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Peptide DV-28 amide: An inhibitor of bradykinin-induced arterial smooth muscle relaxation encoded by Bombina orientalis skin kininogen-2

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  • Skin Kininogens From Bombinid Toads Encode An Array Of Bradykinin-Related Peptides And One Such Kini
  • Kinestatin
  • In Order To Determine If The Skin Secretion Of The Closely-Related Toad
  • Bombina Orientalis
  • Contained A Bradykinin Inhibitory Peptide Related To Kinestatin
  • We Screened Reverse Phase Hplc Fractions Of Defensive Skin Secretion Using A Rat Tail Artery Smooth
  • A Fraction Was Located That Inhibited Bradykinin-Induced Relaxation Of The Preparation And This Cont
  • 5 Da As Determined By Maldi-Tof Ms
  • Automated Edman Degradation Of This Peptide Established The Identity Of A 28-Mer As: Dmyeikgfksahgrp
  • With A Disulfide-Bridge Between Cys18 And Cys24 And An Amidated C-Terminal Val Residue
  • Peptide Dv-28 Was Found To Correspond To Residues 133–160 Of Skin Pre-Kininogen-2 Of B
  • Orientalis That Also Encodes Two Copies Of (Thr6)-Bradykinin
  • The C-Terminal Residue
  • Gly-161
  • Of The Precursor Open-Reading Frame
  • Acts As The C-Terminal Amide Donor Of Mature Dv-28
  • Dv-28 Amide Thus Represents A New Class Of Bradykinin Inhibitor Peptide From Amphibian Skin Secretio
  • Biology


Chapter 2 Androgen Action During Prostate Carcinogenesis Diping Wang and Donald J. Tindall Abstract Androgens are critical for normal prostate development and function, as well as prostate cancer initiation and progression. Androgens function mainly by regulating target gene expression through the androgen receptor (AR). Many studies have shown that androgen-AR signaling exerts actions on key events during prostate carcinogenesis. In this review, androgen action in distinct aspects of prostate carcinogenesis, including (i) cell proliferation, (ii) cell apoptosis, and (iii) prostate cancer metastasis will be discussed. Key words: Androgen receptor, prostate cancer, androgen metabolism, androgen signaling, castration-resistant prostate cancer. 1. Androgen Signaling Androgens are the male sex hormones, which control the differ- entiation and maturation of male reproductive organs, including the prostate gland. Testosterone is the principal androgen in cir- culation and is synthesized by Leydig cells in the testes, under the regulation of luteinizing hormone (LH), which is further regulated by gonadotropin-releasing hormone (GnRH). Adrenal glands also synthesize a small amount of androgens, such as dehy- droepiandrosterone (DHEA) and androstenedione (4-dione) (1). Testosterone enters prostate cells by passive diffusion, where it is converted enzymatically by 5-α reductases to the more potent androgen dihydrotestosterone (DHT) (2). Binding of androgens to the androgen receptor (AR), a ligand-modulated transcrip- tion factor, induces a conformational change in the AR, causing release of heat shock proteins and translocation of the AR to the F. Saatcioglu (ed.), Androgen Action, Methods in Molecular Biology 776, DOI 10.1007/978-1-61779-243-4_2, © Springer Science+Business Media, LLC 2011 25 26 Wang and Tindall nucleus, where it transcriptionally regulates the expression of tar- get genes (3). In addition to the classic genomic effects of sex steroids, accu- mulating

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