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Related Concept Videos

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...
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...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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...
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...
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...

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Related Experiment Video

Updated: Jun 2, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Roles of the Ras/Raf/MEK/ERK pathway in leukemia therapy.

L S Steelman1, R A Franklin, S L Abrams

  • 1Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA.

Leukemia
|April 16, 2011
PubMed
Summary
This summary is machine-generated.

The Ras/Raf/MEK/ERK pathway is crucial in leukemia therapy, influencing treatment sensitivity and resistance. Understanding its dysregulation is key to developing effective leukemia treatments and improving patient outcomes.

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

Published on: July 17, 2019

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Last Updated: Jun 2, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

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

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • The Ras/Raf/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway plays a significant role in leukemia development and treatment response.
  • Dysregulation of this pathway, often due to genetic mutations, contributes to uncontrolled leukemia cell proliferation and resistance to apoptosis.

Purpose of the Study:

  • To review the mechanisms by which the Ras/Raf/MEK/ERK pathway contributes to drug resistance in leukemia.
  • To explore the interplay between the Ras/Raf/MEK/ERK pathway and other signaling cascades, such as the PI3K/PTEN/Akt/mTOR pathway, in the context of leukemia therapy.

Main Methods:

  • Literature review of studies investigating the Ras/Raf/MEK/ERK pathway in leukemia.
  • Analysis of genetic alterations and signaling crosstalk impacting therapeutic sensitivity.

Main Results:

  • Aberrant activation of the Ras/Raf/MEK/ERK pathway promotes chemoresistance and resistance to targeted therapies in leukemia.
  • Cross-talk between the Ras/Raf/MEK/ERK pathway and the PI3K/PTEN/Akt/mTOR pathway influences therapeutic outcomes.
  • Certain chemotherapeutic drugs can activate the Ras/Raf/MEK/ERK pathway, contributing to treatment resistance.

Conclusions:

  • Targeting the Ras/Raf/MEK/ERK pathway holds potential for overcoming drug resistance in leukemia.
  • Modulating this pathway could enhance the efficacy of current leukemia therapies and improve patient health.