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Related Concept Videos

Phase II Reactions: Methylation Reactions01:17

Phase II Reactions: Methylation Reactions

Methylation is a phase II biotransformation process involving the attachment of a methyl group to a substrate. Enzymes known as methyltransferases orchestrate this reaction.
The mechanism of methylation unfolds in two stages. The first stage sees a methyltransferase enzyme facilitating the transfer of a methyl group from S-adenosylmethionine (SAM) to the substrate, forming S-adenosylhomocysteine (SAH). The second stage involves further metabolism of SAH into homocysteine, which can be recycled...
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
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Diversity in Cell Signaling Responses01:22

Diversity in Cell Signaling Responses

The physiological function of a cell and cellular communication are outcomes of a range of extrinsic signals, intracellular signaling pathways, and cellular responses. No two cell types express the same repertoire of signaling components. Receptors are highly selective for their cognate ligands, but once activated, they can alter multiple cellular processes such as DNA transcription, protein synthesis, and metabolic activity. 
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Global Regulatory Systems

Global regulatory systems in bacteria enable rapid and coordinated responses to environmental changes by integrating sensory inputs with gene expression, ensuring efficient adaptation to fluctuating conditions. Key global regulatory mechanisms include regulons, two-component systems, sigma factors, and secondary messengers.Regulons and Global RegulatorsA regulon is a collection of genes and operons controlled by a common global regulator. These regulators enable bacteria to prioritize resource...
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...
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Amplifying Signals via Enzymatic Cascade

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A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
09:16

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration

Published on: January 22, 2016

Systems-scale analysis reveals pathways involved in cellular response to methamphetamine.

Lijie Sun1, Hong-Mei Li, Manfredo J Seufferheld

  • 1Department of Entomology, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.

Plos One
|May 3, 2011
PubMed
Summary

Methamphetamine (METH) disrupts cellular processes, including energy metabolism and spermatogenesis. Network analysis revealed METH induces a Warburg-like effect, and dietary sugar partially mitigates METH toxicity.

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Area of Science:

  • Toxicology
  • Systems Biology
  • Genomics

Background:

  • Methamphetamine (METH) is an illicit drug with known disruptive effects on cellular processes.
  • Key molecular mechanisms underlying METH toxicity remain incompletely understood.
  • Network analysis of multi-omics data offers a powerful approach to elucidate complex toxicological responses.

Purpose of the Study:

  • To investigate the molecular pathways affected by acute methamphetamine toxicity using network analysis.
  • To identify cellular processes and genes impacted by METH exposure in Drosophila melanogaster.
  • To test the role of carbohydrate metabolism in METH-induced toxicity.

Main Methods:

  • Network analysis of proteomic and transcriptomic data from Drosophila melanogaster exposed to METH.
  • Evaluation of gene expression changes related to energy metabolism, homeostasis, and oxidative stress.
  • Assessment of the impact of dietary sugar on METH toxicity.

Main Results:

  • METH exposure induced alterations in energy metabolism, suggesting a Warburg-like effect (aerobic glycolysis).
  • Increased dietary sugars partially ameliorated METH's toxic effects.
  • METH impacted genes and proteins involved in muscular homeostasis, oxidative status, oxidative phosphorylation, spermatogenesis, and iron/calcium homeostasis.

Conclusions:

  • METH induces a toxic syndrome characterized by altered carbohydrate metabolism.
  • Dysregulation of calcium and iron homeostasis, increased oxidative stress, and disrupted mitochondrial function are key features of METH toxicity.
  • Identified candidate genes provide molecular insights into METH-induced spermatogenesis dysfunction.