Thromb Haemost 1991; 65(01): 052-058
DOI: 10.1055/s-0038-1647453
Original Article
Schattauer GmbH Stuttgart

Characterization of a Mouse Factor IX cDNA and Developmental Regulation of the Factor IX Gene Expression in Liver[*]

Shou-Nan Yao
The Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
,
Audrey H DeSilva
The Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
,
Sumiko Kurachi
The Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
,
Linda C Samuelson
The Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
,
Kotoku Kurachi
The Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
› Author Affiliations
Further Information

Publication History

Received 07 June 1990

Accepted after revision 28 August 1990

Publication Date:
02 July 2018 (online)

Summary

A mouse factor IX cDNA was isolated and characterrzed. The cDNA was 1,837 bp in length and contained the coding region as well as short 5’ and 3’ untranslated sequences. Northern blot analysis of liver RNA showed two mRNA species of 3.2 kb (major) and 2.2 kb (minor) for the mouse factor IX. An antisgnse RNA probe prepared from the mouse cDNA was employed to determine the steady state level of factor IX mRNA in mouse liver at various developmental stages. The factor IX mRNA level was very low (2–5% of the adult level) during the gestational period until day –3 (gestational day 17) followed by a rapid increase at day –2 through birth. This phase of rapid increase was followed by a gradual increase before it reached the adult level at around 20 to 24 days. At birth, the factor IX mRNA level was found to be at about 43% of that of the adult. The rnRNA levels in mouse liver agreed well with the plasma factor IX activity levels. These results indicate that reduced factor IX activity in newborns is due to the low levels of factor IX mRNA available for translation.

* This work was supported in part by research grants from the National Institutes of Health (HL38644 and HL39099) and a research grant from the Hemophilia Foundation of Michigan to K. K.


 
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