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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 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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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.
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Related Experiment Video

Updated: Sep 2, 2025

Co-immunoprecipitation Assay for Studying Functional Interactions Between Receptors and Enzymes
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Progress in programmed cell death-1/programmed cell death-ligand 1 pathway inhibitors and binding mode analysis.

Xiaoyun Li1, Qin Zeng2, Fengjiao Xu2

  • 1Department of Pharmacy, Chun'an County Hospital of Traditional Chinese Medicine, Hangzhou, 311700, Zhejiang, China.

Molecular Diversity
|August 10, 2022
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Summary

This study reviews programmed cell death protein 1 (PD-1)/programmed cell death protein ligand 1 (PD-L1) inhibitors. Molecular-level binding mode analysis can accelerate the development of these crucial immunotherapy drugs.

Keywords:
Binding mode analysisImmune checkpointMonoclonal antibodies drugsPD-1/PD-L1 inhibitors

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Area of Science:

  • Immunology
  • Medicinal Chemistry
  • Molecular Biology

Background:

  • Programmed cell death protein 1 (PD-1) and its ligand PD-L1 are key regulators of the immune system.
  • Dysregulation of the PD-1/PD-L1 pathway is implicated in various diseases, making it a target for therapeutic intervention.
  • The development of PD-1/PD-L1 inhibitors is a rapidly advancing field in drug discovery.

Purpose of the Study:

  • To review the molecular mechanisms of the PD-1/PD-L1 signaling pathway.
  • To summarize the progress and challenges in the development of PD-1/PD-L1 inhibitors.
  • To analyze the binding modes of novel PD-1/PD-L1 inhibitors to inform future drug design.

Main Methods:

  • Literature review of PD-1/PD-L1 signaling and inhibitor research.
  • Analysis of molecular interactions between inhibitors and PD-1/PD-L1 proteins.
  • Examination of existing and emerging PD-1/PD-L1 inhibitor candidates.

Main Results:

  • The PD-1/PD-L1 pathway plays a critical role in immune suppression.
  • Numerous PD-1/PD-L1 inhibitors are in clinical development, with several approved monoclonal antibodies (mAbs).
  • Understanding drug-target binding modes at the molecular level is essential for efficient drug screening.

Conclusions:

  • Molecular modeling and binding mode analysis are vital for accelerating the development of PD-1/PD-L1 inhibitors.
  • Detailed analysis of inhibitor-protein interactions can guide the design of more effective and specific drugs.
  • This review provides insights for the rational development of next-generation PD-1/PD-L1 targeted therapies.