| http://purl.uniprot.org/citations/16203735 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16203735 | http://www.w3.org/2000/01/rdf-schema#comment | "The CATERPILLER (CLR, also NOD and NLR) proteins share structural similarities with the nucleotide binding domain (NBD)-leucine-rich repeat (LRR) superfamily of plant disease-resistance (R) proteins and are emerging as important immune regulators in animals. CLR proteins contain NBD-LRR motifs and are linked to a limited number of distinct N-terminal domains including transactivation, CARD (caspase activation and recruitment), and pyrin domains (PyD). The CLR gene, Monarch-1/Pypaf7, is expressed by resting primary myeloid/monocytic cells, and its expression in these cells is reduced by Toll-like receptor (TLR) agonists tumor necrosis factor (TNF) alpha and Mycobacterium tuberculosis. Monarch-1 reduces NFkappaB activation by TLR-signaling molecules MyD88, IRAK-1 (type I interleukin-1 receptor-associated protein kinase), and TRAF6 (TNF receptor (TNFR)-associated factor) as well as TNFR signaling molecules TRAF2 and RIP1 but not the downstream NFkappaB subunit p65. This indicates that Monarch-1 is a negative regulator of both TLR and TNFR pathways. Reducing Monarch-1 expression with small interference RNA in myeloid/monocytic cells caused a dramatic increase in NFkappaB activation and cytokine expression in response to TLR2/TLR4 agonists, TNFalpha, or M. tuberculosis infection, suggesting that Monarch-1 is a negative regulator of inflammation. Because Monarch-1 is the first CLR protein that interferes with both TLR2 and TLR4 activation, the mechanism of this interference is significant. We find that Monarch-1 associates with IRAK-1 but not MyD88, resulting in the blockage of IRAK-1 hyperphosphorylation. Mutants containing the NBD-LRR or PyD-NBD also blocked IRAK-1 activation. This is the first example of a CLR protein that antagonizes inflammatory responses initiated by TLR agonists via interference with IRAK-1 activation."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m502820200"xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Ting J.P."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Williams K.L."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Moore C."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Su L."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Braunstein M."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Duncan J.A."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Coffield V.M."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Vogel S.N."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Kurtz S."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Lich J.D."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Rallabhandi P."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Reed W."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/author | "Accavitti-Loper M.A."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/pages | "39914-39924"xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/title | "The CATERPILLER protein monarch-1 is an antagonist of toll-like receptor-, tumor necrosis factor alpha-, and Mycobacterium tuberculosis-induced pro-inflammatory signals."xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://purl.uniprot.org/core/volume | "280"xsd:string |
| http://purl.uniprot.org/citations/16203735 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16203735 |
| http://purl.uniprot.org/citations/16203735 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16203735 |
| http://purl.uniprot.org/uniprot/P59046#attribution-60E3C829F904F4D9C7BB9AEA887E5D13 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/16203735 |
| http://purl.uniprot.org/uniprot/#_P51617-mappedCitation-16203735 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16203735 |