The DOI matches its Crossref record; 145 of the 145 references it cites were found in a registry or an index.
Tumor Necrosis Factor Receptors: Pleiotropic Signaling Complexes and Their Differential Effects
Open accessAbstract
Since its discovery in 1975, TNFα has been a subject of intense study as it plays significant roles in both immunity and cancer. Such attention is well deserved as TNFα is unique in its engagement of pleiotropic signaling via its two receptors: TNFR1 and TNFR2. Extensive research has yielded mechanistic insights into how a single cytokine can provoke a disparate range of cellular responses, from proliferation and survival to apoptosis and necrosis. Understanding the intracellular signaling pathways induced by this single cytokine via its two receptors is key to further revelation of its exact functions in the many disease states and immune responses in which it plays a role. In this review, we describe the signaling complexes formed by TNFR1 and TNFR2 that lead to each potential cellular response, namely, canonical and non-canonical NF-κB activation, apoptosis and necrosis. This is followed by a discussion of data from in vivo mouse and human studies to examine the differential impacts of TNFR1 versus TNFR2 signaling.
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Metadata
- Authors
- Gough, P., & Myles, I. A.
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2020-11-25
- Volume
- 11
- Pages
- 585880-585880
- ISSN
- 1664-3224 (ISSN-L)
- OpenAlex
- W3109152315
- Cited by
- 268
- References
- 145
- FWCI
- 8.05
- Type
- journal article
- Language
- en
- Open access
- gold
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- Gough, P., & Myles, I. A. (2020). Tumor Necrosis Factor Receptors: Pleiotropic Signaling Complexes and Their Differential Effects. Frontiers in Immunology. https://doi.org/10.3389/fimmu.2020.585880
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
