Journal articles: '(3) Rome I Regulation'

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Rammeloo, Stephan. "‘From Rome to Rome’ – Cross-border employment contract. European Private International Law: Intertemporal law and foreign overriding mandatory laws." Maastricht Journal of European and Comparative Law 24, no. 2 (April 2017): 298–322. http://dx.doi.org/10.1177/1023263x17709754.

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To what extent are Greek saving laws, resulting in payment cuts in the public sector (that is employment conditions), capable of overriding the applicable (German) law? A dispute arising from an employment relationship between the Greek Republic and an employee habitually carrying out work in Germany, gave rise to preliminary questions having regard to the temporal scope of EU Regulation No. 593/2008 (the ‘Rome I Regulation’)1 and, closely related thereto, the functional reach of Article 9(3) of that Regulation in respect of ‘foreign’ mandatory laws, in light of the principle of sincere cooperation enshrined in Article 4(3) TEU. An analysis of the Advocate General’s Opinion and the Court of Justice of the European Union’s (CJEU) ruling is followed by critical commentary and suggestions for future EU legislative amendments to the Rome I regime.

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Kronenberg, Alexander. "Foreign overriding mandatory provisions under the regulation (EC) No 593/2008 (Rome I Regulation). Judgment of the European Court of Justice of 18 october 2016, case c-135/15 = Leyes de policía de terceros estados en el ámbito del reglamento (CE) No 593/2008 (Reglamento Roma I). Comentario a la STJUE de 18 de octubre de 2016, asunto c-135/15." CUADERNOS DE DERECHO TRANSNACIONAL 10, no. 2 (October 5, 2018): 873. http://dx.doi.org/10.20318/cdt.2018.4409.

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Abstract: The role and treatment of foreign overriding mandatory provisions in international contract law have been subject to academic discussions for a long time. This has not changed with the introduction of Article 9 of the Rome I Regulation. In the judgment discussed in this case note, the European Court of Justice addressed some of the contentious issues in relation to Article 9(3) of the Rome I Regulation. This note examines and evaluates the solutions found by the ECJ and puts them into context. It also points out some questions the ECJ did not discuss; these questions remain open for now but will need to be addressed in the future.Keywords: Article 9(3) Rome I Regulation, foreign overriding mandatory provisions, conflict-of-law level consideration, substantive law level consideration, principle of sincere cooperation.Resumen: El tratamiento de las leyes de policía de terceros estados en derecho de contratos internacionales ha sido objeto de la polémica desde hace tiempo. Esto no ha cambiado con la entrada en vigor del artículo 9 del Reglamento Roma I. Con la sentencia comentada el Tribunal de Justicia de la Unión Europea ha tratado algunas de la cuestiones debatidas respecto al artículo 9.3 del Reglamento Roma I. Este comentario analiza, evalúa y pone en contexto las soluciones encontradas por el TJUE. También aborda las cuestiones que no han sido comentadas por el TJUE; estas cuestiones permanecen abiertas por el momento pero deberán ser examinadas en el futuro.Palabras clave: leyes de policía de terceros estados, consideración en nivel conflictual, consideración en nivel sustantivo, principio de cooperación leal.

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Folkard, Joshua. "THE EFFECT OF ROME II ON NATIONAL PROCEDURAL LAW." Cambridge Law Journal 74, no. 1 (March 2015): 37–40. http://dx.doi.org/10.1017/s0008197315000215.

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AT common law, in cases where the substantive claim is governed by foreign law, questions of procedure are nonetheless governed by the lex fori. In the context of damages, although the existence of damage is a question for the lex causae, its quantification and assessment is determined according to the law of the forum (Boys v Chaplin [1971] A.C. 356). The distinction between substance and procedure is preserved by Article 1(3) of Council Regulation (EC) No 864/2007 (“Rome II”) which provides, with certain exceptions, that Rome II “shall not apply to evidence and procedure”. That rule is, however, qualified by Article 15, which requires the law applicable under the Regulation (i.e. “the law applicable to non-contractual obligations”) to govern, inter alia, “the existence, the nature and the assessment of damage or the remedy claimed” (Article 15(c)). The decision of the Court of Appeal in Wall v Mutuelle De Poitiers Assurances [2014] EWCA Civ 138; [2014] 3 All E.R. 340 concerns the definition of “procedure” in Article 1(3) and the meaning of “applicable law” in Article 15(c). It raises the important question of how far Rome II has encroached on the traditional view of national procedural autonomy in the conflict of laws.

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Lozano-Durán, Rosa, and Silke Robatzek. "14-3-3 Proteins in Plant-Pathogen Interactions." Molecular Plant-Microbe Interactions® 28, no. 5 (May 2015): 511–18. http://dx.doi.org/10.1094/mpmi-10-14-0322-cr.

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14-3-3 proteins define a eukaryotic-specific protein family with a general role in signal transduction. Primarily, 14-3-3 proteins act as phosphosensors, binding phosphorylated client proteins and modulating their functions. Since phosphorylation regulates a plethora of different physiological responses in plants, 14-3-3 proteins play roles in multiple signaling pathways, including those controlling metabolism, hormone signaling, cell division, and responses to abiotic and biotic stimuli. Increasing evidence supports a prominent role of 14-3-3 proteins in regulating plant immunity against pathogens at various levels. In this review, potential links between 14-3-3 function and the regulation of plant-pathogen interactions are discussed, with a special focus on the regulation of 14-3-3 proteins in response to pathogen perception, interactions between 14-3-3 proteins and defense-related proteins, and 14-3-3 proteins as targets of pathogen effectors.

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Khudhair, Nagam, Yu Cuiping, Ahmed Khalid, and Xuejun Gao. "Role 14-3-3 Protein in Regulation Some Cellular Processes." Current Research Journal of Biological Sciences 6, no. 5 (November 20, 2014): 197–204. http://dx.doi.org/10.19026/crjbs.6.5193.

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Banerjee, Hridesh, and Lawrence P. Kane. "Immune regulation by Tim-3." F1000Research 7 (March 14, 2018): 316. http://dx.doi.org/10.12688/f1000research.13446.1.

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T-cell immunoglobulin and mucin domain 3 (Tim-3) is a transmembrane protein that in both mice and humans has been shown to possess various functions in a context-dependent manner. Thus, Tim-3 has been associated with both inhibitory and co-stimulatory function, depending in part on the specific cell type and immune response course. Though originally described on T cells, Tim-3 is now known to be expressed by both lymphoid and non-lymphoid cells within the immune system and even by non-immune cells. In addition, though widely thought of as a negative regulator of immunity, Tim-3 has been shown in more recent studies to have a positive function on both myeloid and lymphoid cells, including T cells. Tim-3 is often expressed at a high level on exhausted T cells in tumors and chronic infection and may engage in crosstalk with other so-called “checkpoint” molecules such as PD-1. Thus, Tim-3 has emerged as a possible therapeutic target, which is being actively explored both pre-clinically and clinically. However, recent research suggests a more complex in vivo role for this protein, compared with other targets in this area.

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Jackson, S. P., C. L. Yap, and K. E. Anderson. "Phosphoinositide 3-kinases and the regulation of platelet function." Biochemical Society Transactions 32, no. 2 (April 1, 2004): 387–92. http://dx.doi.org/10.1042/bst0320387.

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A clear understanding of the role of PI (phosphoinositide) 3-kinases in supporting the haemostatic function of platelets has been slow to evolve. In fact, insight into the roles of individual PI 3-kinase isoforms in platelet function remains rudimentary. However, based on in vitro studies using wortmannin and LY294002, there is evidence for an important role for PI 3-kinases in regulating a broad range of functional platelet responses, including primary platelet adhesion, cytoskeletal remodelling and platelet aggregation. One of the critical platelet responses involves affinity regulation of the major platelet integrin αIIbβ3, the primary receptor mediating platelet aggregation and thrombus growth. The input signals regulating integrin αIIbβ3 can be divided into three main groups: (1) Gq-coupled receptors linked to the activation of PLCβ (phospholipase Cβ); (2) Gi-coupled receptors linked to the regulation of adenylate cyclase and Rap1b; and (3) adhesion receptor signalling involving Src kinase-dependent activation of PLCγ isoforms. PI 3-kinases have not been demonstrated to play a critical role in Gq-dependent platelet activation; however, one or more PI 3-kinase isoforms appears to be important for Gi-dependent activation of Rap1b and adhesion receptor activation of PLCγ isoforms. Thus distinct co-operative PI 3-kinase signalling mechanisms appear to play an important role in regulating the adhesive function of integrin αIIbβ3.

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Jaroszek, Agata. "European Online Marketplace – New Measures for Consumer Protection against “Old Conflict of Laws Rules”." Masaryk University Journal of Law and Technology 9, no. 1 (June 30, 2015): 21–41. http://dx.doi.org/10.5817/mujlt2015-1-3.

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The paper aims at discussing the rationale for protecting consumers under the new directive on consumer rights (CRD) and its relation to conflict of law rules under the Regulation on the law applicable to contractual obligations (Rome I).The author is of the opinion the newly adopted legal framework for consumer protection under the directive on consumer rights seems to be more predictable especially in terms of supporting consumers with more mandatory information before the conclusion of a contract with a professional as well as a single 14 day withdrawal period for all Member States. However, the level of consumer protection in the purchase of digital content is insufficient and from the perspective of conflict of laws rules for consumer contracts under Rome I, a consumer who actively makes a purchase from a professional from another Member State or a third country cannot expect the special protective rules envisaged in the regime under CRD and Rome I to be applied by default; rather, the general rules come into play.

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Dulloo, A. G., S. Samec, and J. Seydoux. "Uncoupling protein 3 and fatty acid metabolism." Biochemical Society Transactions 29, no. 6 (November 1, 2001): 785–91. http://dx.doi.org/10.1042/bst0290785.

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A role for uncoupling protein (UCP) 3 in fatty acid metabolism is reviewed within the context of our proposal, first put forward in 1998, that this homologue of UCP1 may be involved in the regulation of lipids as fuel substrate rather than in the mediation of thermogenesis. Since then, the demonstrations of muscle-type differences in UCP3 gene regulation in response to dietary manipulations (starvation, high-fat feeding) or to pharmacological interferences with the flux of lipid substrates between adipose-tissue stores and skeletal-muscle mitochondrial oxidation are all in accord with this proposed role for UCP3 in regulating lipids as fuel substrate. However, given the current limitations of gene-knockout technology for evaluating/interpreting the functional importance of genes encoding mitochondrial membrane proteins, the transition from ‘associative’ to ‘cause-and-effect’ evidence for a physiological role of UCP3 in regulating fatty acid metabolism will have to await the development of assays that are sensitive to changes in UCP3 activity. Furthermore, in evaluating the physiological regulators of UCP3, the available evidence points to the existence of adipose-derived factor(s) which, independently of circulating levels of free fatty acids, initiates events leading to the transcription of genes encoding UCP3 and key enzymes of lipid oxidation in the fast glycolytic or fast oxidative-glycolytic muscles, i.e. in the bulk of the skeletal-muscle mass. It is proposed that in tissues where UCP3 co-exists with UCP2 (skeletal muscle, brown adipose tissue, heart) they may act in concert in the overall regulation of lipid oxidation, concomitant to the prevention of lipid-induced oxidative damage.

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Trapani, Laura, and Valentina Pallottini. "Hypercholesterolemia and 3-Hydroxy 3-Methylglutaryl Coenzyme A Reductase Regulation during Ageing." Scientific World JOURNAL 9 (2009): 564–74. http://dx.doi.org/10.1100/tsw.2009.81.

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We present here a brief description of the path that cholesterol covers from its intestinal absorption to its effect exerted on some enzyme regulation. Some mechanisms underlying hypercholesterolemia onset and, in particular, the role and the regulation of 3-hydroxy 3-methylglutaryl Coenzyme A reductase (HMGR) during adult life and during aging, have been described. In addition some pharmacological interventions to control proper HMGR regulation and, in turn, cholesterol homeostasis maintenance will be introduced.

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Smith, Courtney, Alice Li, Nithya Krishnamurthy, and Mark Lemmon. "210 Regulation of TIM-3 by phosphatidylserine." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (November 2020): A229. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0210.

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BackgroundImmune checkpoint blockade has proven effective in targeting exhausted T-cells to reactivate the immune system against cancer. However, the majority of patients fail to respond to currently available therapies, which primarily target PD-1. Thus, a key challenge for checkpoint blockade therapy is to identify and understand new therapeutic targets. Another immune checkpoint receptor is TIM-3, which – like PD-1 – is expressed on exhausted T-cells in the tumor microenvironment.1, 2 TIM-3 belongs to a family of phosphatidylserine (PS) receptors, including TIM-1 and TIM-4, which have well-documented roles in the engulfment of apoptotic cells by phagocytes.3 However, the role of PS in regulating TIM-3 function is less clear. We therefore investigated how TIM-3 modulates T-cell signaling and how PS influences TIM-3 activity, with the ultimate goal of improving the translation of candidate TIM-3 therapies to the clinic.MethodsSurface plasmon resonance (SPR) was used to quantify the interaction between human TIM-3 and PS. A Jurkat T-cell model was used to investigate the role of TIM-3 in T-cell receptor (TCR) signaling and to determine the role of PS in regulating TIM-3 function.ResultsTIM-3 bound PS-containing membranes with low micromolar affinity in vitro. In the Jurkat cell model system, high – but not low – surface levels of TIM-3 promoted T-cell signaling, suggesting a threshold of receptor expression needed to modulate T-cell signaling, similar to what has recently been reported for PD-1.4 However, chimeric receptors that maintained the TIM-3 cytoplasmic tail but were unable to bind PS failed to enhance T-cell signaling like the full-length TIM-3 receptor. Cells expressing mutant TIM-3, which displayed reduced PS binding as quantified by SPR, also displayed reduced T-cell signaling compared to cells expressing wild-type TIM-3. Importantly, treatment of TIM-3-expressing cells with a functional TIM-3 antibody that blocks PS binding also reduced T-cell signaling compared with untreated TIM-3-expressing cells.ConclusionsOur results support a role for PS as a ligand capable of modulating TIM-3 activity. Using chimeric receptors, TIM-3 mutants, changes in receptor expression, and a functional TIM-3 antibody, we show that preventing the interaction between TIM-3 and PS blocks TIM-3 activity. These data suggest that blocking the PS-TIM-3 interaction is a key mechanism for functional antibodies targeting TIM-3. Ultimately, this work supports the development and use of clinical antibodies that block the interaction of TIM-3 with PS and provides new mechanistic insight into how TIM-3 modulates TCR signaling.AcknowledgementsThis work was supported by the PhRMA Foundation Pre-Doctoral Fellowship in Pharmacology/Toxicology.ReferencesFourcade J, Sun Z, Benallaoua M, et al. Upregulation of Tim-3 and PD-1 expression is associated with tumor antigen-specific CD8+ T cell dysfunction in melanoma patients. J Exp Med. 2010;207(10):2175–2186.Zhou Q, Munger ME, Veenstra RG, et al. Coexpression of Tim-3 and PD-1 identifies a CD8+ T-cell exhaustion phenotype in mice with disseminated acute myelogenous leukemia. Blood. 2011;117(17):4501–4510.Kobayashi N, Karisola P, Peña-Cruz V, et al. TIM-1 and TIM-4 glycoproteins bind phosphatidylserine and mediate uptake of apoptotic cells. Immunity. 2007;27(6):927–940.Hui E, Cheung J, Zhu J, et al. T cell costimulatory receptor CD28 is a primary target for PD-1-mediated inhibition. Science. 2017;355(6332):1428–1433.

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Fitchen, Jonathan. "Choice of Law in International Claims Based on Restrictions of Competition: Article 6(3) of the Rome II Regulation." Journal of Private International Law 5, no. 2 (August 2009): 337–70. http://dx.doi.org/10.1080/17536235.2009.11424362.

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BRUCKMANN, Astrid, H. Yde STEENSMA, M. Joost TEIXEIRA de MATTOS, and G. Paul H. van HEUSDEN. "Regulation of transcription by Saccharomyces cerevisiae 14-3-3 proteins." Biochemical Journal 382, no. 3 (September 7, 2004): 867–75. http://dx.doi.org/10.1042/bj20031885.

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14-3-3 proteins form a family of highly conserved eukaryotic proteins involved in a wide variety of cellular processes, including signalling, apoptosis, cell-cycle control and transcriptional regulation. More than 150 binding partners have been found for these proteins. The yeast Saccharomyces cerevisiae has two genes encoding 14-3-3 proteins, BMH1 and BMH2. A bmh1 bmh2 double mutant is unviable in most laboratory strains. Previously, we constructed a temperature-sensitive bmh2 mutant and showed that mutations in RTG3 and SIN4, both encoding transcriptional regulators, can suppress the temperature-sensitive phenotype of this mutant, suggesting an inhibitory role of the 14-3-3 proteins in Rtg3-dependent transcription [van Heusden and Steensma (2001) Yeast 18, 1479–1491]. In the present paper, we report a genome-wide transcription analysis of a temperature-sensitive bmh2 mutant. Steady-state mRNA levels of 60 open reading frames were increased more than 2.0-fold in the bmh2 mutant, whereas those of 78 open reading frames were decreased more than 2.0-fold. In agreement with our genetic experiments, six genes known to be regulated by Rtg3 showed elevated mRNA levels in the mutant. In addition, several genes with other cellular functions, including those involved in gluconeogenesis, ergosterol biosynthesis and stress response, had altered mRNA levels in the mutant. Our data show that the yeast 14-3-3 proteins negatively regulate Rtg3-dependent transcription, stimulate the transcription of genes involved in ergosterol metabolism and in stress response and are involved in transcription regulation of multiple other genes.

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Wei, Yu, Juan Du, and Zhangwu Zhao. "Integrative Role of 14-3-3ε in Sleep Regulation." International Journal of Molecular Sciences 22, no. 18 (September 9, 2021): 9748. http://dx.doi.org/10.3390/ijms22189748.

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Sleep is a crucial factor for health and survival in all animals. In this study, we found by proteomic analysis that some cancer related proteins were impacted by the circadian clock. The 14-3-3ε protein, expression of which is activated by the circadian transcription factor Clock, regulates adult sleep of Drosophila independent of circadian rhythm. Detailed analysis of the sleep regulatory mechanism shows that 14-3-3ε directly targets the Ultrabithorax (Ubx) gene to activate transcription of the pigment dispersing factor (PDF). The dopamine receptor (Dop1R1) and the octopamine receptor (Oamb), are also involved in the 14-3-3ε pathway, which in 14-3-3ε mutant flies causes increases in the dopR1 and OAMB, while downregulation of the DopR1 and Oamb can restore the sleep phenotype caused by the 14-3-3ε mutation. In conclusion, 14-3-3ε is necessary for sleep regulation in Drosophila.

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de Boer, A. H. "Plant 14-3-3 proteins assist ion channels and pumps." Biochemical Society Transactions 30, no. 4 (August 1, 2002): 416–21. http://dx.doi.org/10.1042/bst0300416.

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Turgor pressure is a cellular parameter, important for a range of physiological processes in plants, like cell elongation, gas exchange and gravitropic/phototropic bending. Regulation of turgor pressure involves ion and water transport at the expense of metabolic energy (ATP). The primary pump in the plasma membrane (the H+-ATPase) is a key player in turgor regulation since it provides the driving force for ion uptake, followed by water influx through osmosis. Using the phytotoxin fusicoccin (a well-known activator of the ATPase) as a tool, 14-3-3 proteins were identified as regulators of the H+-ATPase. Since fusicoccin has a dramatic effect on K+ accumulation and cellular respiration as well, we studied whether 14-3-3 proteins play a role in the regulation of the mitochondrial F0F1-ATP synthase and ion channels in the vacuolar and plasma membranes. Besides the plasma membrane H+-ATPase, we have identified thus far at least four other transport proteins that are regulated by 14-3-3 proteins. The mechanism of regulation will be described and the possibility that 14-3-3 proteins act as coordinators of ion transporters with varied but interdependent functions will be discussed.

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Makarieva, A. M., A. V. Nefiodov, V. E. Morozov, A. A. Aleynikov, and R. G. Vasilov. "SCIENCE IN THE VANGUARD OF RETHINKING THE ROLE OF FORESTS IN THE THIRD MILLENNIUM: COMMENTS ON THE DRAFT CONCEPT OF THE FEDERAL LAW “FOREST CODE OF THE RUSSIAN FEDERATION." FOREST SCIENCE ISSUES 3, no. 3 (December 2, 2020): 1–25. http://dx.doi.org/10.31509/2658-607x-2020-3-3-1-25.

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In this work, in the light of the latest scientific data, multiple aspects of the regulatory influence of forest ecosystems on climate are considered from the standpoint of the concept of biotic regulation of the environment: carbon absorption in the biomass of trees and soil, regulation of local temperature regime through the transpiration and reflectivity of forest cover, regulation of continental transport of atmospheric moisture and cloudiness. It is shown that under conditions of increasing climatic destabilization, the value of the climate-regulating function of forests and, in particular, its aspects associated with the water cycle, rapidly increases in comparison with the traditional economic functions of the forest. The Forest Code, as the main document regulating the impact of Russian citizens on the forest, should take into account the dynamically developing situation and assign a special role to climate-regulating forests. Considering that natural forest ecosystems have finite stability and climate-regulating potential, which commercially-scaled timber harvesting and other methods of exploitation can completely destroy, it is proposed to achieve a balance between the economic and climate-regulating functions of forests through their spatial delineation. Economic activity must be carried out intensively in previously developed territories where forests have been perturbed beyond their self-recovery threshold. Intact forests, performing a climate-regulating function, are proposed to be separated into a distinct legal category, subject only to protection and intensive study. It is shown that the advancement of the category of climate-regulating forests in the international climate agenda is vital for the protection of the national interests of Russia.

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Kageyama, Kazunori, Komaki Hanada, Yasumasa Iwasaki, and Toshihiro Suda. "Regulation and role of suppressor of cytokine signaling-3 in hypothalamic 4B cells." Journal of Endocrinology 201, no. 3 (March 16, 2009): 369–76. http://dx.doi.org/10.1677/joe-08-0506.

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Corticotropin-releasing factor (CRF) plays a central role in regulating stress responses. In the hypothalamic paraventricular nucleus (PVN), CRF, produced in response to stress, stimulates the release of ACTH from the anterior pituitary. ACTH then stimulates the release of glucocorticoids from the adrenal glands; circulating glucocorticoids are critical for recovery from stress conditions. Cytokines are also implicated in the regulation of CRF expression. Among them, interleukin (IL)-6 plays a role in the regulation of CRF. Factors other than glucocorticoids are likely to be involved in limiting the stimulation of CRF during stress. Suppressor of cytokine signaling (SOCS)-3 acts as a potent negative regulator of cytokine signaling. Little is known about the ability of the inhibitory signaling pathways to limit activation of the CRF gene in parvocellular PVN neurons. Hypothalamic 4B cells are useful for exploring the mechanisms, because these cells show characteristics of the parvocellular neurons of the PVN. In the present study, we examined whether SOCS-3 is regulated by IL-6 and cAMP in hypothalamic 4B cells. We also explored the involvement of SOCS-3 in the regulation of CRF gene expression. SOCS-3 was found to be regulated by IL-6 and via the cAMP/protein kinase A pathway in the hypothalamic cells. SOCS-3 knockdown increased IL-6- or forskolin-induced CRF gene transcription and mRNA levels. Therefore, SOCS-3, induced by a cAMP stimulant and IL-6, would be involved in the negative regulation of CRF gene expression in hypothalamic cells.

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Moreno-Aliaga, María J., Silvia Lorente-Cebrián, and J. Alfredo Martínez. "Regulation of adipokine secretion byn-3 fatty acids." Proceedings of the Nutrition Society 69, no. 3 (June 14, 2010): 324–32. http://dx.doi.org/10.1017/s0029665110001801.

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Obesity leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome. White adipose tissue (WAT) metabolism and WAT-derived factors (fatty acids and adipokines) play an important role in the development of these metabolic disturbances. In fact, dysregulated adipokine secretion from the expanded WAT of obese individuals contributes to the development of systemic low-grade inflammation, insulin resistance and metabolic syndrome. Then-3 PUFA EPA and DHA have been widely reported to have protective effects in a range of chronic inflammatory conditions including obesity. In fact,n-3 PUFA have been shown to ameliorate low-grade inflammation in adipose tissue associated with obesity and up-regulate mitochondrial biogenesis and induce beta-oxidation in WAT in mice. Moreover, the ability ofn-3 PUFA to regulate adipokine gene expression and secretion has been observed bothin vitroandin vivoin rodents and human subjects. The present article reviews: (1) the physiological role of adiponectin, leptin and pre-B cell colony-enhancer factor/visfatin, three adipokines with immune-modulatory properties involved in the regulation of metabolism and insulin sensitivity and (2) the actions ofn-3 PUFA on these adipokines focusing on the underlying mechanisms and the potential relationship with the beneficial effects of these fatty acids on obesity-associated metabolic disorders. It can be concluded that the ability ofn-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of WAT metabolism and the secretion of bioactive adipokines including leptin, adiponectin and visfatin.

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Suchyna, Thomas M., and HaiXia Huang. "Role of Muscle Specific Caveolin-3 in Mechanosensitive Channel Regulation." Biophysical Journal 100, no. 3 (February 2011): 281a. http://dx.doi.org/10.1016/j.bpj.2010.12.1743.

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MONTALVETTI, Andrea, Javier PE±A-DÍAZ, Ramón HURTADO, Luis Miguel RUIZ-PÉREZ, and Dolores GONZÁLEZ-PACANOWSKA. "Characterization and regulation of Leishmania major 3-hydroxy-3-methylglutaryl-CoA reductase." Biochemical Journal 349, no. 1 (June 26, 2000): 27–34. http://dx.doi.org/10.1042/bj3490027.

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In eukaryotes the enzyme 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase catalyses the synthesis of mevalonic acid, a common precursor to all isoprenoid compounds. Here we report the isolation and overexpression of the gene coding for HMG-CoA reductase from Leishmania major. The protein from Leishmania lacks the membrane domain characteristic of eukaryotic cells but exhibits sequence similarity with eukaryotic reductases. Highly purified protein was achieved by ammonium sulphate precipitation followed by chromatography on hydroxyapatite. Kinetic parameters were determined for the protozoan reductase, obtaining Km values for the overall reaction of 40.3±5.8 μM for (R,S)-HMG-CoA and 81.4±5.3 μM for NADPH; Vmax was 33.55±1.8 units·mg-1. Gel-filtration experiments suggested an apparent molecular mass of 184 kDa with subunits of 46 kDa. Finally, in order to achieve a better understanding of the role of this enzyme in trypanosomatids, the effect of possible regulators of isoprenoid biosynthesis in cultured promastigote cells was studied. Neither mevalonic acid nor serum sterols appear to modulate enzyme activity whereas incubation with lovastatin results in significant increases in the amount of reductase protein. Western- and Northern-blot analyses indicate that this activation is apparently performed via post-transcriptional control.

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Chakraborty, Ashmita, and Indraneel Saha. "Regulatory effects of prolactin on breeding and migratory behaviours in birds." South Asian Journal of Experimental Biology 11, no. 3 (May 24, 2021): 337–44. http://dx.doi.org/10.38150/sajeb.11(3).p337-344.

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Prolactin is an adenohypophyseal hormone of vertebrates produced by the neuroendocrine signaling of the hypothalamus. It plays important role in different vertebrate species and referred to as “The Parental Hormone” or “The Hormone of Maternity”. In birds the role of Prolactin is limited as the parental hormone but the behavioral functions like the regulation of season-al reproduction, combating stress of predators, nest building abilities and regulations of migratory cycle are diversified. The classical role of Prolactin in different birds’ species like pigeons and doves is secretion of crop sac “milk” after hatching of eggs and regulation of migration in different type of mi-grants. Reports have suggested that acute and chronic stressors and ener-getic constraints depress prolactin levels disrupting the parental effort in nest building, mate selection, incubation and crop milk production. Although prolactin is diverse in its function but acts through the same receptors throughout the vertebrate series. However, this review establishes that pro-lactin plays an intense role in regulating breeding behaviours and migration in birds along with the interactions of other hormones. Prolactin helps the birds to carry out wide range of behaviour and become evolutionarily suc-cessful.

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Casals, N., N. Roca, M. Guerrero, G. Gil-Gómez, J. Ayté, C. J. Ciudad, and F. G. Hegardt. "Regulation of the expression of the mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase gene. Its role in the control of ketogenesis." Biochemical Journal 283, no. 1 (April 1, 1992): 261–64. http://dx.doi.org/10.1042/bj2830261.

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We have explored the role of mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase in regulating ketogenesis. We had previously cloned the cDNA for mitochondrial HMG-CoA synthase and have now studied the regulation in vivo of the expression of this gene in rat liver. The amount of processed mitochondrial HMG-CoA synthase mRNA is rapidly changed in response to cyclic AMP, insulin, dexamethasone and refeeding, and is greatly increased by starvation, fat feeding and diabetes. We conclude that one point of ketogenic control is exercised at the level of genetic expression of mitochondrial HMG-CoA synthase.

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Lindemans, C. A., and P. J. Coffer. "Regulation of granulocyte apoptosis by phosphatidylinositol 3-kinase." Biochemical Society Transactions 32, no. 3 (June 1, 2004): 480–84. http://dx.doi.org/10.1042/bst0320480.

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Granulocytes are critical components of the innate immune system whose lifespan is limited by an intrinsic, constitutive, apoptotic pathway. However, the lifespan of these cells can be extended at an inflammatory locus through interaction with survival factors. Although a wide variety of factors can modulate granulocyte survival, they often utilize a common subset of intracellular signal transduction pathways. Over the last decade, evidence has accumulated that the PI3K (phosphatidylinositol 3-kinase) family of lipid kinases may be critical in regulating the ability of granulocytes to survive at inflammatory loci. Studies utilizing both pharmacological inhibitors of PI3K and isoform-specific knockout mice have demonstrated that this enzyme is needed for the anti-apoptotic effects of granulocyte survival factors. More recently, a serine/threonine protein kinase, termed protein kinase B (also known as c-akt), has been demonstrated to be important in modulating the prosurvival effects of PI3K activation. This can occur through modulation of the expression or phosphorylation of members of the Bcl-2 (B-cell lymphocytic-leukaemia proto-oncogene 2) family of apoptosis regulators. This review summarizes recent results that have implicated a role for PI3K in regulating granulocyte survival.

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Undi, Ram Babu, Usha Gutti, Itishri Sahu, Shilpa Sarvothaman, Satya Ratan Pasupuleti, Ravinder Kandi, and Ravi Kumar Gutti. "Wnt Signaling: Role in Regulation of Haematopoiesis." Indian Journal of Hematology and Blood Transfusion 32, no. 2 (August 28, 2015): 123–34. http://dx.doi.org/10.1007/s12288-015-0585-3.

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Pehmøller, Christian, Jonas T. Treebak, Jesper B. Birk, Shuai Chen, Carol MacKintosh, D. Grahame Hardie, Erik A. Richter, and Jørgen F. P. Wojtaszewski. "Genetic disruption of AMPK signaling abolishes both contraction- and insulin-stimulated TBC1D1 phosphorylation and 14-3-3 binding in mouse skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 297, no. 3 (September 2009): E665—E675. http://dx.doi.org/10.1152/ajpendo.00115.2009.

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TBC1D1 is a Rab-GTPase-activating protein (GAP) known to be phosphorylated in response to insulin, growth factors, pharmacological agonists that activate 5′-AMP-activated protein kinase (AMPK), and muscle contraction. Silencing TBC1D1 in L6 muscle cells by siRNA increases insulin-stimulated GLUT4 translocation, and overexpression of TBC1D1 in 3T3-L1 adipocytes with low endogenous TBC1D1 expression inhibits insulin-stimulated GLUT4 translocation, suggesting a role of TBC1D1 in regulating GLUT4 translocation. Aiming to unravel the regulation of TBC1D1 during contraction and the potential role of AMPK in intact skeletal muscle, we used EDL muscles from wild-type (WT) and AMPK kinase dead (KD) mice. We explored the site-specific phosphorylation of TBC1D1 Ser237 and Thr596 and their relation to 14-3-3 binding, a proposed mechanism for regulation of GAP function of TBC1D1. We show that muscle contraction increases 14-3-3 binding to TBC1D1 as well as phosphorylation of Ser237 and Thr596 in an AMPK-dependent manner. AMPK activation by AICAR induced similar Ser237 and Thr596 phosphorylation of, and 14-3-3 binding to, TBC1D1 as muscle contraction. Insulin did not increase Ser237 phosphorylation or 14-3-3 binding to TBC1D1. However, insulin increased Thr596 phosphorylation, and intriguingly this response was fully abolished in the AMPK KD mice. Thus, TBC1D1 is differentially regulated in response to insulin and contraction. This study provides genetic evidence to support an important role for AMPK in regulating TBC1D1 in response to both of these physiological stimuli.

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Welham, M. J., M. P. Storm, E. Kingham, and H. K. Bone. "Phosphoinositide 3-kinases and regulation of embryonic stem cell fate." Biochemical Society Transactions 35, no. 2 (March 20, 2007): 225–28. http://dx.doi.org/10.1042/bst0350225.

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ES (embryonic stem) cell lines are derived from the epiblast of pre-implantation embryos and like the inner cell mass cells from which they are derived exhibit the remarkable property of pluripotency, namely the ability to differentiate into all cell lineages comprising the adult organism. ES cells and their differentiated progeny offer tremendous potential to regenerative medicine, particularly as cellular therapies for the treatment of a wide variety of chronic disorders, such as Type 1 diabetes, Parkinson's disease and retinal degeneration. In order for this potential to be realized, a detailed understanding of the molecular mechanisms regulating the fundamental properties of ES cells, i.e. pluripotency, proliferation and differentiation, is required. In the present paper, we review the evidence that PI3K (phosphoinositide 3-kinase)-dependent signalling plays a role in regulation of both ES cell pluripotency and proliferation.

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Marth, Thomas, and Brian L. Kelsall. "Regulation of Interleukin-12 by Complement Receptor 3 Signaling." Journal of Experimental Medicine 185, no. 11 (June 2, 1997): 1987–95. http://dx.doi.org/10.1084/jem.185.11.1987.

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Complement receptor type 3 (CR3, CD11b/CD18) serves as a receptor for a number of endogenous ligands and infectious organisms, and is involved in adhesion and host defense functions. Here, we report that signaling via CR3 plays an important role in regulating production of interleukin-12 (IL-12), a key mediator of cell-mediated immunity (CMI). We demonstrate with a variety of stimuli a dose-dependent, specific downregulation of IL-12 secretion by human monocytes in vitro after exposure to antibodies to CR3 (anti-CD11b and anti-CD18), as well as to the natural CR3 ligands, iC3b, and Histoplasma capsulatum. CR3 antibodies also suppressed interferon-γ (IFN-γ) production in cultures of human peripheral blood mononuclear cells (PBMC). We determined that one mechanism by which CR3 antibodies may suppress IL-12 production is by the inhibition of IFN-γ–induced tyrosine phosphorylation. Finally, in a murine model of IL-12–dependent septic shock, we provide evidence that administration of CR3 antibodies leads to suppression of IL-12 and IFN-γ in vivo. Our studies thus define a novel role for CR3 in regulating CMI functions via IL-12.

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Vareilles-Sommières, Pascal de. "Rationale of the Exclusion of Choice of Law by the Parties in Articles 6(4) and 8(3) of Rome II Regulation." Oslo Law Review 6, no. 01 (May 14, 2019): 62–66. http://dx.doi.org/10.18261/issn.2387-3299-2019-01-08.

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Van Haastert, P. J. M. "Intracellular adenosine 3′,5′-phosphate formation is essential for down-regulation of surface adenosine 3′,5′-phosphate receptors in Dictyostelium." Biochemical Journal 303, no. 2 (October 15, 1994): 539–45. http://dx.doi.org/10.1042/bj3030539.

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Dictyostelium discoideum cells contain cell surface cyclic AMP (cAMP) receptors that bind cAMP as a first messenger and intracellular cAMP receptors that bind cAMP as a second messenger. Prolonged incubation of Dictyostelium cells with cAMP induces a sequential process of phosphorylation, sequestration and down-regulation of the surface receptors. The role of intracellular cAMP in down-regulation of surface receptors was investigated. Down-regulation of receptors does not occur under conditions that specifically inhibit the formation of intracellular cAMP (the drug caffeine or mutant cells lacking adenylate cyclase) or conditions that inhibit the function of intracellular cAMP (mutants lacking protein kinase A activity). Cell-permeable non-hydrolysable cAMP derivatives were used to investigate further the requirement of intracellular cAMP for down-regulation. The Sp isomer of 6-thioethylpurineriboside 3′,5′-phosphorothioate (6SEth-cPuMPS) does not bind to the surface receptor, enters the cell and has relative high affinity for protein kinase A. 6SEth-cPuMPS alone has no effect on down-regulation. However, together with an agonist of the surface receptor, the analogue induces down-regulation in caffeine-treated wild-type cells and in mutant cells lacking adenylate cyclase, but not in mutant cells lacking protein kinase A. These results indicate that intracellular cAMP formation and activation of protein kinase A are essential for down-regulation of the surface cAMP receptor.

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Sayas, C. "Regulation of neuronal cytoskeleton by lysophosphatidic acid: role of GSK-3." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1582, no. 1-3 (May 23, 2002): 144–53. http://dx.doi.org/10.1016/s1388-1981(02)00149-x.

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Raabe, Karel, David Honys, and Christos Michailidis. "The role of eukaryotic initiation factor 3 in plant translation regulation." Plant Physiology and Biochemistry 145 (December 2019): 75–83. http://dx.doi.org/10.1016/j.plaphy.2019.10.015.

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Dontenwill, M., E. Tibiriça, H. Greney, F. Bennaï, J. Feldman, J. Stutzmann, G. Bricca, A. Belcourt, and P. Bousquet. "Role of imidazoline receptors in cardiovascular regulation." American Journal of Cardiology 74, no. 13 (December 1994): A3—A6. http://dx.doi.org/10.1016/0002-9149(94)90035-3.

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A. Griffith, Jennifer, Shane Connelly, and Chase E. Thiel. "Emotion regulation and intragroup conflict: when more distracted minds prevail." International Journal of Conflict Management 25, no. 2 (April 8, 2014): 148–70. http://dx.doi.org/10.1108/ijcma-04-2012-0036.

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Purpose – In order to shed light on whether and how leaders should help manage group members' emotions related to intragroup conflict, the aim of this paper was to investigate the effects of several outcomes associated with two cognitive emotion regulation strategies, cognitive reappraisal and distraction, in the presence of two distinct types of conflict, relationship or task-oriented. Design/methodology/approach – A 2×3 between subjects' experimental design was employed to investigate the influence of intragroup conflict and emotion regulations strategies on individual-level discrete emotions and group processes and outcomes. Findings – Results suggest that emotion regulation plays an important role in moderating the negative consequences associated with relationships conflict. Specifically, distraction served a critical function to those in the relationship conflict conditions such that both cohesion levels and task performance levels were elevated when group members used distraction as a means of regulating emotions. Research limitations/implications – This study extends research in the area of emotion regulation into a group context and extends other research that suggests distraction may have potential as a means of regulating emotion. Long-term groups with experience in problem solving may have behaved in different ways than participants in this study. Originality/value – Emotion regulation strategies have been studied only in an individual context. This study is particularly valuable in understanding how emotion regulation strategies work differentially when applied to multiple individuals in a shared setting. Additionally, it incorporates the use of distraction as a viable regulation strategy.

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McGowan, B. M., S. A. Stanley, J. Donovan, E. L. Thompson, M. Patterson, N. M. Semjonous, J. V. Gardiner, K. G. Murphy, M. A. Ghatei, and S. R. Bloom. "Relaxin-3 stimulates the hypothalamic-pituitary-gonadal axis." American Journal of Physiology-Endocrinology and Metabolism 295, no. 2 (August 2008): E278—E286. http://dx.doi.org/10.1152/ajpendo.00028.2008.

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The hypothalamus plays a key role in the regulation of both energy homeostasis and reproduction. Evidence suggests that relaxin-3, a recently discovered member of the insulin superfamily, is an orexigenic hypothalamic neuropeptide. Relaxin-3 is thought to act in the brain via the RXFP3 receptor, although the RXFP1 receptor may also play a role. Relaxin-3, RXFP3, and RXFP1 are present in the hypothalamic paraventricular nucleus, an area with a well-characterized role in the regulation of energy balance that also modulates reproductive function by providing inputs to hypothalamic gonadotropin-releasing hormone (GnRH) neurons. Other members of the relaxin family are known to play a role in the regulation of reproduction. However, the effects of relaxin-3 on reproductive function are unknown. We studied the role of relaxin-3 in the regulation of the hypothalamo-pituitary-gonadal (HPG) axis. Intracerebroventricular (5 nmol) and intraparaventricular (540–1,620 pmol) administration of human relaxin-3 (H3) in adult male Wistar rats significantly increased plasma luteinizing hormone (LH) 30 min postinjection. This effect was blocked by pretreatment with a peripheral GnRH antagonist. Central administration of human relaxin-2 showed no significant effect on plasma LH. H3 dose-dependently stimulated the release of GnRH from hypothalamic explants and GT1-7 cells, which express RXFP1 and RXFP3, but did not influence LH or follicle-stimulating hormone release from pituitary fragments in vitro. We have demonstrated a novel role for relaxin-3 in the stimulation of the HPG axis, putatively via hypothalamic GnRH neurons. Relaxin-3 may act as a central signal linking nutritional status and reproductive function.

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Chen, Yunfeng, Zaverio M. Ruggeri, and Xiaoping Du. "14-3-3 proteins in platelet biology and glycoprotein Ib-IX signaling." Blood 131, no. 22 (May 31, 2018): 2436–48. http://dx.doi.org/10.1182/blood-2017-09-742650.

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Abstract Members of the 14-3-3 family of proteins function as adapters/modulators that recognize phosphoserine/phosphothreonine-based binding motifs in many intracellular proteins and play fundamental roles in signal transduction pathways of eukaryotic cells. In platelets, 14-3-3 plays a wide range of regulatory roles in phosphorylation-dependent signaling pathways, including G-protein signaling, cAMP signaling, agonist-induced phosphatidylserine exposure, and regulation of mitochondrial function. In particular, 14-3-3 interacts with several phosphoserine-dependent binding sites in the major platelet adhesion receptor, the glycoprotein Ib-IX complex (GPIb-IX), regulating its interaction with von Willebrand factor (VWF) and mediating VWF/GPIb-IX–dependent mechanosignal transduction, leading to platelet activation. The interaction of 14-3-3 with GPIb-IX also plays a critical role in enabling the platelet response to low concentrations of thrombin through cooperative signaling mediated by protease-activated receptors and GPIb-IX. The various functions of 14-3-3 in platelets suggest that it is a possible target for the treatment of thrombosis and inflammation.

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Schrauwen, Patrick, and Matthijs Hesselink. "Uncoupling protein 3 and physical activity: the role of uncoupling protein 3 in energy metabolism revisited." Proceedings of the Nutrition Society 62, no. 3 (August 2003): 635–43. http://dx.doi.org/10.1079/pns2003277.

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Physical activity influences energy metabolism in human subjects by increasing activity-induced energy expenditure and resting metabolic rate for several hours after exercise. On the other hand, physical activity increases mechanical energy efficiency, suggesting that trained subjects would need less energy for daily activities. The underlying mechanism by which physical activity influences energy metabolism is largely unknown. The skeletal muscle-specific homologue of uncoupling protein (UCP) 1, UCP3, could possibly play a major role in energy expenditure. UCP3 is, like UCP1, able to uncouple respiration from ATP production. A strong link or association between the UCP3 gene and energy metabolism was found. Furthermore, UCP3 mRNA expression is related to sleeping metabolic rate, and thyroid hormone, a powerful stimulator of energy expenditure, up regulates UCP3. Finally, mice overexpressing UCP3 are hyperphagic but lean. These findings indicated that UCP3 is related to energy metabolism and that UCP3 could have a role in the effect of physical activity on energy expenditure. Thus, acute exercise up regulates UCP3, whereas endurance training results in the down-regulation of UCP3 protein content. Only a minimal amount of physical activity is needed for down-regulation of UCP3. Moreover, there is very strong evidence that UCP3 is negatively related to mechanical energy efficiency, suggesting that the down-regulation of UCP3 with training increases mechanical energy efficiency. Taken together, although the exact function of UCP3 is still unknown, exercise and training studies clearly show that under certain circumstances UCP3 is strongly related to human energy metabolism, possibly as a secondary effect of its (yet) unknown primary function.

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YIP-SCHNEIDER, Michele T., Wenyan MIAO, Amy LIN, Darlene S. BARNARD, Guri TZIVION, and Mark S. MARSHALL. "Regulation of the Raf-1 kinase domain by phosphorylation and 14-3-3 association." Biochemical Journal 351, no. 1 (September 26, 2000): 151–59. http://dx.doi.org/10.1042/bj3510151.

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The Raf-1 kinase domain is kept in an inactive state by the N-terminal regulatory domain. Activation of the kinase domain occurs following release from the N-terminal repression and possible catalytic upregulation. To distinguish the regulatory mechanisms that directly influence the catalytic activity of the enzyme from those which act through the inhibitory domain, the catalytic domain of Raf-1 (CR3) was expressed in COS-7 cells. The role of phosphorylation in the direct regulation of this domain was determined by substituting non-phosphorylatable amino acids for known serine and tyrosine phosphorylation sites. The intrinsic activity of each mutant protein was determined as well as stimulation by v-Src and phorbol esters. Both v-Src and phorbol esters were potent activators of CR3, requiring the serine 338/339 (p21-activated protein kinase, Pak) and tyrosine 340/341 (Src) phosphorylation sites for full stimulation of CR3. In contrast, loss of the serine 497/499 protein kinase C phosphorylation sites had little effect on CR3 activation by either v-Src or phorbol esters. Loss of serine 621, a 14-3-3 adaptor-protein-binding site, prevented activation of CR3 by v-Src or phorbol esters and partially decreased the high basal activity of the kinase fragment. When co-expressed in COS-7 cells, 14-3-3 associated strongly with full-length Raf-1, weakly with wild-type CR3 and not at all with the A621 and D621 CR3 mutants. The role of 14-3-3 in maintaining the activity of the catalytic domain of Raf-1 was investigated further by performing peptide-competition studies with wild-type CR3, wild-type CR3 and v-Src or constitutively active CR3 (CR3[YY340/341DD]). In each case, incubation of the proteins with a phosphoserine-621 Raf-1 peptide, which we show displaced Raf-1 and CR3[YY340/341DD] from 14-3-3, was found to substantially reduce catalytic activity. Taken together, our results support a model of Raf regulation in which the activity of the Raf-1 catalytic domain is directly upregulated by phosphorylation, following relief of inhibition by the N-terminal regulatory domain upon Ras-GTP binding. Moreover, the presence of serine 621 in the free catalytic fragment is required for full CR3 activation by stimulatory factors, and the continuous presence of 14-3-3 at this site is necessary for retaining activity once the kinase is activated.

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Bostick, John W., Yetao Wang, Zeli Shen, Yong Ge, Jeffrey Brown, Zong-ming E. Chen, Mansour Mohamadzadeh, James G. Fox, and Liang Zhou. "Dichotomous regulation of group 3 innate lymphoid cells by nongastric Helicobacter species." Proceedings of the National Academy of Sciences 116, no. 49 (November 18, 2019): 24760–69. http://dx.doi.org/10.1073/pnas.1908128116.

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Intestinal innate lymphoid cells (ILCs) contribute to the protective immunity and homeostasis of the gut, and the microbiota are critically involved in shaping ILC function. However, the role of the gut microbiota in regulating ILC development and maintenance still remains elusive. Here, we identified opposing effects on ILCs by two Helicobacter species, Helicobacter apodemus and Helicobacter typhlonius, isolated from immunocompromised mice. We demonstrated that the introduction of both Helicobacter species activated ILCs and induced gut inflammation; however, these Helicobacter species negatively regulated RORγt+ group 3 ILCs (ILC3s), especially T-bet+ ILC3s, and diminished their proliferative capacity. Thus, these findings underscore a previously unknown dichotomous regulation of ILC3s by Helicobacter species, and may serve as a model for further investigations to elucidate the host–microbe interactions that critically sustain the maintenance of intestinal ILC3s.

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Huber, Steven C., Markus Bachmann, and Joan L. Huber. "Post-translational regulation of nitrate reductase activity: a role for Ca2+ and 14-3-3 proteins." Trends in Plant Science 1, no. 12 (December 1996): 432–38. http://dx.doi.org/10.1016/s1360-1385(96)10046-7.

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Panni, Simona, Christiane Landgraf, Rudolf Volkmer-Engert, Gianni Cesareni, and Luisa Castagnoli. "Role of 14-3-3 proteins in the regulation of neutral trehalase in the yeastSaccharomyces cerevisiae." FEMS Yeast Research 8, no. 1 (February 2008): 53–63. http://dx.doi.org/10.1111/j.1567-1364.2007.00312.x.

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Yamazaki, Osamu, Daigoro Hirohama, Kenichi Ishizawa, and Shigeru Shibata. "Role of the Ubiquitin Proteasome System in the Regulation of Blood Pressure: A Review." International Journal of Molecular Sciences 21, no. 15 (July 28, 2020): 5358. http://dx.doi.org/10.3390/ijms21155358.

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The kidney and the vasculature play crucial roles in regulating blood pressure. The ubiquitin proteasome system (UPS), a multienzyme process mediating covalent conjugation of the 76-amino acid polypeptide ubiquitin to a substrate protein followed by proteasomal degradation, is involved in multiple cellular processes by regulating protein turnover in various tissues. Increasing evidence demonstrates the roles of UPS in blood pressure regulation. In the kidney, filtered sodium is reabsorbed through diverse sodium transporters and channels along renal tubules, and studies conducted till date have provided insights into the complex molecular network through which ubiquitin ligases modulate sodium transport in different segments. Components of these pathways include ubiquitin ligase neuronal precursor cell-expressed developmentally downregulated 4-2, Cullin-3, and Kelch-like 3. Moreover, accumulating data indicate the roles of UPS in blood vessels, where it modulates nitric oxide bioavailability and vasoconstriction. Cullin-3 not only regulates renal salt reabsorption but also controls vascular tone using different adaptor proteins that target distinct substrates in vascular smooth muscle cells. In endothelial cells, UPS can also contribute to blood pressure regulation by modulating endothelial nitric oxide synthase. In this review, we summarize current knowledge regarding the role of UPS in blood pressure regulation, focusing on renal sodium reabsorption and vascular function.

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Rinné, Susanne, Aytug K. Kiper, Constanze Schmidt, Beatriz Ortiz-Bonnin, Simone Zwiener, Guiscard Seebohm, and Niels Decher. "Stress-Kinase Regulation of TASK-1 and TASK-3." Cellular Physiology and Biochemistry 44, no. 3 (2017): 1024–37. http://dx.doi.org/10.1159/000485402.

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Background/Aims: TASK channels belong to the two-pore-domain potassium (K2P) channel family. TASK-1 is discussed to contribute to chronic atrial fibrillation (AFib) and has been together with uncoupling protein 1 found as a marker protein of brown adipose tissue (BAT) fat. In addition, TASK-1 was linked in a genome-wide association study to an increased body mass index. A recent study showed that TASK-1 inhibition is causing obesity in mice by a BAT whitening and that these effects are linked to the mineralocorticoid receptor pathway, albeit the mechanism remained elusive. Therefore, we aimed to probe whether K2P channels are regulated by serum- and glucocorticoid-inducible kinases (SGKs) which are known to modify many cellular functions by modulating ion channels. Methods: To this end we used functional co-expression studies and chemiluminescence-assays in Xenopus oocytes, together with fluorescence imaging and quantitative PCR experiments. Results: SGKs and proteinkinase B (PKB) induced a strong, dose- and time-dependent current reduction of TASK-1 and TASK-3. SGK co-expression reduced the surface expression of TASK-1/3, leading to a predominant localization of the channels into late endosomes. The down regulation of TASK-3 channels was abrogated by the dynamin inhibitor dynasore, confirming a role of SGKs in TASK-1/3 channel endocytosis. Conclusion: Stress-mediated changes in SGK expression pattern or activation is likely to alter TASK-1/3 expression at the surface membrane. The observed TASK-1 regulation might contribute to the pathogenesis of chronic AFib and provide a mechanistic link between increased mineralocorticoid levels and TASK-1 reduction, both linked to BAT whitening.

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Castañeda, Azucena, Carolina Serrano, José Antonio Hernández-Trejo, Itzel Zenidel Gutiérrez-Martínez, Wilber Montejo-López, Mauricio Gómez-Suárez, Marcela Hernández-Ruiz, et al. "pVHL suppresses Akt/β-catenin-mediated cell proliferation by inhibiting 14-3-3ζ expression." Biochemical Journal 474, no. 16 (July 27, 2017): 2679–89. http://dx.doi.org/10.1042/bcj20161097.

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The mechanisms controlling degradation of cytosolic β-catenin are important for regulating β-catenin co-transcriptional activity. Loss of von Hippel–Lindau protein (pVHL) has been shown to stabilize β-catenin, increasing β-catenin transactivation and β-catenin-mediated cell proliferation. However, the role of phosphoinositide 3-kinase (PI3K)/Akt in the regulation of β-catenin signaling downstream from pVHL has never been addressed. Here, we report that hyperactivation of PI3K/Akt in cells lacking pVHL contributes to the stabilization and nuclear accumulation of active β-catenin. PI3K/Akt hyperactivation is facilitated by the up-regulation of 14-3-3ζ and the down-regulation of 14-3-3ε, 14-3-3η and 14-3-3θ. Up-regulation of 14-3-3ζ in response to pVHL is important for the recruitment of PI3K to the cell membrane and for stabilization of soluble β-catenin. In contrast, 14-3-3ε and 14-3-3η enhanced PI3K/Akt signaling by inhibiting PI3K and PDK1, respectively. Thus, our results demonstrated that 14-3-3 family members enhance PI3K/Akt/β-catenin signaling in order to increase proliferation. Inhibition of Akt activation and/or 14-3-3 function strongly reduces β-catenin signaling and decreases cell proliferation. Thus, inhibition of Akt and 14-3-3 function efficiently reduces cell proliferation in 786-0 cells characterized by hyperactivation of β-catenin signaling due to pVHL loss.

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Gong, Wei, Michael Russell, Keiko Suzuki, and Karl Riabowol. "Subcellular Targeting of p33ING1b by Phosphorylation-Dependent 14-3-3 Binding Regulates p21WAF1 Expression." Molecular and Cellular Biology 26, no. 8 (April 15, 2006): 2947–54. http://dx.doi.org/10.1128/mcb.26.8.2947-2954.2006.

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ABSTRACT ING1 is a type II tumor suppressor that affects cell growth, stress signaling, apoptosis, and DNA repair by altering chromatin structure and regulating transcription. Decreased ING1 expression is seen in several human cancers, and mislocalization has been noted in diverse types of cancer cells. Aberrant targeting may, therefore, functionally inactivate ING1. Bioinformatics analysis identified a sequence between the nuclear localization sequence and plant homeodomain domains of ING1 that closely matched the binding motif of 14-3-3 proteins that target cargo proteins to specific subcellular locales. We find that the widely expressed p33ING1b splicing isoform of ING1 interacts with members of the 14-3-3 family of proteins and that this interaction is regulated by the phosphorylation status of ING1. 14-3-3 binding resulted in significant amounts of p33ING1b protein being tethered in the cytoplasm. As shown previously, ectopic expression of p33ING1b increased levels of the p21Waf1 cyclin-dependent kinase inhibitor upon UV-induced DNA damage. Overexpression of 14-3-3 inhibited the up-regulation of p21Waf1 by p33ING1b, consistent with the idea that mislocalization blocks at least one of ING1's biological activities. These data support the idea that the 14-3-3 proteins play a crucial role in regulating the activity of p33ING1b by directing its subcellular localization.

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Leijten, L., P. A. Wilce, M. Davidson, M. Banks, and L. Martin. "Regulation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity in mouse uterine epithelial cells." Biochemical Journal 241, no. 1 (January 1, 1987): 279–84. http://dx.doi.org/10.1042/bj2410279.

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The regulation of 3-hydroxy-3-methylglutaryl-CoA reductase was studied in mouse uterine epithelium. The enzyme was rapidly inactivated during incubation with ATP/Mg2+ in vitro, and could be re-activated by incubation with partially purified rat liver phosphoprotein phosphatase. Enzyme activity was rapidly inhibited by mevalonate injection in vivo to approx. 30% of control. The percentage of total enzyme active in vivo was measured by inclusion of NaF in the isolation buffers. The percentage of enzyme active in vivo 18 h after stimulation by oestrogens remained at approx. 25% after inhibition of activity by mevalonate injection, cholesterol feeding or progesterone pretreatment. However, 9 h after oestrogen stimulation, cholesterol feeding inhibited enzyme activity to 57% of control, 94% of which was in the active form. We conclude that, although all components for a reversible phosphorylative regulation of 3-hydroxy-3-methylglutaryl-CoA reductase activity are present in uterine epithelial cells, a role in the rapid changes in epithelial enzyme activity has not been demonstrated.

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Graca, Luis, Alain Le Moine, Stephen P. Cobbold, and Herman Waldmann. "Antibody-Induced Transplantation Tolerance: The Role of Dominant Regulation." Immunologic Research 28, no. 3 (2003): 181–92. http://dx.doi.org/10.1385/ir:28:3:181.

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Sutrisno, Bambang. "Constitutionality Degree of Indonesia Local Regulation in Political Law Perspective." Rechtsidee 3, no. 1 (June 30, 2016): 41. http://dx.doi.org/10.21070/jihr.v3i1.131.

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The Politics of Law holds responsibility to give the surety of all regulations, including Local Regulation, for capable of reflecting the collective will of the public as the owner of the highest sovereignty. Politics of law is always working to bring together the ius constituendum and ius constitutum at the encounter between realism and idealism. Local Regulation as subsystems of national law, is expected to serve as a guiding instrument and guard direction for development and continuous improvement of Local Government. Therefore the existence of local regulations holds a strategic role for legal certainty, which is a necessary to create a conducive business climate and stability of the country. How To Cite: Sutrisno, B. (2016). Constitutionality Degree of Indonesia Local Regulation in Political Law Perspective. Rechtsidee, 3(1), 41-52. doi:http://dx.doi.org/10.21070/jihr.v3i1.131

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Donnelly, M. J., and J. M. P. Holly. "THE ROLE OF IGFBP-3 IN THE REGULATION OF IGFBP-4 PROTEOLYSIS." Journal of Endocrinology 149, no. 3 (June 1996): R1—R7. http://dx.doi.org/10.1677/joe.0.149r001.

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ABSTRACT The biological effects of insulin-like growth factors (IGFs) are mediated by cell surface receptors but their bioavailability is regulated by IGF binding proteins (IGFBPs) which bind IGF with higher affinity than the receptor. Proteolytic cleavage of the binding proteins reduces their affinity for IGF making the IGF more available to the cell receptor. In the current study we have examined the regulation of IGFBP-4 protease produced by cultured human dermal fibroblasts. IGF-I and the analogs of IGF-I (LR3 and Des[1-3]) induced a dose dependent increase in both proliferation and IGFBP-3 production. Low concentrations of IGF-I induced a marked loss of IGFBP-4 by Western ligand blotting (WLB). This effect was confirmed by the ability of media collected from cells exposed to increasing concentrations of IGF-I to fragment recombinant IGFBP-4, an effect blocked by EDTA. IGFBP-4 proteolysis was observed when cells were exposed to Des[1-3] (albeit at higher concentrations) but not with LR3. Both analogs bind to the IGF receptor but do not bind to IGFBP-4 and have reduced (Des[1-3]) or no (LR3) affinity for IGFBP-3. This demonstrated that neither receptor activation nor ligand binding directly to IGFBP-4 was necessary for IGF induced proteolysis. Protease activity correlated with affinity for IGFBP-3 suggesting a role for IGFBP-3 in the regulation of IGFBP-4 proteolysis. This was confirmed by the ability of excess recombinant IGFBP-3 to inhibit the IGF-I and Des[1-3] induced proteolysis of IGFBP-4. Addition of IGF-I to media from cells unexposed to IGF induced IGFBP-4 proteolysis but this was not seen with LR3 which does not bind to IGFBP-3. Fragmentation occured at higher concentrations of Des[1-3] consistent with its reduced affinity for IGFBP-3 This data suggests that IGFBP-4 proteolysis is regulated in a novel manner by IGFBP-3 which is dependent on the relative proportions of the different binding proteins and the levels of IGFs

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Harrison, M. L., P. Rathinavelu, P. Arese, R. L. Geahlen, and P. S. Low. "Role of band 3 tyrosine phosphorylation in the regulation of erythrocyte glycolysis." Journal of Biological Chemistry 266, no. 7 (March 1991): 4106–11. http://dx.doi.org/10.1016/s0021-9258(20)64292-2.

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50

Reizes, Ofer, Deborah J. Clegg, April D. Strader, and Stephen C. Benoit. "A role for syndecan-3 in the melanocortin regulation of energy balance." Peptides 27, no. 2 (February 2006): 274–80. http://dx.doi.org/10.1016/j.peptides.2005.02.030.

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Journal articles on the topic '(3) Rome I Regulation'

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