Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction
By Katherine A. Fitzgerald, E. Palsson-McDermott, A. Bowie, C. Jefferies, A. Mansell, G. Brady, E. Brint, A. Dunne, Pearl Gray, M. Harte and 5 more. Nature, 2001
1,382 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology
View Paper: https://www.semanticscholar.org/paper/47ee62088bb39c11c09130110ffcf5f3bd436764
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
In Immunology
Citations in the corpus
- Microglia Initiate Central Nervous System Innate and Adaptive Immune Responses through Multiple TLRs1 (2004, background): “However, MyD88-independent pathways have also been identified, including activation of IFN regulatory factor-3, resulting in expression of several IFNinducible genes (32, 33).”
- TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling (2020, background): “When in the plasma membrane, TLR4 interacts with the first adaptor pair, TIRAP (also called Mal [70]) and MyD88 [71, 72].”
- LPS-TLR4 Signaling to IRF-3/7 and NF-κB Involves the Toll Adapters TRAM and TRIF (2003, methodology): “, that the Mal/TIRAP dominant negative mutant powerfully inhibited LPS-induced signaling to NF- B (18, 19) and IFN- expression (12, 20), whereas the Mal/TIRAP knockout mouse both retained the ability to induce NF- B (21, 22) and IFN- expression (22).”