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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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...
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Apoptosis01:30

Apoptosis

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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...
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Mitochondrial Membranes01:45

Mitochondrial Membranes

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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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Mitochondrial Precursor Proteins01:39

Mitochondrial Precursor Proteins

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Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
Most of the mitochondrial...
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Meiosis vs. Mitosis02:57

Meiosis vs. Mitosis

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Cell division is necessary for growth and reproduction in organisms. Mitosis aids cell growth and development by dividing somatic cells. In contrast, meiosis causes the division of germ cells and plays an essential role in sexual reproduction. Due to their unique functional requirements, mitosis and meiosis differ from each other in multiple aspects.
Before the start of mitosis and meiosis I, the cell synthesizes DNA, resulting in two homologous copies of each chromosome. DNA synthesis is...
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Autophagic Cell Death01:18

Autophagic Cell Death

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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
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Related Experiment Video

Updated: Mar 23, 2026

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue
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Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue

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Mitosis and mitochondrial priming for apoptosis.

Robert Pedley, Andrew P Gilmore

    Biological Chemistry
    |March 27, 2016
    PubMed
    Summary

    Cells initiate apoptosis if mitosis is delayed, a process exploited by chemotherapy. Recent studies reveal how cell cycle progression tunes apoptotic sensitivity, clarifying this crucial cellular safeguard.

    Area of Science:

    • Cell Biology
    • Molecular Biology
    • Genetics

    Background:

    • Cell division errors, like inaccurate chromosome segregation, threaten cell viability and can cause aneuploidy.
    • Cells initiate mitochondrial apoptosis to prevent propagation of errors if mitosis is not exited correctly.
    • Delayed mitotic exit is a target for certain chemotherapeutics, but the underlying apoptotic mechanism remains unclear.

    Purpose of the Study:

    • To elucidate the molecular mechanisms governing the apoptotic timer during mitosis.
    • To understand how cell cycle progression influences a cell's sensitivity to apoptosis.
    • To provide insights into the cellular response to errors in mitotic exit.

    Main Methods:

    • The study likely involved cell culture experiments observing mitotic progression and apoptosis.

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    Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
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    Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
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    Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
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  • Techniques may include molecular biology assays to track protein activity and signaling pathways.
  • Analysis of cell cycle checkpoints and their role in initiating apoptosis.

    • Main Results:

    • Passage through the cell cycle dynamically adjusts a cell's susceptibility to apoptosis.
    • Specific molecular events during mitosis fine-tune the apoptotic response.
    • This adaptive sensitivity ensures appropriate cell death when mitotic errors occur.

    Conclusions:

    • The cell cycle acts as a sophisticated timer, modulating apoptotic sensitivity.
    • Understanding this mechanism is key to developing more effective cancer therapies.
    • This research clarifies a fundamental process of cell cycle regulation and cell death.