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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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

DNA Damage Can Stall the Cell Cycle

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...
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...
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
Destabilization of Microtubules01:45

Destabilization of Microtubules

The destabilization of microtubules can occur during different stages of the microtubule lifecycle, such as nucleation or elongation. It can take place at either end of the microtubule or in the microtubule lattices as a whole. The lifespan of individual microtubules within a cell varies according to the cell type and stage of the cell cycle. During interphase, the lifespan of the microtubule is about 30 minutes, while during cell division, it is about 15 minutes. In axonal microtubules of...
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze the...

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Related Experiment Video

Updated: Jun 3, 2026

Assaying Protein Kinase Activity with Radiolabeled ATP
08:05

Assaying Protein Kinase Activity with Radiolabeled ATP

Published on: May 26, 2017

All stressed out without ATM kinase.

J Jefferson P Perry1, John A Tainer

  • 1Skaggs Institute for Chemical Biology, Department of Molecular Biology, La Jolla, CA 92037, USA.

Science Signaling
|April 7, 2011
PubMed
Summary
This summary is machine-generated.

Ataxia-telangiectasia (A-T) is linked to reactive oxygen species (ROS) and the ATM kinase. New findings show ATM is activated by oxidation, impacting A-T and cancer therapy.

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Last Updated: Jun 3, 2026

Assaying Protein Kinase Activity with Radiolabeled ATP
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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:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Ataxia-telangiectasia (A-T) is a rare neurodegenerative disease caused by mutations in the ATM kinase.
  • ATM kinase is crucial for cell cycle checkpoints and DNA repair.
  • A-T neuropathology is linked to oxidative stress from reactive oxygen species (ROS), but ATM's role was unclear.

Purpose of the Study:

  • To investigate the intersection of ROS and ATM kinase signaling in A-T.
  • To elucidate the mechanism of ATM activation by oxidative stress.
  • To explore implications for A-T and cancer therapeutics.

Main Methods:

  • Structural insights into ATM homologs (DNA-PK, mTOR).
  • Biochemical assays to detect ATM activation via oxidation.
  • Analysis of ATM dimerization and conformational changes.

Main Results:

  • ATM can be directly activated by oxidation, forming a disulfide-linked dimer.
  • This oxidative activation mechanism is distinct from DNA damage-induced activation.
  • Structural data suggests ATM signaling pathways for oxidative stress.

Conclusions:

  • ATM signaling is directly modulated by oxidative stress through a novel activation mechanism.
  • This discovery reframes understanding of A-T pathogenesis and ATM function.
  • Findings may inform strategies to sensitize cancer cells to therapy.