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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...
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Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
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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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Examining BCL-2 Family Function with Large Unilamellar Vesicles
08:35

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Published on: October 5, 2012

Bcl-3 regulates UVB-induced apoptosis.

Ingrid García1, Gabriela Cosío, Floria Lizárraga

  • 1National Institute of Cancerology, Av. San Fernando 22 Tlalpan, 14080 Mexico, Mexico.

Human Cell
|March 16, 2013
PubMed
Summary
This summary is machine-generated.

B cell leukemia-3 (Bcl-3) protects cells from apoptosis by regulating both intrinsic and extrinsic pathways. Silencing Bcl-3 accelerates caspase activation and impacts DNA repair proteins.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • B cell leukemia-3 (Bcl-3) is recognized as an anti-apoptotic gene.
  • The precise mechanisms by which Bcl-3 regulates apoptosis remain unclear.
  • Understanding Bcl-3's role is crucial for developing targeted cancer therapies.

Purpose of the Study:

  • To elucidate the specific role of Bcl-3 in apoptosis.
  • To investigate the impact of Bcl-3 silencing on apoptotic pathways.
  • To identify key proteins regulated by Bcl-3 during apoptosis induction.

Main Methods:

  • Evaluating the effect of Bcl-3 silencing on protein expression.
  • Analyzing extrinsic and intrinsic apoptotic pathways.
  • Utilizing ultraviolet light B (UVB) to induce DNA damage.

Main Results:

  • Bcl-3 silencing accelerated caspase-3, caspase-8, and caspase-9 activation.
  • Increased tBid mitochondrial content was observed in Bcl-3 silenced cells.
  • Diminished levels of p53 and DNA-PK were noted in Bcl-3 silenced cells.

Conclusions:

  • Bcl-3 plays a protective role against apoptosis.
  • Bcl-3 regulates both extrinsic and intrinsic apoptotic pathways.
  • Bcl-3 influences DNA repair mechanisms through proteins like p53 and DNA-PK.