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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...
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...
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.
RNA Splicing01:32

RNA Splicing

Splicing is the process by which eukaryotic RNA is edited before its translation into protein. The RNA strand transcribed from eukaryotic DNA is called the primary transcript. The primary transcripts that become mRNAs are called precursor messenger RNAs (pre-mRNAs). Eukaryotic pre-mRNA contains alternating sequences of exons and introns. Exons are nucleotide sequences that code for proteins, whereas introns are the non-coding regions. In RNA splicing, introns are removed and exons are bonded...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.

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Related Experiment Video

Updated: May 17, 2026

Exploring Caspase Mutations and Post-Translational Modification by Molecular Modeling Approaches
05:56

Exploring Caspase Mutations and Post-Translational Modification by Molecular Modeling Approaches

Published on: October 13, 2022

Splice variants in apoptotic pathway.

K Miura1, W Fujibuchi, M Unno

  • 1Department of Surgery, Tohoku University Graduate School of Medicine, Sendai, 980-8574 Japan. k-miura@surg1.med.tohoku.ac.jp

Experimental Oncology
|October 17, 2012
PubMed
Summary
This summary is machine-generated.

Apoptosis, programmed cell death, is crucial for eliminating harmful cells. Aberrant splicing of apoptotic genes contributes to cancer, offering new therapeutic targets by modulating these splice variants.

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Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
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Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

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Related Experiment Videos

Last Updated: May 17, 2026

Exploring Caspase Mutations and Post-Translational Modification by Molecular Modeling Approaches
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Exploring Caspase Mutations and Post-Translational Modification by Molecular Modeling Approaches

Published on: October 13, 2022

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

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Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
10:06

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

Published on: April 26, 2017

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Apoptosis, or programmed cell death, is a fundamental biological process for removing superfluous or mutated somatic cells.
  • Deregulation of apoptotic signaling pathways is a hallmark of oncogenesis.
  • Alternative pre-messenger RNA (mRNA) splicing generates diverse mRNA and protein isoforms, contributing to genomic and functional diversity.

Purpose of the Study:

  • To review splice variants of key apoptotic genes.
  • To explore the regulatory mechanisms of alternative splicing in these genes.
  • To highlight the potential of targeting splice variants and splicing machinery in cancer therapy.

Main Methods:

  • Literature review of apoptosis and alternative splicing.
  • Summary of splice variants for BCL2L1, BIRC5, CFLAR, and MADD.
  • Discussion of regulatory mechanisms governing alternative splicing of apoptotic genes.

Main Results:

  • Several apoptotic genes, including BCL2L1, BIRC5, CFLAR, and MADD, are subject to alternative pre-mRNA splicing.
  • These splice variants can function as critical pro-apoptotic or anti-apoptotic factors.
  • Understanding aberrant splicing in malignancies is key to developing targeted therapies.

Conclusions:

  • Alternative splicing plays a significant role in regulating apoptotic gene function.
  • Targeting specific splice variants or the splicing machinery itself presents a promising avenue for cancer treatment.
  • Integrating knowledge of apoptosis and aberrant splicing can lead to novel therapeutic strategies.