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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...
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.
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
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...
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...

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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
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Cdc45 degradation during differentiation and apoptosis.

S Pollok1, F Grosse

  • 1Leibniz Institute for Age Research (Fritz Lipmann Institute), Biochemistry Group, Jena, Germany.

Biochemical and Biophysical Research Communications
|September 5, 2007
PubMed
Summary

Cell division cycle protein 45 (Cdc45) is ubiquitylated and degraded by the proteasome pathway in human cells, representing its first known posttranslational modification. This regulation is crucial for DNA replication and cell cycle control.

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Published on: October 6, 2022

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Cell division cycle protein 45 (Cdc45) is essential for eukaryotic DNA replication initiation and elongation.
  • Understanding the regulation of Cdc45 is critical for comprehending cell cycle control and DNA replication fidelity.

Purpose of the Study:

  • To investigate the posttranslational modifications and degradation pathways of Cdc45 in human cells.
  • To determine if Cdc45 is a substrate for the anaphase-promoting complex/cyclosome (APC/C).

Main Methods:

  • Treatment of cultured human cells with proteasomal inhibitors during terminal differentiation.
  • Bioinformatic analysis of the Cdc45 amino acid sequence to identify putative destruction and KEN-boxes.
  • Observation of Cdc45 protein cleavage during apoptosis.

Main Results:

  • Proteasomal inhibitors decelerated the degradation of Cdc45 during terminal differentiation, indicating proteasomal involvement.
  • Vertebrate Cdc45 sequences contain destruction boxes and a KEN-box, suggesting it is an APC/C substrate.
  • Cdc45 protein was not cleaved during apoptosis, consistent with the stability of replication proteins during programmed cell death.

Conclusions:

  • Cdc45 undergoes ubiquitylation and proteasomal degradation, representing its first identified posttranslational modification.
  • These findings establish Cdc45 as a novel substrate of the APC/C, linking it to cell cycle regulation.
  • The stability of Cdc45 during apoptosis highlights specific regulatory mechanisms for replication factors.