
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...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

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Related Experiment Video

Updated: Jun 28, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

Stat1 phosphorylation determines Ras oncogenicity by regulating p27 kip1.

Shuo Wang1, Jennifer F Raven, Joan E Durbin

  • 1Department of Oncology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.

Plos One
|October 23, 2008
PubMed
Summary

Signal transducer and activator of transcription 1 (Stat1) suppresses Ras-driven cancer by inducing p27 Kip1 expression. This pathway, crucial for tumor suppression, offers potential prognostic and therapeutic targets.

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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

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Last Updated: Jun 28, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • p27 Kip1 inactivation is linked to tumorigenesis and impacts cancer prognosis.
  • Signal transducer and activator of transcription 1 (Stat1) is vital for immune responses and tumor surveillance, acting downstream of interferons.

Purpose of the Study:

  • To investigate the role of Stat1 in suppressing Ras transformation, independent of interferon signaling.
  • To elucidate the molecular mechanisms by which Stat1 inhibits Ras-driven oncogenesis.

Main Methods:

  • Utilized cell-based assays to study Ras transformation.
  • Analyzed Stat1 phosphorylation at specific sites (tyrosine 701 and serine 727).
  • Investigated the transcriptional regulation of p27 Kip1 by Stat1 and Stat3.

Main Results:

  • Stat1 suppresses Ras transformation and tumorigenesis independently of interferon response.
  • Stat1 phosphorylation at tyrosine 701, but not serine 727, is essential for this tumor suppressor function.
  • Stat1 transcriptionally induces p27 Kip1 expression in Ras-transformed cells, dependent on Stat1 (Tyr701) phosphorylation and Stat3 activation.
  • Inactivation of p27 Kip1 reverses the tumor suppressor effects of Stat1.

Conclusions:

  • Stat1 and p27 Kip1 coordinate to suppress oncogenic Ras.
  • Stat1 phosphorylation status may serve as a prognostic biomarker and predict treatment response in human cancers.
  • This study reveals a novel Stat1-p27 Kip1 axis in cancer suppression.