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Endocrine and Metabolic Side Effects
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
Ayse Serap Karadag, Emin Ozlu, Bodo C. Melnik
The physiologic effects of retinoids are regulated by retinoic acid receptors (RAR-α, -β, and -γ isoforms) and retinoid X receptor (RXR-α, -β, and -γ isoforms) (21) (Table 17.1). RAR and RXR are members of a broad family of nuclear receptors including steroid, thyroid hormone, vitamin D, liver X receptor (LXR), and peroxisome proliferator-activated receptors (PPARs). They act as ligand-dependent transcription factors. Many tissues are targeted by retinoids through different heterodimeric complexes (3). Importantly, retinoids have also a significant impact on stem cell differentiation (22). ATRA induces differentiation primarily by binding to RARs, which are the transcription factors that associate with RXRs and bind retinoic acid response elements (RAREs) in the nucleus. Binding of ATRA (22): Initiates changes in interactions of RAR/RXRs with co-repressor and co-activator proteins, activating transcription of primary target genes.Alters interactions with proteins that induce epigenetic changes.Induces transcription of genes encoding transcription factors and signaling proteins that further modify gene expression and induce a secondary gene response (e.g., upregulation of p53, FoxO1, FoxO3, TRAIL) and results in alterations in estrogen receptor α signaling (3,20). Proteins that bind at or near RAREs include Sin3a, N-CoR1, PRAME, Trim24, NRIP1, Ajuba, Zfp423, and MN1/TEL. Interactions among retinoids, RARs/RXRs, and these proteins explain in part the powerful effects of retinoids on stem cell differentiation.
Nuclear receptor co-repressor RIP140 regulates diurnal expression of cytochrome P450 2b10 in mouse liver
Published in Xenobiotica, 2020
Mengjing Zhao, Huan Zhao, Luomin Lin, Yi Wang, Menglin Chen, Baojian Wu
Co-regulators are nuclear proteins which participate in the regulation of gene transcription by altering the functions of nuclear receptors (NRs) or other transcriptional factors (Glass & Rosenfeld, 2000). They are regarded as secondary transcription factors and brought to the site of transcription by transcription factors (cannot bind to DNA directly) (O’Malley, 2007). Co-regulators are generally classified into two types, namely, co-activators (enhancing gene transcription) and co-repressors (inhibiting gene transcription) (Glass & Rosenfeld, 2000). receptor-interacting protein 140 (RIP140), also known as NRIP1) is a co-repressor that interacts with NRs such as CAR, PXR and RXR and inhibits their transcriptional activities (Timsit & Negishi, 2007). RIP140 has been implicated in regulation of diverse physiological processes such as lipogenesis, cell differentiation and immune responses (Aziz et al., 2015; Hallberg et al., 2008; Ho et al., 2012; Nautiyal, 2017). It may be also involved in regulation of circadian clock genes via interacting with RORs (Poliandri et al., 2011). However, whether and how RIP140 regulates circadian drug-metabolizing genes remain unexplored.
Clinicopathologic and prognostic roles of circular RNA plasmacytoma variant translocation 1 in various cancers
Published in Expert Review of Molecular Diagnostics, 2021
Jian Zhou, Hui Zhang, Dazhi Zou, Zhen Zhou, Wanchun Wang, Yingquan Luo, Tang Liu
Some circRNAs can increase the complexity of RNA regulatory networks by acting as miRNA sponges, which can suppress the function of microRNAs (miRs) in eukaryotic cells [11–13] (Figure 2). In addition, circRNAs have been proven to be correlated with tumorigenesis, and many studies reported that circRNAs (such as CBL.11, SLC8A1, NEK6 and NRIP1) were related to the regulation of genes and signaling pathways of cancers [14–17]. Moreover, many circRNAs have been identified as useful diagnostic biomarkers for various cancers [18–21]. Additionally, circRNAs were reported to play an important role in thyroid cancer [21], viral infections [22], diabetes [23] and ovarian cancer [24].
Selective release of circRNAs in platelet-derived extracellular vesicles
Published in Journal of Extracellular Vesicles, 2018
Christian Preußer, Lee-Hsueh Hung, Tim Schneider, Silke Schreiner, Martin Hardt, Anna Moebus, Sentot Santoso, Albrecht Bindereif
Moreover, we used the same CD63 antibody in Western blot analysis to assess specific enrichment of exosomes, assaying all 12 fractions after sucrose-density gradient centrifugation (Figure 4(c)). CD63 could be clearly detected in fractions #5 to 7, with the major peak in fraction #6, consistent with the expected density of exosomes (1.10–1.12 g/mL). The endoplasmic reticulum marker calnexin served as a negative control. To examine whether circRNAs are associated with EVs, we used RNA isolated from each fraction across the sucrose gradient (#1–12, from top to bottom) and monitored by RT-PCR the distribution of two abundant circRNAs in platelets, GSE1 and NRIP1 (Figure 4(d)). Clearly both circRNAs could be detected in the fractions where exosomes are highly enriched, indicating that circRNAs are associated with platelet-derived vesicles. Finally, we determined the relative size distribution of the enriched EVs (microvesicles and exosomes) by dynamic light scattering (Figure 4(e)). However, note that without further characterisation this does not allow to distinguish between microvesicles and similar-sized lipoprotein particles or small platelets [30]. In addition, the measured size of the isolated microvesicles appeared on the lower limit of what one expects. Please note that in particular the isolation of these vesicles from blood samples such as apheresis platelets is affected by venipuncture, centrifugation and washing steps, as well as by the presence of lipoprotein particles. Therefore, larger particles sub-types may aggregate and/or precipitate during the first steps of centrifugation. Nevertheless, we chose differential centrifugation to obtain a clean subpopulation of microvesicles. In sum, together with the electron microscopy and Western blot analysis, we conclude that we specifically enriched for either type of platelet-derived vesicles.