Apoptotic Induction
Apoptotic Induction - Related Videos
19:44
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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Cited by 10 •
2012
We have synthesized a novel analogue of pancratistatin with comparable anti-cancer activity as native pancratistatin; interestingly, combinatory treatment with tamoxifen yielded a drastic enhancement in apoptotic and autophagic induction by mitochondrial targeting with minimal effect on noncancerous fibroblasts. Thus, JCTH-4 in combination with tamoxifen could provide a safe anti-cancer therapy.
05:36
Analysis of Efferocytosis of Apoptotic Thymocytes by Peritoneal Macrophages
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2025
This video demonstrates a procedure for analyzing peritoneal macrophage-mediated efferocytosis of apoptotic mouse thymocytes by fluorescence microscopy.
08:59
Live Imaging of Apoptotic Cell Clearance during Drosophila Embryogenesis
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Cited by 10 •
2013
Here we describe an effective method for studying dynamics of apoptotic cell clearance in vivo. This method employs live Drosophila embryos as a powerful model for monitoring phagocytosis of apoptotic cells using specific labeling of apoptotic cells and phagocytes.
11:57
Organotypic Cerebellar Cultures: Apoptotic Challenges and Detection
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Cited by 17 •
2011
This method describes the generation of organotypic cerebellar cultures and the effect of certain apoptotic stimuli on the viability of different cerebellar cell types.
01:30
TUNEL Assay for Detecting Apoptotic Cell Death in a Brain Slice
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2025
To detect apoptotic cell death using the TUNEL assay, treat the brain slice with the enzyme proteinase-K.
FAQs
These routes are distinguished by where the death signal begins. Intrinsic signaling follows intracellular stress and is associated with mitochondrial cytochrome c release, whereas extrinsic signaling starts at cell-surface death receptors. Their different entry points converge on caspase activation, giving investigators two mechanistic contexts for studying regulated cell loss.
Cytochrome c release marks a key mitochondrial event in the intrinsic route. It links intracellular stress to the downstream caspase system, which carries out the cell’s controlled dismantling. This connection helps researchers examine how internal damage signals become an organized death response within a tightly regulated sequence.
Caspases act as the execution machinery shared by the intrinsic and extrinsic routes. Once activated, they dismantle the cell in an orderly sequence, helping explain why this form of cell loss generally limits inflammation. Their position downstream of both pathways also provides a common point for analyzing whether a death signal has been effectively propagated.
In cancer medicine, the goal is to eliminate malignant cells by deliberately engaging their regulated death machinery. Research therefore focuses on whether a treatment can activate apoptotic pathways in cancer cells, overcome resistance to cell death, and improve selectivity. These aims connect pathway biology with therapeutic design and the search for more effective treatments.
Resistance and selectivity represent complementary challenges. A therapy may need to overcome a malignant cell’s failure to respond to death signals, while also activating the process in a sufficiently targeted way. Studying both issues guides drug development, because successful development must address both response and selectivity.
It provides a framework for understanding disorders in which cell loss is misregulated. Excessive loss and insufficient loss represent different disease contexts, making the balance of programmed cell death medically important. Research on these patterns supports broader disease understanding and contributes to drug development beyond cancer-focused investigation.