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Characterization, expression and evolution of mouse beta 2-glycoprotein I (apolipoprotein H)
G C Sellar1, D M Steel, A Zafiropoulos
1Department of Genetics, Trinity College, Dublin, Ireland.
Biochemical and Biophysical Research Communications
|May 16, 1994
Summary
Researchers cloned and sequenced mouse beta 2-glycoprotein I (beta 2I) cDNA. Mouse beta 2I does not act as an acute phase reactant and shows faster evolution than other species.
Area of Science:
- Biochemistry
- Immunology
- Molecular Biology
Background:
- Beta 2-glycoprotein I (beta 2I) is a serum glycoprotein with an unclear function.
- Its ability to bind negatively charged phospholipids suggests potential inhibitory roles.
Purpose of the Study:
- To clone and sequence a full-length mouse beta 2I cDNA.
- To investigate the role of mouse beta 2I as an acute phase reactant.
- To analyze the evolutionary rate of mouse beta 2I.
Main Methods:
- Cloning and sequencing of mouse beta 2I cDNA.
- Experimental induction of inflammation to assess acute phase reactant behavior.
- Phylogenetic analysis of mammalian beta 2I homologues.
Main Results:
- A full-length mouse beta 2I cDNA clone was successfully obtained and sequenced.
- Mouse beta 2I did not exhibit acute phase reactant properties following induced inflammation.
- Phylogenetic analysis indicated that mouse beta 2I is the most divergent and evolves faster than other mammalian beta 2I.
Conclusions:
- Mouse beta 2I's function may differ from other mammalian homologues.
- The rapid evolution of mouse beta 2I suggests unique adaptive pressures or functional divergence.