Clinical Chemistry
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Clinical Chemistry 42: 1042-1050, 1996;
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Melegos, D. N.
Right arrow Articles by Diamandis, E. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Melegos, D. N.
Right arrow Articles by Diamandis, E. P.

Clinical Chemistry, Vol 42, 1042-1050, Copyright © 1996 by American Association for Clinical Chemistry

Prostaglandin D2 synthase: a component of human amniotic fluid and its association with fetal abnormalities

DN Melegos, H Yu and EP Diamandis
Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Canada.

Prostaglandin D2 (PGD2) synthase is responsible for PGD2 production in the brain. Western blot analysis of human amniotic fluid and probing with a polyclonal antibody against prostate-specific antigen (PSA) revealed a strong immunoreactive band with a molecular mass of 25 kDa. The immunoreactive species, which does not react with monoclonal anti- PSA antibodies, was purified to homogeneity from 1 L of amniotic fluid through successive cycles of gel filtration and ion-exchange chromatography. Amino acid sequence analysis (15 cycles) revealed that the protein was highly homologous or identical to PGD2 synthase. On semiquantitative analysis, PGD2 synthase concentration appears to increase dramatically during gestational weeks 12-25 and then declines slowly until term. PGD2 synthase concentration in amniotic fluid was altered in many abnormal pregnancies, most notably its decrease in trisomic fetuses and fetuses with renal abnormalities.


The following articles in journals at HighWire Press have cited this article:


Home page
 Clin. Chem.Home page
B. Bulmer, G. Ward, E. Diamandis, D. Nicol, and J. Clements
Prostaglandin D Synthase Does Not Produce Prostate-specific Antigen Cross-Reactivity in Renal Cell Carcinoma
Clin. Chem., March 1, 2001; 47(3): 607 - 608.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1996 by the American Association for Clinical Chemistry.