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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Biochem Biophys Res Commun. 2002 Apr 26;293(1):327-31.
Conserved physical linkage of GnRH-R and RBM8 in the medaka and human genomes.

Okubo K, Mitani H, Naruse K, Kondo M, Shima A, Tanaka M, Aida K.

Department of Aquatic Bioscience, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo, Tokyo 113-8657, Japan.

Candidate genes for human type II gonadotropin-releasing hormone receptor (GnRH-RII) reside on two separate loci, 1q12-q21 and 14q21-23, yet neither locus generates functional GnRH-RII. Instead, their opposite DNA strands encode functional RNA-binding motif protein 8 (RBM8s), which is also encoded by another locus, 5q13-q14. To elucidate the mechanism through which such multiple human GnRH-RII/RBM8 loci arose, here we have defined an RBM8 locus in a comparative model species, the medaka Oryzias latipes. The medaka RBM8, which exists as a single copy gene, is linked to, but does not overlap with, GnRH-R2 on linkage group (LG) 16, demonstrating the ancient origin of the physical linkage between GnRH-R and RBM8. The medaka LG 16 contains orthologous segments to the human chromosome 1 and therefore the 1q12-q21 locus would be an originating human GnRH-RII/RBM8 segment. Furthermore, like the human RBM8s on 1q12-q21 and 5q13-q14 but not that on 14q21-q23, the medaka RBM8 is a multiexon gene, indicating that the 14q21-q23 and 5q13-q14 loci were generated by retrotransposition and segmental genomic duplication, respectively, of the originating 1q12-q21 locus.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054603&dopt=Abstract

Biochem Biophys Res Commun. 2002 Apr 26;293(1):412-5.
Induction of pro-renin converting enzyme mk9 by thyroid hormone in the guinea-pig liver.

Das SK, Chatterjee D, Uddin M.

Department of Biochemistry, Meharry Medical College, 1005 D.B. Todd Boulevard, Nashville, TN 37208, USA. sdamc.edu

Kallikreins are a group of specific serine proteases and are an integral part of kallikrein-kinin system. The kallikrein-kinin system is hypotensive in nature and counteracts with the renin-angiotensin system in the maintenance of normal blood pressure. So far, four kallikrein-like enzymes, namely, mK9, mK13, mK22, and mK26, have been known to convert the inactive pro-renin into biologically active renin. Some of these enzymes are induced by the thyroid hormone. In the proposed study, we investigated the effects of thyroid hormone on the expression of genes for mk9, mk13, and mk22 enzymes. We used guinea pigs as models because these animals share many characteristics in common to humans. Male adult guinea pigs were intramuscularly injected with 2 mg/kg body weight of thyronine. Forty-eight hours following the last injection, the liver was processed for Northern blot analysis using labeled mK9, mK13, and mK22 specific RNA probes. Only mK9 was found to be transcriptionally regulated by the hormone.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054615&dopt=Abstract

Biochem Biophys Res Commun. 2002 Apr 26;293(1):489-96.
Crystal structure of the liganded anti-gibberellin A(4) antibody 4-B8(8)/E9 Fab fragment.

Murata T, Fushinobu S, Nakajima M, Asami O, Sassa T, Wakagi T, Yamaguchi I.

Department of Applied Biological Chemistry, Division of Agriculture and Agricultural Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan. tkgr1.ch.a.u-tokyo.ac.jp

Gibberellins, a class of plant hormones, consist of more than 120 members. Only a few of them are recognized by a receptor that remains unknown. The haptenic mouse monoclonal antibody, 4-B8(8)/E9, was generated against gibberellin A(4) (GA(4)) to recognize biologically active GA selectivity, and we attempted to confirm the binding properties between the antibody and GA(4). We carried out an X-ray crystallographic analysis of the 4-B8(8)/E9 Fab fragment complexed with GA(4) at a 2.8 A resolution by using the molecular replacement method. The crystal structure of the Fab fragment showed the typical immunoglobulin fold of the beta-barrel structure which is the common motif of all antibodies. A small hapten-combining site was made up of three heavy chain CDR loops. On the other hand, CDRs of the light chain did not interact directly with GA(4). The C/D rings of the GA(4) molecule were in van der Waals contact mainly with the aromatic side chain of Tyr100AH and Phe100BH of CDR-H3. The 3 beta-hydroxyl and 6 beta-carboxyl groups were, respectively, hydrogen-bonded to the main chain of Ala33H and to the Thr53H heavy chain.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054627&dopt=Abstract

Biochem Biophys Res Commun. 2002 Apr 26;293(1):549-53.
Effect of a peroxisome proliferator on 3 beta-hydroxysteroid dehydrogenase.

Wong JS, Ye X, Muhlenkamp CR, Gill SS.

Environmental Toxicology Graduate Program, Department of Cell Biology and Neuroscience, University of California, 5429 Boyce Hall, Riverside, CA 92521, USA.

To better understand the changes that occur following exposure to peroxisome proliferators, we utilized mRNA differential display and microarray to screen for peroxisome proliferator target genes apart from those involved in lipid metabolism in male C57B6 mice by using the ubiquitous plasticizer, di(2-ethylhexyl)phthalate (DEHP). One noted change was the dose-dependent suppression of the mouse hormone metabolizing 3 beta-hydroxysteroid dehydrogenase V (HSD3b5), which is specifically expressed in the male mouse liver. Northern analysis showed that HSD3b5 mRNA levels decreased dramatically upon one-day exposure to 2.0% dietary DEHP, and were nearly undetectable by one week of treatment. Food restriction also significantly suppressed HSD3b5 expression; however, in this case the suppression was delayed and to a lesser extent. Another mouse 3 beta-hydroxysteroid dehydrogenase, HSD3b4, predominantly expressed in kidneys, was also regulated by DEHP and food restriction. The sex-specific gene, HSD3b5, was affected more by DEHP and food restriction than the tissue-specific gene, HSD3b4.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054636&dopt=Abstract

Biochem Biophys Res Commun. 2002 Apr 26;293(1):554-9.
Thyroid hormonal activity of the flame retardants tetrabromobisphenol A and tetrachlorobisphenol A.

Kitamura S, Jinno N, Ohta S, Kuroki H, Fujimoto N.

School of Medicine, Institute of Pharmaceutical Science, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan. skitamiroshima-u.ac.jp

The thyroid hormonal-disrupting activity of the flame retardants tetrabromobisphenol A (TBBPA) and tetrachlorobisphenol A (TCBPA) was examined and compared with that of bisphenol A, a typical estrogenic xenobiotic. TBBPA and TCBPA, halogenated derivatives of bisphenol A, markedly inhibited the binding of triiodothyronine (T(3); 1 x 10(-10) M) to thyroid hormone receptor in the concentration range of 1 x 10(-6) to 1 x 10(-4) M, but bisphenol A did not. The thyroid hormonal activity of TBBPA and TCBPA was also examined using rat pituitary cell line GH3 cells, which grow and release growth hormone (GH) depending on thyroid hormone. TBBPA and TCBPA enhanced the proliferation of GH3 cells and stimulated their production of GH in the concentration range of 1 x 10(-6) to 1 x 10(-4) M, while bisphenol A was inactive. TBBPA, TCBPA, and bisphenol A did not show antagonistic action, i.e., these compounds did not inhibit the hormonal activity of T(3) to induce growth and GH production of GH3 cells. TBBPA and TCBPA, as well as bisphenol A, enhanced the proliferation of MtT/E-2 cells, whose growth is estrogen-dependent. These results suggest that TBBPA and TCBPA act as thyroid hormone agonists, as well as estrogens.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12054637&dopt=Abstract

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