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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...
Overview of Cell Death01:30

Overview of Cell Death

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 20th century...
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...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

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...
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

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...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...

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Related Experiment Video

Updated: May 22, 2026

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Thioredoxin system in cell death progression.

Jun Lu1, Arne Holmgren

  • 1Division of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.

Antioxidants & Redox Signaling
|April 26, 2012
PubMed
Summary
This summary is machine-generated.

The thioredoxin (Trx) system is vital for cellular redox balance and antioxidant defense. Its regulation of apoptosis, particularly through Trx interacting protein (TXNIP), influences cell fate and presents therapeutic targets.

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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

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Last Updated: May 22, 2026

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Area of Science:

  • Cellular biology
  • Biochemistry
  • Oxidative stress research

Background:

  • The thioredoxin (Trx) system, including Trx reductase (TrxR) and Trx, is crucial for cellular redox balance and antioxidant functions.
  • Mammalian cells utilize cytosolic Trx1 and mitochondrial Trx2 systems for proliferation and viability.
  • The redox state of Trx regulates apoptosis by interacting with apoptosis signal-regulating kinase 1 (ASK1) and its inhibitor, Trx interacting protein (TXNIP).

Purpose of the Study:

  • To review research progress on the regulation of apoptosis by Trx systems.
  • To explore the role of Trx redox state and TrxR activity in cell death.
  • To classify compounds that inhibit TrxR and understand their reaction mechanisms.

Main Methods:

  • Literature review of research progress on Trx systems and apoptosis regulation.
  • Analysis of the molecular mechanisms involving Trx, TrxR, ASK1, and TXNIP.
  • Classification of electrophilic compounds inhibiting TrxR based on reaction mechanisms.

Main Results:

  • Trx system components are critical for maintaining cellular redox balance and antioxidant function.
  • Trx's interaction with ASK1 and TXNIP modulates stress-induced apoptosis.
  • TrxR activity and redox state are key determinants of cell fate in apoptosis.
  • TrxR can be inactivated by various compounds, potentially generating reactive oxygen species.

Conclusions:

  • Trx redox state and TrxR activity are critical regulators of cell death.
  • TrxR's unique properties make it a potential pharmaceutical target.
  • Understanding TrxR inhibition mechanisms is essential for developing targeted therapies.