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Overview of Cell Death

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...

Autophagic Cell Death

Autophagic Cell Death

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 pro-apoptotic...

The Intrinsic Apoptotic Pathway

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...

Caspases

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.

The Extrinsic Apoptotic Pathway

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...

Apoptosis

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.

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Related Experiment Video

Updated: Jun 24, 2026

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex

Published on: August 2, 2021

Structure-function correlation of human programmed cell death 5 protein.

Hongwei Yao¹, Lanjun Xu, Yingang Feng

¹Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.

Archives of Biochemistry and Biophysics

|April 11, 2009

Summary

This summary is machine-generated.

Human programmed cell death 5 (PDCD5) protein

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Last Updated: Jun 24, 2026

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Published on: August 2, 2021

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Identifying Protein-protein Interaction Sites Using Peptide Arrays

Identifying Protein-protein Interaction Sites Using Peptide Arrays

Published on: November 18, 2014

Area of Science:

Molecular Biology
Biochemistry
Cell Biology

Background:

Programmed cell death 5 (PDCD5) is a key translocatory protein in cellular apoptosis.
While PDCD5's function is documented, its structure-function relationship remains unexplored.

Purpose of the Study:

To investigate the structure-function correlation of human PDCD5.
To elucidate the role of protein structure and flexibility in PDCD5's apoptotic function.

Main Methods:

Multidimensional Nuclear Magnetic Resonance (NMR) spectroscopy to determine 3D structure and internal dynamics.
Flow cytometry (FACScan) and fluorescence microscopy to assess protein internalization and function of PDCD5 fragments.

Main Results:

The 3D structure of PDCD5 reveals a compact, low-flexibility core with mobile N-terminal alpha-helices and a flexible C-terminal region.
Charged residues are critical for PDCD5's apoptosis-promoting activity and cell translocation.
Functional regions of PDCD5 exhibit higher flexibility.

Conclusions:

PDCD5 possesses a distinct structural organization influencing its function.
Protein flexibility, particularly in charged regions, is essential for PDCD5's role in apoptosis and cell translocation.
This study provides novel insights into the molecular mechanisms of PDCD5-mediated cell death.