Related Experiment Videos
[TNF/TNFR gene and apoptosis]
1Department of Immunology and Parasitology, Yamagata University School of Medicine.
Nihon Rinsho. Japanese Journal of Clinical Medicine
|July 1, 1996
Abstract:
Intracellular signal transduction pathways induced by in the reaction of TNF and TNF receptors has been clarified through finding of various TNF receptor associated intracytoplasmic molecules. The possible role of these signal transduction pathways for apoptosis induced by TNF is discussed.
Insights
Tumor necrosis factor (TNF) signaling pathways and their role in apoptosis have been clarified by identifying TNF receptor-associated intracellular molecules. This research discusses how these pathways contribute to TNF-induced cell death.
Area of Science:
- Cellular Biology
- Molecular Biology
- Immunology
Context:
- Tumor necrosis factor (TNF) and its receptors are crucial in cellular responses.
- Understanding intracellular signaling is key to deciphering TNF's biological effects.
- Apoptosis, or programmed cell death, is a fundamental biological process regulated by various pathways.
Purpose:
- To elucidate the intracellular signal transduction pathways activated by TNF receptor engagement.
- To identify key TNF receptor-associated intracytoplasmic molecules involved in these pathways.
- To discuss the functional role of these identified pathways in TNF-induced apoptosis.
Summary:
- Intracellular signal transduction pathways triggered by the interaction of Tumor Necrosis Factor (TNF) with its receptors have been elucidated.
- This clarification was achieved through the identification of various TNF receptor-associated intracytoplasmic molecules.
- The study further discusses the potential involvement of these signal transduction pathways in mediating TNF-induced apoptosis.
Impact:
- Provides a clearer understanding of TNF-mediated cellular signaling.
- Identifies molecular players in TNF-induced apoptosis, potentially revealing therapeutic targets.
- Contributes to the fundamental knowledge of cell death regulation and immune responses.