Gap junctions are critical for spermatogenesis. They are composed of integral proteins, the connexins. In mammals, a loss of Cx43 expression results in the inhibition of spermatogenesis. We have shown that Cx43 is expressed in the Sertoli cells of rainbow trout and that cAMP and triiodothyronine (T(3)) regulate testicular Cx43 expression in brook trout testis. The objective of this study was to determine if cAMP and T(3) act at the level of the cx43 promoter to regulate its expression. A 607 bp 5' flanking sequence of the cx43 promoter was obtained by Genome Walking. A TATA box was predicted to be located between positions -36 and -30 relative to the transcriptional initiation site. 5'-Rapid amplification of cDNA ends indicated a single transcriptional start site. Single C/EBP (-164 to -156) and tr-beta (-112 to -107) response elements were identified and electrophoretic mobility shift assays indicated the presence of competitive protein binding sites at each region. Immortalized rainbow trout gonadal cell line (RTG-2) which express cx43 and tr-beta transcripts were transfected with a vector containing the Cx43 promoter inserted into a luciferase expression vector. Transactivation of the reporter genes was stimulated by either cAMP or T(3). Sequential deletion and point mutations in either the C/EBP or tr-beta response element indicated that T(3) but not cAMP directly induced luciferase transactivation of the luciferase gene by acting on different sites of the Cx43 promoter. Together, these data indicate that T(3) stimulates cx43 expression via direct regulation of gene transcription.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.ygcen.2010.09.013 | DOI Listing |
Circ Res
November 2024
Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, College of Medicine or College of Pharmacy, Seoul National University, South Korea (M.K., C.-S.L., H.S., H.J.S., H.-S.K.).
Background: Latrophilin-2 (Lphn2), an adhesive GPCR (G protein-coupled receptor), was found to be a specific marker of cardiac progenitors during the differentiation of pluripotent stem cells into cardiomyocytes or during embryonic heart development in our previous studies. Its role in adult heart physiology, however, remains unclear.
Methods: The embryonic lethality resulting from deletion necessitates the establishment of cardiomyocyte-specific, tamoxifen-inducible knockout mice, which was achieved by crossing mice with mice having MerCreMer (tamoxifen-inducible Cre [Cyclization recombinase] recombinase) under the α-myosin heavy chain promoter.
Cell Tissue Res
December 2024
Laboratory for Reproductive Toxicology, INRS-Centre Armand-Frappier Santé Biotechnologie, Université du Québec, 531 Boul Des Prairies, Laval, Québec, H7V 1B7, Canada.
Am J Pathol
October 2024
Jiangxi Provincial Key Laboratory of Drug Targets and Drug Screening, School of Pharmacy, Jiangxi Medical College, Nanchang University, Nanchang, China. Electronic address:
Remote ischemic preconditioning (RIPC) exerts a protective role on myocardial ischemia/reperfusion (I/R) injury by the release of various humoral factors. Lactate is a common metabolite in ischemic tissues. Nevertheless, little is known about the role lactate plays in myocardial I/R injury and its underlying mechanism.
View Article and Find Full Text PDFJ Transl Med
July 2024
Cellular Networks and Molecular Therapeutic Targets, Proteomics Unit, IRCCS-Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144, Rome, Italy.
Background: In the fight against GBM, drug repurposing emerges as a viable and time-saving approach to explore new treatment options. Chlorpromazine, an old antipsychotic medication, has recently arisen as a promising candidate for repositioning in GBM therapy in addition to temozolomide, the first-line standard of care. We previously demonstrated the antitumor efficacy of chlorpromazine and its synergistic effects with temozolomide in suppressing GBM cell malignant features in vitro.
View Article and Find Full Text PDFJ Biol Chem
July 2024
Department of Biochemistry, The University of Texas Southwestern Medical Center, Dallas, Texas, USA; Department of Obstetrics & Gynecology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA; Cecil H. and Ida Green Center for Reproductive Biology Sciences, The University of Texas Southwestern Medical Center, Dallas, Texas, USA; North Texas March of Dimes Birth Defects Center, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Progesterone (P), acting via its nuclear receptor (PR), is critical for pregnancy maintenance by suppressing proinflammatory and contraction-associated protein (CAP)/contractile genes in the myometrium. P/PR partially exerts these effects by tethering to NF-κB bound to their promot-ers, thereby decreasing NF-κB transcriptional activity. However, the underlying mechanisms whereby P/PR interaction blocks proinflammatory and CAP gene expression are not fully understood.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!