{"doi":"10.1126/science.282.5396.2085","title":"Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in\n            <i>Tlr4</i>\n            Gene","abstract":"<jats:p>\n            Mutations of the gene\n            <jats:italic>Lps</jats:italic>\n            selectively impede lipopolysaccharide (LPS) signal transduction in C3H/HeJ and C57BL/10ScCr mice, rendering them resistant to endotoxin yet highly susceptible to Gram-negative infection. The codominant\n            <jats:italic>Lps</jats:italic>\n            <jats:sup>\n              <jats:italic>d</jats:italic>\n            </jats:sup>\n            allele of C3H/HeJ mice was shown to correspond to a missense mutation in the third exon of the Toll-like receptor-4 gene (\n            <jats:italic>Tlr4</jats:italic>\n            ), predicted to replace proline with histidine at position 712 of the polypeptide chain. C57BL/10ScCr mice are homozygous for a null mutation of\n            <jats:italic>Tlr4</jats:italic>\n            . Thus, the mammalian Tlr4 protein has been adapted primarily to subserve the recognition of LPS and presumably transduces the LPS signal across the plasma membrane. Destructive mutations of\n            <jats:italic>Tlr4</jats:italic>\n            predispose to the development of Gram-negative sepsis, leaving most aspects of immune function intact.\n          </jats:p>","journal":"Science","year":1998,"id":5122,"datarank":24.449029216712223,"base_score":8.935113740791747,"endowment":8.935113740791747,"self_citation_contribution":1.3402670611187624,"citation_network_contribution":23.10876215559346,"self_endowment_contribution":1.3402670611187624,"citer_contribution":23.10876215559346,"corpus_percentile":95.6,"corpus_rank":1974,"citation_count":7593,"citer_count":187,"citers_with_citation_signal":187,"citers_with_endowment":187,"datacite_reuse_total":0,"is_dataset":false,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"1998-12-11","authors":[{"id":51937,"name":"Xiaolong He","orcid":"0000-0002-1509-8739","position":1,"is_corresponding":false},{"id":51938,"name":"Irina Smirnova","orcid":null,"position":2,"is_corresponding":false},{"id":51939,"name":"Mu-Ya Liu","orcid":null,"position":3,"is_corresponding":false},{"id":51940,"name":"Christophe Van Huffel","orcid":"0000-0001-6127-3027","position":4,"is_corresponding":false},{"id":51941,"name":"Xin Du","orcid":"0000-0003-2339-8464","position":5,"is_corresponding":false},{"id":51942,"name":"Dale Birdwell","orcid":null,"position":6,"is_corresponding":false},{"id":51943,"name":"Erica Alejos","orcid":null,"position":7,"is_corresponding":false},{"id":51944,"name":"Maria Silva","orcid":null,"position":8,"is_corresponding":false},{"id":51945,"name":"Chris Galanos","orcid":null,"position":9,"is_corresponding":false},{"id":51946,"name":"Marina Freudenberg","orcid":null,"position":10,"is_corresponding":false},{"id":51947,"name":"Paola Ricciardi-Castagnoli","orcid":null,"position":11,"is_corresponding":false},{"id":51948,"name":"Betsy Layton","orcid":null,"position":12,"is_corresponding":false},{"id":51949,"name":"Bruce Beutler","orcid":"0000-0002-3639-246X","position":13,"is_corresponding":false},{"id":51950,"name":"Maria João Silva","orcid":"0000-0002-6060-0716","position":14,"is_corresponding":false},{"id":51951,"name":"Marina A. Freudenberg","orcid":"0000-0001-5894-1805","position":15,"is_corresponding":false},{"id":51952,"name":"Paola Ricciardi‐Castagnoli","orcid":"0000-0002-4749-7187","position":16,"is_corresponding":false},{"id":51936,"name":"Alexander Poltorak","orcid":"0000-0002-5375-6587","position":0,"is_corresponding":true}],"reference_count":43,"raw_metadata":{"citation_network_status":"fetched"},"created_at":"2026-03-01T18:20:47.508186Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}