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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Regulation of Nuclear Protein Sorting01:45

Regulation of Nuclear Protein Sorting

Nuclear protein sorting regulates nucleus composition and gene expression, crucial for determining the fate of a eukaryotic cell. Hence, the entry and exit of molecules across the nuclear envelope is a tightly controlled process. Nuclear protein sorting can be inhibited by one of the following ways: 1) masking cargo signal sequences, 2) modifying the nuclear receptor's affinity for cargo, 3) controlling the nuclear pore size, 4) retaining the cargo during its transit to the cytosol or the...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
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...

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Related Experiment Video

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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

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Published on: June 29, 2011

Nucleolar AATF regulates c-Jun-mediated apoptosis.

Saima E Ferraris1, Kimmo Isoniemi, Elin Torvaldson

  • 1Department of Biosciences, Åbo Akademi University, FIN-20521 Turku, Finland.

Molecular Biology of the Cell
|August 31, 2012
PubMed
Summary

The apoptosis-antagonizing transcription factor (AATF) acts as a nucleolar stress sensor and cofactor for c-Jun. AATF regulates c-Jun activity and promotes stress-induced apoptosis, particularly following UV radiation.

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Last Updated: May 19, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

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Published on: June 29, 2011

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
09:52

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia

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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • The transcription factor c-Jun is crucial for stress-induced apoptosis.
  • The precise molecular mechanisms governing c-Jun's proapoptotic role remain unclear.

Purpose of the Study:

  • To elucidate the role of the apoptosis-antagonizing transcription factor (AATF) in c-Jun-mediated apoptosis.
  • To identify AATF as a novel nucleolar stress sensor and cofactor for c-Jun.

Main Methods:

  • Investigated AATF's function as a cofactor for c-Jun.
  • Analyzed the impact of AATF expression levels on c-Jun activation and target gene expression (FasL, TNF-α).
  • Utilized UV irradiation and c-Jun-deficient cells to assess AATF's role in apoptosis induction and c-Jun binding.

Main Results:

  • AATF acts as a nucleolar stress sensor and is required for c-Jun-mediated apoptosis.
  • Altering AATF levels proportionally affected c-Jun phosphorylation and the expression of proapoptotic genes.
  • UV irradiation induced AATF translocation to the nucleus, facilitating its association with c-Jun and promoting apoptosis.

Conclusions:

  • AATF is a nucleolar-confined cofactor that modulates c-Jun activity.
  • AATF's expression levels and localization are critical determinants of stress-induced c-Jun activity and apoptosis.
  • AATF is essential for UV-induced apoptosis, functioning through its interaction with c-Jun.