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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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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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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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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 TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Related Experiment Video

Updated: Mar 16, 2026

Author Spotlight: Development and Evaluation of a Compound Acne Rodent Model Using C. acnes and Oleic Acid
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The TRAIL to acne pathogenesis: let's focus on death pathways.

Bodo C Melnik1

  • 1Department of Dermatology, Environmental Medicine and Health Theory, University of Osnabrück, Osnabrück, Germany.

Experimental Dermatology
|August 20, 2016
PubMed
Summary

Acne is a pro-survival disease of the sebaceous follicle due to impaired cell death signaling. Treatments like isotretinoin may restore this balance by enhancing cell death pathways.

Keywords:
FoxOsacneapoptosisc-FLIPdeath signallingtumor necrosis factor-related apoptosis-inducing ligand

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Area of Science:

  • Dermatology and molecular biology, focusing on cellular signaling pathways in skin conditions.

Background:

  • Acne vulgaris is hypothesized as a pro-survival disease of the sebaceous follicle.
  • This condition is characterized by impaired Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-mediated apoptosis.

Discussion:

  • The PI3K-Akt-mTORC1 pathway is implicated in driving sebaceous follicle pro-survival in acne.
  • Impaired TRAIL-mediated death signaling contributes to acne pathogenesis.
  • Immortalized sebocyte cultures are inadequate models for studying acne's key features.

Key Insights:

  • Acne pathogenesis involves a disturbed balance between pro-survival and death signaling in the sebaceous follicle.
  • Anti-acne agents, such as isotretinoin, are predicted to enhance death signaling pathways.

Outlook:

  • Further research is needed to validate the role of PI3K-Akt-mTORC1 and TRAIL signaling in acne.
  • Developing new therapeutic strategies targeting these pathways could offer novel acne treatments.