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Related Concept Videos

Activation and Inactivation of G Proteins01:22

Activation and Inactivation of G Proteins

Heterotrimeric G proteins are guanine nucleotide-binding proteins. As the name suggests, heterotrimeric G proteins are composed of three subunits: alpha, beta, and gamma. They remain GDP-bound or GTP-bound inside the cells and switch between inactive/active states. The Gα subunit possesses the nucleotide-binding pocket that binds guanine nucleotides and switches between GDP or GTP-bound states. In contrast, the Gꞵ and Gγ subunits are always bound together with high affinity and are together...
Indirect-Acting Cholinergic Agonists: Mechanism of Action01:18

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Indirect-acting cholinergic agonists work by interacting with an enzyme called acetylcholinesterase (AChE) in the synaptic cleft. They can be reversible or irreversible inhibitors and have different effects on the enzyme.
Reversible inhibitors like edrophonium bind to a specific part of the enzyme called the anionic catalytic site. They form noncovalent bonds, which means they are not strongly attached to the enzyme. This creates a temporary and less stable enzyme–inhibitor complex, leading to...
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X-Inactivation

The human X chromosome contains over ten times the number of genes as in the Y chromosome. Since males have only one X chromosome, and females have two, one might expect females to produce twice as many of the proteins, with undesirable results.
X-inactivation01:58

X-inactivation

The human X chromosome contains over ten times the number of genes as in the Y chromosome. Since males have only one X chromosome, and females have two, one might expect females to produce twice as many of the proteins, with undesirable results.
DNA Damage can Stall the Cell Cycle02:36

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

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The Akt DUBbed InAktive.

Kui Lin1

  • 1Department of Translational Oncology, Research Oncology, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA. klin@gene.com

Science Signaling
|January 10, 2013
PubMed
Summary
This summary is machine-generated.

The phosphoinositide-3 kinase-Akt-mammalian target of rapamycin pathway is regulated by ubiquitination and deubiquitination. These processes act as on-off switches for Akt activity, crucial for preventing pathological consequences.

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Amide Hydrogen/Deuterium Exchange & MALDI-TOF Mass Spectrometry Analysis of Pak2 Activation

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Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Cancer Research

Background:

  • The phosphoinositide-3 kinase-Akt-mammalian target of rapamycin (PI3K-Akt-mTOR) pathway is critical for cell growth and survival.
  • Akt activation is a complex process involving growth factor stimulation and posttranslational modifications.
  • Dysregulation of Akt signaling is implicated in various pathological conditions, including cancer.

Purpose of the Study:

  • To investigate the role of ubiquitination and deubiquitination in regulating Akt activity.
  • To identify key enzymes involved in these posttranslational modifications of Akt.
  • To understand how these regulatory mechanisms maintain Akt activity balance.

Main Methods:

  • Identification of E3 ligase responsible for Lys(63)-linked ubiquitination of Akt.
  • Discovery of cylindromatosis tumor suppressor as a deubiquitinating enzyme (DUB) for Akt.
  • Analysis of Akt ubiquitination and deubiquitination cycles.

Main Results:

  • Akt undergoes Lys(63)-linked ubiquitination mediated by a specific E3 ligase.
  • Cylindromatosis functions as a deubiquitinating enzyme for Akt.
  • Ubiquitination and deubiquitination act as dynamic on-off switches for Akt activity.

Conclusions:

  • Ubiquitination and deubiquitination represent a novel regulatory layer for Akt.
  • These cycles are essential for maintaining Akt activity homeostasis.
  • Disruptions in Akt ubiquitination/deubiquitination balance can lead to pathological outcomes.