The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Links

 

Gene Review

TOLLIP  -  toll interacting protein

Homo sapiens

Synonyms: IL-1RAcPIP, Toll-interacting protein
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

High impact information on TOLLIP

  • Through proteomic analysis, we identify Tollip (Toll-interacting protein) and IRAK-1 (interleukin-1 receptor-associated serine/threonine kinase 1) as caveolin-1-interacting proteins in monocytes [1].
  • We demonstrated that transient transfection of TLR2 signaling-negative regulator Toll-interacting protein or treatment with TLR2-blocking Ab suppressed CPPD and MSU crystal-induced chondrocyte release of NO, an inflammatory mediator that promotes cartilage degeneration [2].
  • Here we report that Exip, but not p38alpha, binds to Toll interacting protein which is involved in interleukin-1 (IL-1) signaling pathway as a component of the receptor proximal complex and impaired NF-kappaB activity [3].
  • METHODS: In order to detect a possible role of TOLLIP variation in the pathogenesis of AD, we screened the entire coding sequence of the TOLLIP gene by SSCP in 50 AD patients [4].
  • Toll-interacting protein (TOLLIP) is an inhibitory adaptor protein within the toll-like receptor (TLR) pathway, a part of the innate immune system that recognizes structurally conserved molecular patterns of microbial pathogens, leading to an inflammatory immune response [4].

References

  1. CD26 mediates dissociation of Tollip and IRAK-1 from caveolin-1 and induces upregulation of CD86 on antigen-presenting cells. Ohnuma, K., Yamochi, T., Uchiyama, M., Nishibashi, K., Iwata, S., Hosono, O., Kawasaki, H., Tanaka, H., Dang, N.H., Morimoto, C. Mol. Cell. Biol. (2005) [Pubmed]
  2. TLR2 signaling in chondrocytes drives calcium pyrophosphate dihydrate and monosodium urate crystal-induced nitric oxide generation. Liu-Bryan, R., Pritzker, K., Firestein, G.S., Terkeltaub, R. J. Immunol. (2005) [Pubmed]
  3. Exip, a splicing variant of p38alpha, participates in interleukin-1 receptor proximal complex and downregulates NF-kappaB pathway. Yagasaki, Y., Sudo, T., Osada, H. FEBS Lett. (2004) [Pubmed]
  4. Association of toll-interacting protein gene polymorphisms with atopic dermatitis. Schimming, T.T., Parwez, Q., Petrasch-Parwez, E., Nothnagel, M., Epplen, J.T., Hoffjan, S. BMC Dermatol. (2007) [Pubmed]
 
WikiGenes - Universities