| First Author | Morrow JF | Year | 1981 |
| Journal | Proc Natl Acad Sci U S A | Volume | 78 |
| Issue | 8 | Pages | 4718-22 |
| PubMed ID | 6946420 | Mgi Jnum | J:6644 |
| Mgi Id | MGI:55118 | Doi | 10.1073/pnas.78.8.4718 |
| Citation | Morrow JF, et al. (1981) Induction of hepatic synthesis of serum amyloid A protein and actin. Proc Natl Acad Sci U S A 78(8):4718-22 |
| abstractText | Major changes in the mRNA population of murine liver occur after administration of bacterial lipopolysaccharide, an agent that causes increases in the concentrations of acute-phase serum proteins. The mRNA for one of these, serum amyloid A, is increased at least 500-fold compared to the normal level. It becomes one of the most abundant hepatic mRNAs, and serum amyloid A synthesis comprises about 2.5% of total hepatic protein synthesis in the acute-phase response. Its synthesis is tissue-specific in that amyloid A mRNA was not detected in the kidney, an important site of amyloid fibril accumulation. The protein synthesized in largest amount by acute-phase liver tissue in culture is cytoplasmic actin. Its relative rate of synthesis is increased about 5-fold compared to the normal tissue; that of serum albumin is decreased to about one-third of its normal rate. The concentration of mRNA for serum albumin is decreased by a similar amount. Starting with induced liver RNA, we have constructed a recombinant plasmid containing most of the DNA sequence encoding the serum amyloid A polypeptide. |
