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Characterization of cDNA coding for human factor XIIIa.

U Grundmann, E Amann, G Zettlmeissl

    Proceedings of the National Academy of Sciences of the United States of America
    |November 1, 1986
    PubMed
    Summary
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    Researchers identified a human placenta cDNA sequence coding for factor XIIIa, an enzyme crucial for blood clot stabilization. This discovery advances understanding of blood coagulation and fibrin crosslinking mechanisms.

    Area of Science:

    • Molecular Biology
    • Hematology
    • Biochemistry

    Background:

    • Factor XIIIa is the active subunit of Factor XIII, essential for stabilizing blood clots via fibrin crosslinking.
    • Understanding the genetic basis of Factor XIIIa is crucial for comprehending hemostasis and related disorders.

    Purpose of the Study:

    • To isolate and characterize the complementary DNA (cDNA) encoding human placental factor XIIIa.
    • To determine the full length of the factor XIIIa cDNA and its corresponding protein sequence.

    Main Methods:

    • Screening of a human placental cDNA library using oligonucleotide probes based on known amino acid sequences of factor XIIIa.
    • Hybridization analysis, including blot-hybridization, to determine mRNA size and identify specific sequences.
    • Rescreening of cDNA libraries with the identified insert to obtain full-length sequences.

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    Main Results:

    • One clone containing a 1704 base pair insert coding for the amino-terminal 541 amino acids of factor XIIIa was identified from 0.36 million recombinants.
    • Factor XIIIa mRNA in placenta is approximately 4000 bases long.
    • The complete isolated factor XIIIa cDNA is 3905 bases, encoding a 732 amino acid protein, lacking a typical leader sequence for secreted proteins.

    Conclusions:

    • A substantial cDNA sequence for human factor XIIIa has been isolated and characterized from placental tissue.
    • The findings provide a detailed molecular basis for factor XIIIa synthesis and function in blood clot formation.
    • The absence of a predicted leader sequence suggests potential intracellular synthesis or alternative secretion mechanisms for factor XIIIa.