scholarly journals Catecholamine oxidation-mediated transcriptional inhibition in Mn neurotoxicity

2020 ◽  
Vol 45 (10) ◽  
pp. 619-624
Author(s):  
Koji Ueda ◽  
Yoshinori Okamoto ◽  
Akira Aoki ◽  
Hideto Jinno
Keyword(s):  
Transcriptional Inhibition ◽  
Catecholamine Oxidation

scholarly journals Interaction of 7SK with the Smn complex modulates snRNP production

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Changhe Ji ◽  
Jakob Bader ◽  
Pradhipa Ramanathan ◽  
Luisa Hennlein ◽  
Felix Meissner ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
Fine Tuning ◽  
Global Changes ◽  
Functional Association ◽  
Transcriptional Inhibition ◽  
Smn Complex ◽  
Core Components

AbstractGene expression requires tight coordination of the molecular machineries that mediate transcription and splicing. While the interplay between transcription kinetics and spliceosome fidelity has been investigated before, less is known about mechanisms regulating the assembly of the spliceosomal machinery in response to transcription changes. Here, we report an association of the Smn complex, which mediates spliceosomal snRNP biogenesis, with the 7SK complex involved in transcriptional regulation. We found that Smn interacts with the 7SK core components Larp7 and Mepce and specifically associates with 7SK subcomplexes containing hnRNP R. The association between Smn and 7SK complexes is enhanced upon transcriptional inhibition leading to reduced production of snRNPs. Taken together, our findings reveal a functional association of Smn and 7SK complexes that is governed by global changes in transcription. Thus, in addition to its canonical nuclear role in transcriptional regulation, 7SK has cytosolic functions in fine-tuning spliceosome production according to transcriptional demand.

Taurine Inhibition of Iron-Stimulated Catecholamine Oxidation

1998 ◽  
pp. 155-162 ◽  
Author(s):  
Ralph Dawson ◽  
Elisa Tang ◽  
Debbie Shih ◽  
Hunter Hern ◽  
Ming Hu ◽  
...  
Keyword(s):  
Catecholamine Oxidation

scholarly journals Dysregulation of In Vitro Decidualization of Human Endometrial Stromal Cells by Insulin via Transcriptional Inhibition of Forkhead Box Protein O1

PLoS ONE ◽  
2017 ◽  
Vol 12 (1) ◽  
pp. e0171004 ◽  
Author(s):  
Dorina Ujvari ◽  
Ivika Jakson ◽  
Shabnam Babayeva ◽  
Daniel Salamon ◽  
Bence Rethi ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Endometrial Stromal Cells ◽  
Transcriptional Inhibition ◽  
Forkhead Box

scholarly journals Mutator Foci Are Regulated by Developmental Stage, RNA, and the Germline Cell Cycle in Caenorhabditis elegans

2020 ◽  
Vol 10 (10) ◽  
pp. 3719-3728 ◽  
Author(s):  
Celja J. Uebel ◽  
Dana Agbede ◽  
Dylan C. Wallis ◽  
Carolyn M. Phillips
Keyword(s):  
Cell Cycle ◽  
Caenorhabditis Elegans ◽  
Epigenetic Inheritance ◽  
Germline Cell ◽  
Late Pachytene ◽  
Larval Stages ◽  
Transcriptional Inhibition ◽  
Male Germline ◽  
Early Embryos ◽  
Adult Hermaphrodite

RNA interference is a crucial gene regulatory mechanism in Caenorhabditis elegans. Phase-separated perinuclear germline compartments called Mutator foci are a key element of RNAi, ensuring robust gene silencing and transgenerational epigenetic inheritance. Despite their importance, Mutator foci regulation is not well understood, and observations of Mutator foci have been largely limited to adult hermaphrodite germlines. Here we reveal that punctate Mutator foci arise in the progenitor germ cells of early embryos and persist throughout all larval stages. They are additionally present throughout the male germline and in the cytoplasm of post-meiotic spermatids, suggestive of a role in paternal epigenetic inheritance. In the adult germline, transcriptional inhibition results in a pachytene-specific loss of Mutator foci, indicating that Mutator foci are partially reliant on RNA for their stability. Finally, we demonstrate that Mutator foci intensity is modulated by the stage of the germline cell cycle and specifically, that Mutator foci are brightest and most robust in the mitotic cells, transition zone, and late pachytene of adult germlines. Thus, our data defines several new factors that modulate Mutator foci morphology which may ultimately have implications for efficacy of RNAi in certain cell stages or environments.

scholarly journals Transcriptional inhibition of the murine erythropoietin receptor gene by an upstream repetitive element.

1993 ◽  
Vol 13 (1) ◽  
pp. 98-104 ◽  
Author(s):  
H Youssoufian ◽  
H F Lodish
Keyword(s):  
Reporter Gene ◽  
Mouse Genome ◽  
Repetitive Element ◽  
Receptor Gene ◽  
Inhibitory Effect ◽  
Erythropoietin Receptor ◽  
Erythroid Cells ◽  
Rnase Protection ◽  
Transcriptional Inhibition ◽  
Sense Orientation

Transcription of the murine erythropoietin receptor (EpoR) gene is inhibited by a novel repetitive element that is located upstream of the EpoR promoter. Reporter gene studies reveal that the inhibitory effect is both distance and orientation dependent. This element is a member of a family of repetitive elements specific to rodents and is present at approximately 10(5) copies per mouse genome. It encodes approximately 500- to 900-bp-long transcripts in both erythroid and nonerythroid cells. RNase protection analysis with a probe from the 5' flanking murine EpoR gene reveals that the direction of transcription is in the sense orientation, relative to the downstream EpoR gene. We suggest that transcriptional inhibition of the EpoR promoter is mediated by read-through transcripts originating in the upstream repetitive element and that this effect may contribute to the basal level of transcription of the murine EpoR gene in erythroid cells.

scholarly journals Nucleolar Association and Transcriptional Inhibition through 5S rDNA in Mammals

PLoS Genetics ◽  
2012 ◽  
Vol 8 (1) ◽  
pp. e1002468 ◽  
Author(s):  
Andrew M. Fedoriw ◽  
Joshua Starmer ◽  
Della Yee ◽  
Terry Magnuson
Keyword(s):  
5S Rdna ◽  
Transcriptional Inhibition

Abstract 162: MicroRNAs Mediate the Hemodynamic Regulation of Endothelium-to-Smooth Muscle Signaling

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Jing Zhou ◽  
Juanjuan Zhu ◽  
Yuefeng Liu ◽  
Shu Chien
Keyword(s):  
Smooth Muscle ◽  
Flow Pattern ◽  
Vascular Endothelial Cells ◽  
Vascular Diseases ◽  
Therapeutic Interventions ◽  
Pharmacological Intervention ◽  
Neointimal Formation ◽  
Transcriptional Inhibition ◽  
Protein Receptors ◽  
Phenotypic Transition

Vascular endothelial cells (ECs) at arterial branches and curvatures experience disturbed blood flow and induce a quiescent-to-activated phenotypic transition of the adjacent smooth muscle cells (SMCs) and a subsequent smooth muscle hyperplasia. However, the mechanism underlying the flow pattern-specific initiation of EC-to-SMC signaling remains elusive. Our previous study has demonstrated that endothelial microRNA-126-3p (miR-126-3p) acts as a key intercellular molecule to increase turnover of the recipient SMCs, and that its release is reduced by atheroprotective laminar shear (LS) to ECs. In the current study we found that atherogenic oscillatory shear (OS), but not atheroprotective pulsatile shear (PS), promotes the regulated exocytosis, particularly the secretion of non-membrane-bound miR-126-3p and other microRNAs (miRNAs) via the activation of soluble N-ethyl-maleimide-sensitive fusion protein attachment protein receptors (SNAREs), VAMP3 and SNAP23. Quantitative PCR arrays identify 15 EC-secreted miRNAs whose levels in the vesicle-poor supernatant of flow perfusate are differentially regulated (P<0.05) by OS versus PS. The fold changes of 11 miRNAs are either greater than 2.0 or less than 0.5. Knockdown of VAMP3 and SNAP23 reduces the secretion of miR-126-3p and miR-200a-3p, as well as the proliferation, migration, and suppression of contractile markers in SMCs caused by EC-coculture. Pharmacological intervention of mTORC1 in ECs blocks endothelial secretion and EC-to-SMC transfer of miR-126-3p through transcriptional inhibition of VAMP3 and SNAP23. Systemic inhibition of VAMP3 and SNAP23 by rapamycin or periadventitial application of the endocytosis inhibitor dynasore ameliorates the disturbed flow-induced neointimal formation, whereas intraluminal overexpression of SNAP23 aggravates it. Our findings demonstrate the flow-pattern-specificity of SNAREs activation and its contribution to the miRNA-mediated EC-SMC communication, uncovering potential targets for future diagnosis and therapeutic interventions for proliferative vascular diseases.

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