The DOI matches its Crossref record; 65 of the 66 references it cites were found in a registry or an index.
MyD88: a central player in innate immune signaling
Open accessAbstract
MyD88 is the canonical adaptor for inflammatory signaling pathways downstream of members of the Toll-like receptor (TLR) and interleukin-1 (IL-1) receptor families. MyD88 links IL-1 receptor (IL-1R) or TLR family members to IL-1R-associated kinase (IRAK) family kinases via homotypic protein-protein interaction. Activation of IRAK family kinases leads to a variety of functional outputs, including the activation of nuclear factor-kappa B (NFκB), mitogen-activated protein kinases, and activator protein 1, making MyD88 a central node of inflammatory pathways. As more details of MyD88-dependent signaling have been elucidated, it has become clear that the functions of this critical signaling component can be influenced by multiple interaction partners in distinct subcellular compartments. In this review, we will focus on recent developments in the understanding of the assembly of MyD88 signaling complexes and the mechanisms leading to the diversification of MyD88-based signaling.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Figures
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Deguine and Barton have shown that the nature of the TLR9 response-IFN type I or pro-inflammatory cytokine production is dependent on the class of CpG motif (class A or B) and the composition of phospholipids in the membrane incorporating TLR9.”
From Risk mitigation of immunogenicity: a key to personalized retinal gene therapy (2021) · cites this paper as [89]
In the citing paper
“It has also been demonstrated that the pro-inflammatory cytokine response requires a localization motif in the tail of TLR9 while the anti-inflammatory IFN type I response, by contrast, requires the AP-3 adaptor [89].”
From Risk mitigation of immunogenicity: a key to personalized retinal gene therapy (2021) · cites this paper as [89]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Role of Adaptor TRIF in the MyD88-Independent Toll-Like Receptor Signaling Pathway
Yamamoto, M., Sato, S., Hemmi, H., Hoshino, K., Kaisho, T., Sanjo, H., Takeuchi, O., Sugiyama, M., Okabe, M., Takeda, K., et al. (2003) · Science · doi:10.1126/science.1087262 · Cited by 3,286
CpG Motifs in Bacterial DNA and Their Immune Effects
Krieg, A. Μ. (2002) · Annual Review of Immunology · doi:10.1146/annurev.immunol.20.100301.064842 · Cited by 2,598
Unresponsiveness of MyD88-deficient mice to endotoxin.
Kawai, T., Adachi, O., Ogawa, T., Takeda, K., & Akira, S. (1999) · Immunity · doi:10.1016/s1074-7613(00)80086-2 · Cited by 2,367
Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function.
Adachi, O., Kawai, T., Takeda, K., Matsumoto, M., Tsutsui, H., Sakagami, M., Nakanishi, K., & Akira, S. (1998) · Immunity · doi:10.1016/s1074-7613(00)80596-8 · Cited by 2,358
MyD88 is an adaptor protein in the hToll/IL-1 receptor family signaling pathways.
Medzhitov, R., Preston-Hurlburt, P., Kopp, E., Stadlen, A., Chen, C.-Q., Ghosh, S., & Janeway, C. (1998) · Molecules and Cells · doi:10.1016/s1097-2765(00)80136-7 · Cited by 1,783
Oncogenically active MYD88 mutations in human lymphoma
Ngo, V. N., Young, R. M., Schmitz, R., Jhavar, S. G., Xiao, W., Lim, K., Kohlhammer, H., Xu, W., Yang, Y., Zhao, H., et al. (2010) · Nature · doi:10.1038/nature09671 · Cited by 1,560
Akira, S. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.r300028200 · Cited by 1,499
Crystal Structure of the TLR1-TLR2 Heterodimer Induced by Binding of a Tri-Acylated Lipopeptide
Jin, M. S., Kim, S. E., Heo, J. Y., Lee, M. E., Kim, H. M., Paik, S., Lee, H., & Lee, J. (2007) · Cell · doi:10.1016/j.cell.2007.09.008 · Cited by 1,391
Toll-like receptors control activation of adaptive immune responses
Schnare, M., Barton, G. M., Czopik, A. K., Takeda, K., Akira, S., & Medzhitov, R. M. (2001) · Nature Immunology · doi:10.1038/ni712 · Cited by 1,364
Self-citationTRAM couples endocytosis of Toll-like receptor 4 to the induction of interferon-β
Kagan, J. C., Su, T., Horng, T., Chow, A. Y., Akira, S., & Medzhitov, R. M. (2008) · Nature Immunology · doi:10.1038/ni1569 · Cited by 1,310
Cited by
Sorted by citations
Gut Microbiota as a Trigger for Metabolic Inflammation in Obesity and Type 2 Diabetes
Scheithauer, T. P. M., Rampanelli, E., Nieuwdorp, M., Vallance, B. A., Verchere, C. B., van Raalte, D. H., & Herrema, H. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.571731 · Cited by 715
Cross Talk Pathways Between Coagulation and Inflammation
Foley, J. H., & Conway, E. M. (2016) · Circulation Research · doi:10.1161/circresaha.116.306853 · Cited by 595
Calder, P. C., Bosco, N., Bourdet‐Sicard, R., Capuron, L., Delzenne, N. M., Dore, J. M., Franceschi, C., Lehtinen, M. J., Recker, T., Salvioli, S., et al. (2017) · Ageing Research Reviews · doi:10.1016/j.arr.2017.09.001 · Cited by 524
The emerging mechanisms and functions of microautophagy
Wang, L., Klionsky, D. J., & Shen, H. (2022) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-022-00529-z · Cited by 495
NLRP12-PANoptosome activates PANoptosis and pathology in response to heme and PAMPs
Sundaram, B., Nagakannan, P., Mall, R., Wang, Y., Sarkar, R., Kim, H. J., Malireddi, R. K. S., Karki, R., Janke, L. J., Vogel, P., et al. (2023) · Cell · doi:10.1016/j.cell.2023.05.005 · Cited by 443
Metadata
- Authors
- Deguine, J., & Barton, G. M.
- Affiliations
- University of California, Berkeley (US)
- Corresponding author
- Deguine, Jacques
- Barton, Gregory M.
- Venue
- F1000Prime Reports
- Publisher
- H1 Connect
- Published
- 2014-11-04
- Volume
- 6
- Pages
- 97-97
- ISSN
- 2051-7599 (ISSN-L)
- PMC
- PMC4229726
- OpenAlex
- W2158738222
- Cited by
- 692
- References
- 66
- Citations by year
- 2026: 50 · 2025: 86 · 2024: 104 · 2023: 91 · 2022: 80 · 2021: 85 · 2020: 60 · 2019: 56 · 2018: 30 · 2017: 18 · 2016: 18 · 2015: 14
- FWCI
- 1.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- F1000Prime Reports (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- Burroughs Wellcome Fund
- Lupus Research Institute
- Lupus Research Alliance
- National Institutes of Health
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- MyD88, Toll-like receptors, interleukin-1 receptor, innate immune signaling, NF-κB activation, MAPK signaling, activator protein-1, signaling complex assembly, protein-protein interaction, subcellular compartmentalization
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
