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Cd14  -  CD14 antigen

Mus musculus

Synonyms: Monocyte differentiation antigen CD14, Myeloid cell-specific leucine-rich glycoprotein
 
 
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Disease relevance of Cd14

 

High impact information on Cd14

  • The Heedless phenotype was positionally ascribed to a premature stop codon in Cd14 [3].
  • Activation of STAT-3 and three STAT-3 responsive genes, Socs3, Cd14, and serum amyloid A2 were also blocked [4].
  • To resolve this controversy and to establish a mouse model suitable for elucidation of the functions of human CD14 (hCD14) in vivo, we generated several lines of transgenic mice bearing different copy numbers of the hCd14 transgene on a murine Cd14(-/-) background [5].
  • The macrophage activation by CAZ-released endotoxin as well as LPS was mainly dependent on the presence of serum factor and CD14 antigen [6].
  • TNF-alpha induced a transient increase in levels of CD14 in plasma with a peak at 6 to 8 h, and this increase in levels of CD14 antigen in plasma was accompanied by increased levels of CD14 mRNA in lung, liver, and kidney [7].
 

Biological context of Cd14

 

Anatomical context of Cd14

  • A mutant cell line, J7.DEF3, defective in expression of a CD14 antigen, responded equally well to taxol by producing TNF as did the parent J774.1 cells [9].
  • Increased profibrogenic cytokine mRNA expression in the liver after bile duct ligation was significantly blunted in CD14(-/-) mice compared with the wild type [1].
  • Both of these agents down-regulated CD45 (leukocyte common antigen) and monocyte-associated CD14 antigen on K-562 cells [10].
 

Other interactions of Cd14

  • Because strain differences are known for Gbp1 and Pla2g2a, further analyses focused on Cd14 [11].
  • Recombinant murine interleukin-1beta (IL-1beta) induced a transient increase in plasma levels of CD14 with a peak at 8 h, and this increase in plasma CD14 antigen was accompanied by increased levels of CD14 messenger ribonucleic acid (mRNA) in all organs examined [12].
  • Studies utilizing a mutant cell line (J7.DEF3), which is defective in the expression of a CD14 antigen, showed that the increase in NO and iNOS mRNA caused by LTA is profoundly depressed in J7.DEF3 cells compared to that in parent J774 cells [13].

References

  1. LPS signaling enhances hepatic fibrogenesis caused by experimental cholestasis in mice. Isayama, F., Hines, I.N., Kremer, M., Milton, R.J., Byrd, C.L., Perry, A.W., McKim, S.E., Parsons, C., Rippe, R.A., Wheeler, M.D. Am. J. Physiol. Gastrointest. Liver Physiol. (2006) [Pubmed]
  2. Survival of Vi-capsulated and Vi-deleted Salmonella typhi strains in cultured macrophage expressing different levels of CD14 antigen. Hirose, K., Ezaki, T., Miyake, M., Li, T., Khan, A.Q., Kawamura, Y., Yokoyama, H., Takami, T. FEMS Microbiol. Lett. (1997) [Pubmed]
  3. CD14 is required for MyD88-independent LPS signaling. Jiang, Z., Georgel, P., Du, X., Shamel, L., Sovath, S., Mudd, S., Huber, M., Kalis, C., Keck, S., Galanos, C., Freudenberg, M., Beutler, B. Nat. Immunol. (2005) [Pubmed]
  4. Proinflammatory cytokine production in liver regeneration is Myd88-dependent, but independent of Cd14, Tlr2, and Tlr4. Campbell, J.S., Riehle, K.J., Brooling, J.T., Bauer, R.L., Mitchell, C., Fausto, N. J. Immunol. (2006) [Pubmed]
  5. Mice expressing high levels of soluble CD14 retain LPS in the circulation and are resistant to LPS-induced lethality. Jacque, B., Stephan, K., Smirnova, I., Kim, B., Gilling, D., Poltorak, A. Eur. J. Immunol. (2006) [Pubmed]
  6. Biological characterization of endotoxins released from antibiotic-treated Pseudomonas aeruginosa and Escherichia coli. Kirikae, T., Kirikae, F., Saito, S., Tominaga, K., Tamura, H., Uemura, Y., Yokochi, T., Nakano, M. Antimicrob. Agents Chemother. (1998) [Pubmed]
  7. Role of tumor necrosis factor alpha in induction of murine CD14 gene expression by lipopolysaccharide. Fearns, C., Loskutoff, D.J. Infect. Immun. (1997) [Pubmed]
  8. Establishment and characterization of somatic hybrids between human differentiated macrophages and mouse myeloma NS1 cells. Bohbot, A., Faradji, A., Schmitt, M., Oberling, F., Uttwiller, F., Ruch, J.V., Braun, S., Hartmann, D., Bartholeyns, J., Poindron, P. Int. J. Cell Cloning (1990) [Pubmed]
  9. CD14 is not involved in Rhodobacter sphaeroides diphosphoryl lipid A inhibition of tumor necrosis factor alpha and nitric oxide induction by taxol in murine macrophages. Kirikae, F., Kirikae, T., Qureshi, N., Takayama, K., Morrison, D.C., Nakano, M. Infect. Immun. (1995) [Pubmed]
  10. Tyrosine kinase inhibitor-induced differentiation of K-562 cells: alterations of cell cycle and cell surface phenotype. Hunáková, L., Sedlák, J., Klobusická, M., Duraj, J., Chorváth, B. Cancer Lett. (1994) [Pubmed]
  11. Cd14, Gbp1, and Pla2g2a: three major candidate genes for experimental IBD identified by combining QTL and microarray analyses. de Buhr, M.F., Mähler, M., Geffers, R., Hansen, W., Westendorf, A.M., Lauber, J., Buer, J., Schlegelberger, B., Hedrich, H.J., Bleich, A. Physiol. Genomics (2006) [Pubmed]
  12. Effect of recombinant interleukin-1beta on murine CD14 gene expression in vivo. Fearns, C., Ulevitch, R.J. Shock (1998) [Pubmed]
  13. Induction of NO synthesis by lipoteichoic acid from Staphylococcus aureus in J774 macrophages: involvement of a CD14-dependent pathway. Hattor, Y., Kasai, K., Akimoto, K., Thiemermann, C. Biochem. Biophys. Res. Commun. (1997) [Pubmed]
 
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