Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

8.5K
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...
8.5K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

2.3K
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...
2.3K
Initiation of Translation02:33

Initiation of Translation

24.5K
Initiating translation is complex because it involves multiple molecules. Initiator tRNA, ribosomal subunits, and eukaryotic initiation factors (eIFs) are all required to assemble on the initiation codon of mRNA. This process consists of several steps that are mediated by different eIFs.
First, the initiator tRNA must be selected from the pool of elongator tRNAs by eukaryotic initiation factor 2 (eIF2). The initiator tRNA (Met-tRNAi) has conserved sequence elements including modified bases at...
24.5K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

5.1K
The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.1K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

1.8K
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
1.8K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.6K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.6K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Pericytes Are Odontoblast Progenitor Cells Depending on ER Stress.

Journal of dental research·2025
Same author

Low energy virtual monochromatic CT with deep learning image reconstruction to improve delineation of endoleaks.

Clinical radiology·2024
Same author

Urticaria due to natto (fermented soybeans).

Clinical and experimental dermatology·2021
Same author

Gamma-delta T cell large granular lymphocyte leukaemia with multiple cutaneous nodules that showed spontaneous regression.

Journal of the European Academy of Dermatology and Venereology : JEADV·2018
Same author

Recurrent Spindle Cell Carcinoma Shows Features of Mesenchymal Stem Cells.

Journal of dental research·2018
Same author

Combination of low-dose total skin electron beam therapy and subsequent localized skin electron beam therapy as a therapeutic option for advanced-stage mycosis fungoides.

Clinical and experimental dermatology·2017

Related Experiment Video

Updated: Apr 24, 2026

Author Spotlight: Deciphering the Role of ATM in Ataxia-Telangiectasia and the Associated Cerebellar Degeneration
08:41

Author Spotlight: Deciphering the Role of ATM in Ataxia-Telangiectasia and the Associated Cerebellar Degeneration

Published on: December 27, 2024

1.5K

Translational initiation regulated by ATM in dendritic cells development.

E Y So1, T Ouchi1

  • 1Department of Cancer Genetics, Roswell Park Cancer Institute, Buffalo, NY, USA.

Cell Death & Disease
|September 12, 2014
PubMed
Summary

Ataxia telangiectasia mutated (ATM) protein is crucial for dendritic cell (DC) development from bone marrow (BM) cells. ATM deficiency impairs protein translation, leading to reduced DC development and T cell activation.

More Related Videos

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

941
Toeprinting Analysis of Translation Initiation Complex Formation on Mammalian mRNAs
10:37

Toeprinting Analysis of Translation Initiation Complex Formation on Mammalian mRNAs

Published on: May 10, 2018

12.3K

Related Experiment Videos

Last Updated: Apr 24, 2026

Author Spotlight: Deciphering the Role of ATM in Ataxia-Telangiectasia and the Associated Cerebellar Degeneration
08:41

Author Spotlight: Deciphering the Role of ATM in Ataxia-Telangiectasia and the Associated Cerebellar Degeneration

Published on: December 27, 2024

1.5K
Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

941
Toeprinting Analysis of Translation Initiation Complex Formation on Mammalian mRNAs
10:37

Toeprinting Analysis of Translation Initiation Complex Formation on Mammalian mRNAs

Published on: May 10, 2018

12.3K

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Ataxia telangiectasia mutated (ATM) protein regulates DNA repair, cell cycle, growth, and stem cell renewal.
  • Granulocyte macrophage colony-stimulating factor (GM-CSF) is vital for dendritic cell (DC) development.

Purpose of the Study:

  • To investigate the role of ATM in GM-CSF-induced DC development from bone marrow (BM) cells.
  • To elucidate the molecular mechanisms underlying ATM's function in DC development.

Main Methods:

  • Utilized wild-type and ATM-null bone marrow (BM) cells.
  • Stimulated BM cells with GM-CSF.
  • Analyzed protein expression and phosphorylation (Jak2, STAT5, mTOR, 4EBP1, Erk, p38, Akt).
  • Assessed BM proliferation and DC development.
  • Restored DC development using constitutively active Akt or STAT5 in ATM-null BM cells.

Main Results:

  • ATM inactivation decreased BM proliferation and DC development.
  • ATM deficiency delayed and prolonged hypophosphorylation of 4EBP1 upon GM-CSF stimulation.
  • Akt and STAT5 signaling pathways were implicated in ATM-dependent DC development.
  • Restoring Akt or STAT5 activity in ATM-null BM cells rescued DC development.

Conclusions:

  • ATM deficiency impairs GM-CSF-induced DC development by hindering the initiation of protein translation in BM cells.
  • ATM plays a critical role in regulating key signaling pathways essential for DC maturation and function.
  • Targeting ATM or its downstream pathways may offer therapeutic strategies for immune disorders related to DC dysfunction.