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Related Concept Videos

General Transcription Factors01:30

General Transcription Factors

Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012 for this...
Transcription Factors02:16

Transcription Factors

Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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 heterodimer of NF-κB...

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Activating transcription factor 4 modulates BDNF release from microglial cells.

Pengling Sun1, Xiangnan Li, Chengwen Chen

  • 1Department of Anesthesiology, Neuroscience Research Centre, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.

Journal of Molecular Neuroscience : MN
|September 28, 2013
PubMed
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Activating transcription factor 4 (ATF4) activation in microglial cells increases brain-derived neurotrophic factor (BDNF) release, a key molecule in pathogenic pain. This study clarifies a mechanism linking ATF4 to BDNF secretion in pain pathways.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Pathogenic pain mechanisms remain largely unclear.
  • Activating transcription factor 4 (ATF4) is crucial for cell activation.
  • Brain-derived neurotrophic factor (BDNF) plays a significant role in pathogenic pain.

Purpose of the Study:

  • To investigate the role of ATF4 in inducing BDNF release from microglial cells.
  • To explore the relationship between ATF4, BDNF, and microglial cell apoptosis.

Main Methods:

  • Cultured mouse microglial cells.
  • Overexpressed ATF4 using gene transfection.
  • Measured BDNF levels via ELISA.
  • Assessed apoptosis using flow cytometry.
  • Utilized protease-activated receptor-2 (PAR2) agonist tryptase.

Main Results:

  • Microglial cells express both ATF4 and PAR2.
  • ATF4 overexpression significantly increased BDNF release.
  • ATF4-overexpressing cells showed increased apoptosis, which was inhibited by tryptase.
  • Tryptase treatment maintained high BDNF secretion in ATF4-overexpressing cells.

Conclusions:

  • ATF4 activation increases BDNF release from microglial cells.
  • This suggests a novel pathway involving ATF4 in pain pathogenesis.
  • PAR2 signaling may modulate ATF4-induced BDNF release and apoptosis.