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"Defective LPS signaling in C3H/Hej
and C57BL/10ScCR mice: Mutations in Tlr4 gene,"
by A. Poltorak and 13 others, Science, 282(5396):2085-8, 11 December
1998.
[Authors' affiliations: Howard Hughes Medical
Institute, and University of Texas Southwestern Medical Center, Dallas; CNR,
Milan, Italy; Max Planck Institute for Immunobiology, Freiburg, Germany]
Abstract: "Mutations of the gene Lps
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 Lps-d allele of
C3H/Hej mice was shown to correspond to a missense mutation in the third exon
of the toll-like receptor-4 gene (Tlr4), predicted to replace proline
with histidine at position 712 of the polypeptide chain. C57BL/10ScCr mice are
homozygous for a null mutation of Tlr4. 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 Tlr4 predispose to the development of Gram-negative
sepsis, leaving most aspects of immune function intact."
This 1998 report in Science was cited 30
times in current journal articles indexed in the ISI database during
July-August 2000. Of all papers published in biology in the last two years
(aside from reviews), only one managed to collect more citations during that
two-month period. Prior to the most recent bimonthly count, citations to the
paper have accrued as follows:
May-June 2000: 29 citations
March-April 2000: 24
January-February 2000: 22
November-December 1999: 19
September-October 1999: 21
July-August 1999: 17
May-June 1999: 10
March-April 1999: 9
Total citations to date: 181
SOURCE: Hot
Papers Database (Available from the ISI
Research Services Group in a CD-ROM version containing data on
hundreds of highly cited papers published during the last two years.
User interface permits searching by author, organization, journal,
field, and more. Total citations, as well as citations accrued during
successive bimonthly periods, can be assessed and graphed. Database is
combined with subscription to the ISI newsletter Science
Watch®; updated discs containing the
most recent bimonthly data are mailed with each new issue, six times a
year.)
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