ABSTRACT
The gonadoblastoma gene, testis-specific protein Y-encoded (TSPY), on the Y chromosome and its X-homologue, TSPX, are cell cycle regulators and function as a proto-oncogene and a tumor suppressor respectively in human oncogenesis. TSPY and TSPX competitively bind to the androgen receptor (AR) and AR variants, such as AR-V7, at their conserved SET/NAP domain, and exacerbate and repress the transactivation of the AR/AR-V7 target genes in ligand dependent and independent manners respectively. The inhibitory domain has been mapped to the carboxyl acidic domain of TSPX, truncation of which renders TSPX to be stimulatory while its transposition to the C-terminus of TSPY results in an inhibitory hybrid protein. TSPY and TSPX co-localize with the endogenous AR, in the presence of ligand, on the promoters and differentially regulate the expression of the endogenous AR target genes in the androgen-responsive LNCaP prostate cancer cells. Transcriptome analysis shows that TSPY and TSPX expressions differentially affect significant numbers of canonical pathways, upstream regulators and cellular functions. Significantly, among the common ones, TSPY activates and TSPX inhibits numerous growth-related and oncogenic canonical pathways and cellular functions in the respective cell populations. Hence, TSPY and TSPX exert opposing effects on the transactivation functions of AR and AR-Vs important for various physiological and disease processes sensitive to male sex hormone actions, thereby not only affecting the pathogenesis of male-specific prostate cancer but also likely contributing to sex differences in the health and diseases of man.
Subject(s)
Cell Cycle Proteins/genetics , Nuclear Proteins/genetics , Prostatic Neoplasms/genetics , Receptors, Androgen/genetics , Transcriptome/genetics , Cell Cycle Proteins/biosynthesis , Cell Line, Tumor , Chromosomes, Human, X/genetics , Chromosomes, Human, Y/genetics , DNA-Binding Proteins , Gene Expression Regulation, Developmental , Gonadoblastoma/genetics , Humans , Male , Nuclear Proteins/biosynthesis , Prostatic Neoplasms/pathology , Protein Domains/genetics , Proto-Oncogene Mas , Receptors, Androgen/biosynthesis , Testis/growth & development , Testis/pathology , Transcriptional Activation/geneticsABSTRACT
OBJECTIVES: This study was conducted to investigate the effects of dietary supplementation of Perilla frutescens seed (PFS) on growth performance, blood profiles, meat quality and meat nutrient characteristics in finishing castrated male Songliao black pigs. METHODS: A total of 80 castrated male Songliao black pigs with an average initial body weight (BW) of 84.1 ± 2.1 kg were used in a 75 days feeding trial. All pigs were randomly assigned into four dietary treatments: CON, basal diet; PFS3.0, basal diet + 3.0% of PFS; PFS6.0, basal diet + 6.0% of PFS and PFS9.0, basal diet + 9.0% of PFS. RESULTS: As a result of this experiment, dietary supplementation of PFS improved the growth performance parameters, blood albumin and blood lipid parameters. Whereas, on FBW, average daily feed intake and average daily gain there showed a non-dose-dependent manner that pigs in PFS9.0 had lowest performance compared with other two PFS treatments. Furthermore, meat colour of yellowness, pH, cook meat rate, moisture, crude protein and crude fat were increased by PFS addition. However, lower growth performance was observed in PFS9.0 group. As well as, dietary inclusion of PFS also alters the meat amino acid composition and meat fatty acids composition. Particularly, umami amino acid contents and polyunsaturated fatty acid were all enhanced by PFS addition. CONCLUSIONS: In summary, dietary supplementation of PFS have beneficial effects on the performance and meat quality and nutritional values in Songliao black pigs.
Subject(s)
Animal Feed , Perilla frutescens , Amino Acids/pharmacology , Animal Feed/analysis , Animals , Body Composition , Diet/veterinary , Dietary Supplements , Male , Seeds , SwineABSTRACT
Transgenic mouse lines were generated that express the Cre recombinase under the control of the distal promoter of the mouse Lck gene. Cre recombination in four of these lines of transgenic mice was characterized at the single cell level using ROSA26-regulated loxP-Stop-loxP-betageo and loxP-Stop-loxP-YFP reporter mouse lines. Two of the lines showed T cell-restricted Cre recombination, whereas the other two also expressed Cre in B cells, NK cells, and monocytes. Cre recombination began at a late stage of T cell development (at or after up-regulation of the TCR during positive selection) in the two T cell-restricted lines. Lines of mice that express the Cre recombinase at late stages of thymocyte development are of value for determining the impact of mutations on T cell function in the absence of complicating effects on early thymocyte selection.