Literature DB >> 3108254

The factor IX phospholipid-binding site is required for calcium-dependent activation of factor IX by factor XIa.

H A Liebman, B C Furie, B Furie.   

Abstract

To determine the functional role of the metal-dependent conformational changes in Factor IX, two populations of conformation-specific anti-Factor IX antibodies were prepared. Anti-Factor IX X Mg(II) antibodies bind to Factor IX in the presence of Mg(II) and other metal ions, but not in the absence of metal ions. Anti-Factor IX X Ca(II)-specific antibodies bind to Factor IX in the presence of Ca(II) and Sr(II), but not in the presence of Mn(II), Mg(II), and Ba(II). In the presence of a metal ion that induces the conformational transition recognized by the anti-Factor IX X Mg(II) antibodies, the concentrations of CaCl2 and SrCl2 needed for the half-maximal binding of the anti-Factor IX X Ca(II)-specific antibodies to Factor IX were reduced 3- and 20-fold, respectively. Factor IX binding to phospholipid vesicles was inhibited by the Fab fragments of the anti-Factor IX X Ca(II)-specific antibodies, but was not inhibited by the Fab fragments of the anti-Factor IX X Mg(II) antibodies. Factor XIa activation of Factor IX was also inhibited by the Fab fragments of the anti-Factor IX X Ca(II)-specific antibodies, but not by the anti-Factor IX X Mg(II) antibodies. These results support the hypothesis that Factor IX undergoes two metal-dependent conformational transitions: FIX----FIX'----FIX*. The first transition (FIX----FIX') is metal-dependent but cation-nonselective; the second transition (FIX'----FIX*) is metal-selective for Ca(II) or Sr(II). The second transition results in the expression of conformational determinants necessary for membrane binding and the Ca(II)-dependent activation of Factor IX by Factor XIa. These results suggest chemical similarity between a surface of a domain of Factor XIa and phospholipid vesicles, both of which interact with Factor IX in the presence of Ca(II).

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Year:  1987        PMID: 3108254

Source DB:  PubMed          Journal:  J Biol Chem        ISSN: 0021-9258            Impact factor:   5.157


  6 in total

1.  Modification of the N-terminus of human factor IX by defective propeptide cleavage or acetylation results in a destabilized calcium-induced conformation: effects on phospholipid binding and activation by factor XIa.

Authors:  E G Wojcik; M Van Den Berg; S R Poort; R M Bertina
Journal:  Biochem J       Date:  1997-05-01       Impact factor: 3.857

2.  gamma-Carboxyglutamic acids 36 and 40 do not contribute to human factor IX function.

Authors:  S Gillis; B C Furie; B Furie; H Patel; M C Huberty; M Switzer; W B Foster; H A Scoble; M D Bond
Journal:  Protein Sci       Date:  1997-01       Impact factor: 6.725

3.  In vitro and in vivo functional characterization of bovine vitamin K-dependent gamma-carboxylase expressed in Chinese hamster ovary cells.

Authors:  A Rehemtulla; D A Roth; L C Wasley; A Kuliopulos; C T Walsh; B Furie; B C Furie; R J Kaufman
Journal:  Proc Natl Acad Sci U S A       Date:  1993-05-15       Impact factor: 11.205

4.  Factor IX Zutphen: a Cys18-->Arg mutation results in formation of a heterodimer with alpha 1-microglobulin and the inability to form a calcium-induced conformation.

Authors:  E G Wojcik; M van den Berg; I K van der Linden; S R Poort; R Cupers; R M Bertina
Journal:  Biochem J       Date:  1995-11-01       Impact factor: 3.857

5.  The first EGF-like domain from human factor IX contains a high-affinity calcium binding site.

Authors:  P A Handford; M Baron; M Mayhew; A Willis; T Beesley; G G Brownlee; I D Campbell
Journal:  EMBO J       Date:  1990-02       Impact factor: 11.598

6.  The role of beta-hydroxyaspartate and adjacent carboxylate residues in the first EGF domain of human factor IX.

Authors:  D J Rees; I M Jones; P A Handford; S J Walter; M P Esnouf; K J Smith; G G Brownlee
Journal:  EMBO J       Date:  1988-07       Impact factor: 11.598

  6 in total

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