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Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

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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...
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Abnormal Proliferation02:23

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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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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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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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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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...
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Caspases01:24

Caspases

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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...
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m6A: An Emerging Role in Programmed Cell Death.

Fajuan Tang1,2, Lin Chen1,2, Hu Gao1,2

  • 1Department of Emergency, West China Second University Hospital, Sichuan University, Chengdu, China.

Frontiers in Cell and Developmental Biology
|February 10, 2022
PubMed
Summary

N6-methyladenosine (m6A) is a key RNA modification regulating gene expression. This review explores how m6A, through its writers, erasers, and readers, influences various programmed cell death pathways.

Keywords:
apoptosisautophagyferroptosism6Anecroptosispyroptosis

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Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells
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Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells
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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Epigenetics

Background:

  • Programmed cell death encompasses diverse active cell extinction processes like apoptosis and ferroptosis.
  • N6-methyladenosine (m6A) is a prevalent and reversible RNA modification crucial for gene regulation.
  • m6A modification impacts mRNA metabolism, miRNA maturation, and the stability of non-coding RNAs.

Purpose of the Study:

  • To review the multifaceted roles of m6A modification in regulating programmed cell death.
  • To elucidate the mechanisms by which m6A regulators (writers, erasers, readers) influence cell death pathways.

Main Methods:

  • Literature review synthesizing current research on m6A and programmed cell death.
  • Analysis of molecular mechanisms linking m6A regulators to cell death pathways.
  • Integration of findings on m6A's impact on mRNA, miRNA, circRNA, and lncRNA metabolism in cell death.

Main Results:

  • m6A modification is intricately involved in modulating apoptosis, ferroptosis, pyroptosis, and necroptosis.
  • Writers, erasers, and readers of m6A dynamically regulate target gene expression to promote or inhibit cell death.
  • m6A-dependent regulation of RNA stability and translation is a key mechanism in programmed cell death.

Conclusions:

  • m6A is a critical regulator of programmed cell death, impacting multiple cell death modalities.
  • Dysregulation of m6A pathways contributes to various disease processes.
  • Targeting m6A regulators offers potential therapeutic strategies for diseases involving aberrant cell death.