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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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The Intrinsic Apoptotic Pathway01:31

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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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Necrosis01:16

Necrosis

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Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
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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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Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Export of Misfolded Proteins out of the ER01:32

Export of Misfolded Proteins out of the ER

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After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
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Evaluation of Caspase Activation to Assess Innate Immune Cell Death
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Both Caspase and Calpain are Involved in Endoplasmic Reticulum-Targeted BNIP3-Induced Cell Death.

J Zeng1,2, Y Y Huang1,2, X M Xu1,2

  • 1Department of Orthodontics, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, Sichuan, China.

Folia Biologica
|August 28, 2020
PubMed
Summary
This summary is machine-generated.

Bcl-2/E1B-19K-interacting protein 3 (BNIP3) targeting the endoplasmic reticulum induces cell death. This cell death requires both caspases and calpains, suggesting a mixed cell death pathway.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Bcl-2/E1B-19K-interacting protein 3 (BNIP3) regulates cell death and is implicated in endoplasmic reticulum stress.
  • While initially thought to target mitochondria, BNIP3 localizes to the endoplasmic reticulum under physiological conditions.

Purpose of the Study:

  • To investigate the molecular mechanisms of BNIP3-induced cell death specifically within the endoplasmic reticulum.
  • To determine the role of caspases and calpains in endoplasmic reticulum-targeted BNIP3-mediated cell death.

Main Methods:

  • Engineered a BNIP3 variant targeted to the endoplasmic reticulum by replacing its transmembrane domain with a cytochrome b5 segment.
  • Utilized SW480 colon carcinoma cells for experiments.
  • Assessed cell death induction and inhibition using a pan-caspase inhibitor (z-VAD-fmk) and a calpain inhibitor (PD150606).

Main Results:

  • Endoplasmic reticulum-targeted BNIP3 induced cell death effectively in SW480 cells, comparable to wild-type BNIP3.
  • Both caspase and calpain inhibitors significantly suppressed the cell death induced by endoplasmic reticulum-targeted BNIP3.
  • This indicates that BNIP3-induced cell death in the ER involves both caspase-dependent and calpain-dependent pathways.

Conclusions:

  • Endoplasmic reticulum-targeted BNIP3 triggers a mixed mode of cell death.
  • Caspases and calpains are crucial mediators in the cell death pathway initiated by BNIP3 in the endoplasmic reticulum.