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Updated: Aug 29, 2026

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
Published on: June 9, 2017
Involvement of protein kinase C-delta in DNA damage-induced apoptosis
1Department of Molecular Biology & Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107, USA. abasu@hsc.unt.edu
Abstract:
Apoptosis is a highly orchestrated cell suicidal program required to maintain a balance between cell proliferation and cell death. A defect in apoptotic machinery can cause cancer. Many anticancer drugs are known to kill tumor cells by inducing apoptosis, and a defect in apoptosis can lead to anticancer drug resistance. Apoptosis is regulated by a complex cellular signaling network. Several members of the protein kinase C (PKC) family serve as substrates for caspases and PKCdelta isozyme has been intimately associated with DNA damage-induced apoptosis. It can act both upstream and downstream of caspases. In response to apoptotic stimuli, the full-length and the catalytic fragment of PKCdelta may translocate to distinct cellular compartments, including mitochondria and the nucleus, to reach their targets. Both activation and intracellular distribution of PKCdelta may have significant impact on apoptosis. This review intends to assimilate recent views regarding the involvement of PKCdelta in DNA damage-induced apoptosis.
Insights
Protein kinase C delta (PKCdelta) plays a key role in programmed cell death (apoptosis) following DNA damage. Its activation and cellular location influence cancer drug effectiveness and resistance.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Apoptosis, or programmed cell death, is crucial for maintaining cellular homeostasis and preventing diseases like cancer.
- Dysregulation of apoptosis is linked to cancer development and resistance to anticancer therapies.
- The protein kinase C (PKC) family, particularly PKCdelta, is implicated in the complex signaling networks governing apoptosis.
Purpose of the Study:
- To review the current understanding of PKCdelta's role in DNA damage-induced apoptosis.
- To explore how PKCdelta activation and subcellular localization impact apoptotic pathways.
- To highlight the significance of PKCdelta in the context of cancer and drug resistance.
Main Methods:
- Literature review of studies investigating PKCdelta and apoptosis.
- Analysis of research on PKCdelta's interaction with caspases and its translocation to cellular compartments.
- Synthesis of findings related to PKCdelta's function in response to DNA damage.
Main Results:
- PKCdelta acts as a key regulator in DNA damage-induced apoptosis, functioning both upstream and downstream of caspases.
- Activation of PKCdelta and its translocation to mitochondria and the nucleus are critical for its apoptotic function.
- PKCdelta's activity influences the efficacy of anticancer drugs and the development of drug resistance.
Conclusions:
- PKCdelta is a significant mediator of apoptosis following DNA damage.
- Understanding PKCdelta's intricate role offers potential therapeutic strategies for cancer treatment.
- Further research into PKCdelta signaling pathways is warranted for developing novel anticancer drugs.
Related Concept Videos
DNA Damage Can Stall the Cell Cycle
DNA Damage can Stall the Cell Cycle
The Intrinsic Apoptotic Pathway
The Extrinsic Apoptotic Pathway
Caspases
Inhibition of Cdk Activity

