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NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
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Role of Hematopoietic Growth Factors01:28

Role of Hematopoietic Growth Factors

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Hematopoietic growth factors are molecules that regulate the differentiation rate of hematopoietic stem cells (HSCs). Erythropoietin (EPO), primarily produced by the kidneys, plays a crucial role in erythrocyte production. When oxygen levels in the blood are low, EPO is released into the bloodstream, reaching the bone marrow, where it stimulates HSCs to differentiate and mature into erythrocytes, which are vital for oxygen transport.
Thrombopoietin (TPO), mainly released by the liver,...
4.1K
Regulation of Hematopoietic Stem Cells01:01

Regulation of Hematopoietic Stem Cells

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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
4.2K
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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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
8.9K
Co-activators and Co-repressors02:04

Co-activators and Co-repressors

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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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Related Experiment Video

Updated: Mar 1, 2026

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α
11:27

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

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NF-κB in Hematological Malignancies.

Véronique Imbert1, Jean-François Peyron2

  • 1Centre Méditerranéen de Médecine Moléculaire, INSERM U1065, Université Côte d'Azur, 06204 Nice, France. Veronique.IMBERT@unice.fr.

Biomedicines
|June 1, 2017
PubMed
Summary

Nuclear Factor Κ-light-chain-enhancer of activated B cells (NF-κB) pathway deregulation drives hematological malignancies. Genetic alterations and microenvironment signaling contribute to aberrant NF-κB activation in cancer.

Keywords:
NF-κBleukemialymphoma

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Area of Science:

  • Molecular biology
  • Immunology
  • Oncology

Background:

  • Nuclear Factor Κ-light-chain-enhancer of activated B cells (NF-κB) transcription factors regulate immunity, stress, apoptosis, and differentiation.
  • Constitutive activation of NF-κB pathways is implicated in cancer, diabetes, inflammation, and autoimmunity.
  • Deregulation of NF-κB signaling is a key factor in the development of various diseases.

Purpose of the Study:

  • This review focuses on the mechanisms underlying NF-κB deregulation in hematological malignancies.
  • It examines how genetic alterations and microenvironmental factors contribute to aberrant NF-κB activation in these cancers.

Main Methods:

  • Review of existing literature on NF-κB signaling pathways.
  • Analysis of genetic alterations (translocations, amplifications, mutations) affecting NF-κB regulators.
  • Investigation of microenvironment-driven NF-κB activation in cancer cells.

Main Results:

  • Positive NF-κB regulators can function as oncogenes, often altered by chromosomal translocations or mutations.
  • Negative NF-κB regulators act as tumor suppressors and are frequently inactivated by deletions or point mutations.
  • NF-κB activation in cancer cells can be driven by microenvironmental cues independent of genetic mutations.

Conclusions:

  • Aberrant NF-κB signaling, driven by genetic mutations or microenvironmental factors, is a critical mechanism in hematological malignancies.
  • Understanding these deregulation mechanisms is crucial for developing targeted therapies.
  • Targeting NF-κB pathways offers potential therapeutic strategies for hematological cancers.