Prediction of microRNAs affecting mRNA expression during retinal development.

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Prediction of microRNAs affecting mRNA expression during retinal development.

  • Conversely
  • Background: Micrornas (Mirnas) Are Small Rna Molecules (~22 Nucleotides) Which Have Been Shown To Pl
  • Conditional Inactivation Of Mirnas In The Eye Causes Loss Of Visual Function And Progressive Retinal
  • In Addition To Inhibiting Translation
  • Mirnas Can Mediate Degradation Of Targeted Mrnas
  • We Have Previously Shown That Candidate Mirnas Affecting Transcript Levels In A Tissue Can Be Deduce
  • The Purpose Of This Study Was To Predict Mirnas Which Affect Mrna Levels In Developing And Adult Ret
  • Results: Microarray Expression Data From Ciliary Epithelial Retinal Stem Cells (Ce-Rscs)
  • Developing And Adult Mouse Retina Were Generated Or Downloaded From Public Repositories
  • Analysis Of Gene Expression Profiles Detected The Effects Of Multiple Mirnas In Ce-Rscs And Retina
  • The Expression Of 20 Selected Mirnas Was Confirmed By Rt-Pcr And The Cellular Distribution Of Repres
  • The Expression Levels Of Mirnas Correlated With The Significance Of Their Predicted Effects Upon Mrn
  • Highly Expressed Mirnas Included Mir-124
  • Mir-125A
  • Mir-125B
  • Mir-204 And Mir-9
  • Over-Expression Of Three Mirnas With Significant Predicted Effects Upon Global Mrna Levels Resulted
  • Conclusions: This Study Has Detected The Effect Of Mirnas Upon Mrna Expression In Immature And Adult
  • The Validity Of These Observations Is Supported By The Experimental Confirmation Of Candidate Mirna
  • Identified Mirnas Are Likely To Be Important In Retinal Development And Function
  • Misregulation Of These Mirnas Might Contribute To Retinal Degeneration And Disease
  • Manipulation Of Their Expression Could Potentially Be Usedas A Therapeutic Tool In The Future


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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