Gotowe bibliografie tematyczne / GPCR function and regulation

Gotowa bibliografia na temat „GPCR function and regulation”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 10 lutego 2022

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Artykuły w czasopismach na temat "GPCR function and regulation"

Liu, Nannan, Yifan Wang, Ting Li i Xuechun Feng. "G-Protein Coupled Receptors (GPCRs): Signaling Pathways, Characterization, and Functions in Insect Physiology and Toxicology". International Journal of Molecular Sciences 22, nr 10 (17.05.2021): 5260. http://dx.doi.org/10.3390/ijms22105260.

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G-protein-coupled receptors (GPCRs) are known to play central roles in the physiology of many organisms. Members of this seven α-helical transmembrane protein family transduce the extracellular signals and regulate intracellular second messengers through coupling to heterotrimeric G-proteins, adenylate cyclase, cAMPs, and protein kinases. As a result of the critical function of GPCRs in cell physiology and biochemistry, they not only play important roles in cell biology and the medicines used to treat a wide range of human diseases but also in insects’ physiological functions. Recent studies have revealed the expression and function of GPCRs in insecticide resistance, improving our understanding of the molecular complexes governing the development of insecticide resistance. This article focuses on the review of G-protein coupled receptor (GPCR) signaling pathways in insect physiology, including insects’ reproduction, growth and development, stress responses, feeding, behaviors, and other physiological processes. Hormones and polypeptides that are involved in insect GPCR regulatory pathways are reviewed. The review also gives a brief introduction of GPCR pathways in organisms in general. At the end of the review, it provides the recent studies on the function of GPCRs in the development of insecticide resistance, focusing in particular on our current knowledge of the expression and function of GPCRs and their downstream regulation pathways and their roles in insecticide resistance and the regulation of resistance P450 gene expression. The latest insights into the exciting technological advances and new techniques for gene expression and functional characterization of the GPCRs in insects are provided.

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Melhem, Hassan, Berna Kaya, C. Korcan Ayata, Petr Hruz i Jan Hendrik Niess. "Metabolite-Sensing G Protein-Coupled Receptors Connect the Diet-Microbiota-Metabolites Axis to Inflammatory Bowel Disease". Cells 8, nr 5 (14.05.2019): 450. http://dx.doi.org/10.3390/cells8050450.

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Increasing evidence has indicated that diet and metabolites, including bacteria- and host-derived metabolites, orchestrate host pathophysiology by regulating metabolism, immune system and inflammation. Indeed, autoimmune diseases such as inflammatory bowel disease (IBD) are associated with the modulation of host response to diets. One crucial mechanism by which the microbiota affects the host is signaling through G protein-coupled receptors (GPCRs) termed metabolite-sensing GPCRs. In the gut, both immune and nonimmune cells express GPCRs and their activation generally provide anti-inflammatory signals through regulation of both the immune system functions and the epithelial integrity. Members of GPCR family serve as a link between microbiota, immune system and intestinal epithelium by which all these components crucially participate to maintain the gut homeostasis. Conversely, impaired GPCR signaling is associated with IBD and other diseases, including hepatic steatosis, diabetes, cardiovascular disease, and asthma. In this review, we first outline the signaling, function, expression and the physiological role of several groups of metabolite-sensing GPCRs. We then discuss recent findings on their role in the regulation of the inflammation, their existing endogenous and synthetic ligands and innovative approaches to therapeutically target inflammatory bowel disease.

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Chaudhary, Preeti Kumari, Sanggu Kim, Youngheun Jee, Seung-Hun Lee, Kyung-Mee Park i Soochong Kim. "Role of GRK6 in the Regulation of Platelet Activation through Selective G Protein-Coupled Receptor (GPCR) Desensitization". International Journal of Molecular Sciences 21, nr 11 (30.05.2020): 3932. http://dx.doi.org/10.3390/ijms21113932.

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Platelet G protein-coupled receptors (GPCRs) regulate platelet function by mediating the response to various agonists, including adenosine diphosphate (ADP), thromboxane A2, and thrombin. Although GPCR kinases (GRKs) are considered to have the crucial roles in most GPCR functions, little is known regarding the regulation of GPCR signaling and mechanisms of GPCR desensitization by GRKs in platelets. In this study, we investigated the functional role of GRK6 and the molecular basis for regulation of specific GPCR desensitization by GRK6 in platelets. We used GRK6 knockout mice to evaluate the functional role of GRK6 in platelet activation. Platelet aggregation, dense- and α-granule secretion, and fibrinogen receptor activation induced by 2-MeSADP, U46619, thrombin, and AYPGKF were significantly potentiated in GRK6−/− platelets compared to the wild-type (WT) platelets. However, collagen-related peptide (CRP)-induced platelet aggregation and secretion were not affected in GRK6−/− platelets. Interestingly, platelet aggregation induced by co-stimulation of serotonin and epinephrine which activate Gq-coupled 5HT2A and Gz-coupled α2A adrenergic receptors, respectively, was not affected in GRK6−/− platelets, suggesting that GRK6 was involved in specific GPCR regulation. In addition, platelet aggregation in response to the second challenge of ADP and AYPGKF was restored in GRK6−/− platelets whereas re-stimulation of the agonist failed to induce aggregation in WT platelets, indicating that GRK6 contributed to P2Y1, P2Y12, and PAR4 receptor desensitization. Furthermore, 2-MeSADP-induced Akt phosphorylation and AYPGKF-induced Akt, extracellular signal-related kinase (ERK), and protein kinase Cδ (PKCδ) phosphorylation were significantly potentiated in GRK6−/− platelets. Finally, GRK6−/− mice exhibited an enhanced and stable thrombus formation after FeCl3 injury to the carotid artery and shorter tail bleeding times, indicating that GRK6−/− mice were more susceptible to thrombosis and hemostasis. We conclude that GRK6 plays an important role in regulating platelet functional responses and thrombus formation through selective GPCR desensitization.

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Chini, B., i M. Parenti. "G-protein coupled receptors in lipid rafts and caveolae: how, when and why do they go there?" Journal of Molecular Endocrinology 32, nr 2 (1.04.2004): 325–38. http://dx.doi.org/10.1677/jme.0.0320325.

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This review describes the advances in our understanding of the role of G-protein coupled receptor (GPCR) localisation in membrane microdomains known as lipid rafts and caveolae. The growing interest in these specialised regions is due to the recognition that they are involved in the regulation of a number of cell functions, including the fine-tuning of various signalling molecules. As a number of GPCRs have been found to be enriched in lipid rafts and/or caveolae by means of different experimental approaches, we first discuss the pitfalls and uncertainties related to the use of these different procedures. We then analyse the addressing signals that drive and/or stabilise GPCRs in lipid rafts and caveolae, and explore the role of rafts/caveolae in regulating GPCR trafficking, particularly in receptor exo- and endocytosis. Finally, we review the growing evidence that lipid rafts and caveolae participate in the regulation of GPCR signalling by affecting both signalling selectivity and coupling efficacy.

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Walther, Cornelia, i Stephen S. G. Ferguson. "Minireview: Role of Intracellular Scaffolding Proteins in the Regulation of Endocrine G Protein-Coupled Receptor Signaling". Molecular Endocrinology 29, nr 6 (1.06.2015): 814–30. http://dx.doi.org/10.1210/me.2015-1091.

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Abstract The majority of hormones stimulates and mediates their signal transduction via G protein-coupled receptors (GPCRs). The signal is transmitted into the cell due to the association of the GPCRs with heterotrimeric G proteins, which in turn activates an extensive array of signaling pathways to regulate cell physiology. However, GPCRs also function as scaffolds for the recruitment of a variety of cytoplasmic protein-interacting proteins that bind to both the intracellular face and protein interaction motifs encoded by GPCRs. The structural scaffolding of these proteins allows GPCRs to recruit large functional complexes that serve to modulate both G protein-dependent and -independent cellular signaling pathways and modulate GPCR intracellular trafficking. This review focuses on GPCR interacting PSD95-disc large-zona occludens domain containing scaffolds in the regulation of endocrine receptor signaling as well as their potential role as therapeutic targets for the treatment of endocrinopathies.

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Cottrell, GS. "Roles of proteolysis in regulation of GPCR function". British Journal of Pharmacology 168, nr 3 (16.01.2013): 576–90. http://dx.doi.org/10.1111/j.1476-5381.2012.02234.x.

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N'Diaye, Elsa-Noah, Aylin C. Hanyaloglu, Kimberly K. Kajihara, Manojkumar A. Puthenveedu, Ping Wu, Mark von Zastrow i Eric J. Brown. "The Ubiquitin-like Protein PLIC-2 Is a Negative Regulator of G Protein-coupled Receptor Endocytosis". Molecular Biology of the Cell 19, nr 3 (marzec 2008): 1252–60. http://dx.doi.org/10.1091/mbc.e07-08-0775.

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The activity of many signaling receptors is regulated by their endocytosis via clathrin-coated pits (CCPs). For G protein-coupled receptors (GPCRs), recruitment of the adaptor protein arrestin to activated receptors is thought to be sufficient to drive GPCR clustering in CCPs and subsequent endocytosis. We have identified an unprecedented role for the ubiquitin-like protein PLIC-2 as a negative regulator of GPCR endocytosis. Protein Linking IAP to Cytoskeleton (PLIC)-2 overexpression delayed ligand-induced endocytosis of two GPCRs: the V2 vasopressin receptor and β-2 adrenergic receptor, without affecting endocytosis of the transferrin or epidermal growth factor receptor. The closely related isoform PLIC-1 did not affect receptor endocytosis. PLIC-2 specifically inhibited GPCR concentration in CCPs, without affecting membrane recruitment of arrestin-3 to activated receptors or its cellular levels. Depletion of cellular PLIC-2 accelerated GPCR endocytosis, confirming its regulatory function at endogenous levels. The ubiquitin-like domain of PLIC-2, a ligand for ubiquitin-interacting motifs (UIMs), was required for endocytic inhibition. Interestingly, the UIM-containing endocytic adaptors epidermal growth factor receptor protein substrate 15 and Epsin exhibited preferential binding to PLIC-2 over PLIC-1. This differential interaction may underlie PLIC-2 specific effect on GPCR endocytosis. Identification of a negative regulator of GPCR clustering reveals a new function of ubiquitin-like proteins and highlights a cellular requirement for exquisite regulation of receptor dynamics.

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Caballero, Adriana, Sarah A. Mahn, Mudassir S. Ali, M. Rose Rogers i Adriano Marchese. "Heterologous regulation of CXCR4 lysosomal trafficking". Journal of Biological Chemistry 294, nr 20 (1.04.2019): 8023–36. http://dx.doi.org/10.1074/jbc.ra118.005991.

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G protein–coupled receptor (GPCR) signaling is regulated by members of the protein kinase C (PKC) and GPCR kinase (GRK) families, although the relative contribution of each to GPCR function varies among specific GPCRs. The CXC motif receptor 4 (CXCR4) is a member of the GPCR superfamily that binds the CXC motif chemokine ligand 12 (CXCL12), initiating signaling that is subsequently terminated in part by internalization and lysosomal degradation of CXCR4. The purpose of this study is to define the relative contribution of PKC and GRK to CXCR4 signaling attenuation by studying their effects on CXCR4 lysosomal trafficking and degradation. Our results demonstrate that direct activation of PKC via the phorbol ester phorbol 12-myristate 13-acetate (PMA) mimics CXCL12-mediated desensitization, internalization, ubiquitination, and lysosomal trafficking of CXCR4. In agreement, heterologous activation of PKC by stimulating the chemokine receptor CXCR5 with its ligand, CXCL13, also mimics CXCL12-mediated desensitization, internalization, ubiquitination, and lysosomal degradation of CXCR4. Similar to CXCL12, PMA promotes PKC-dependent phosphorylation of serine residues within CXCR4 C-tail that are required for binding and ubiquitination by the E3 ubiquitin ligase AIP4 (atrophin-interacting protein 4). However, inhibition of PKC activity does not alter CXCL12-mediated ubiquitination and degradation of CXCR4, suggesting that other kinases are also required. Accordingly, siRNA-mediated depletion of GRK6 results in decreased degradation and ubiquitination of CXCR4. Overall, these results suggest that PKC and GRK6 contribute to unique aspects of CXCR4 phosphorylation and lysosomal degradation to ensure proper signal propagation and termination.

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Poll, Brian G., Lihe Chen, Chung-Lin Chou, Viswanathan Raghuram i Mark A. Knepper. "Landscape of GPCR expression along the mouse nephron". American Journal of Physiology-Renal Physiology 321, nr 1 (1.07.2021): F50—F68. http://dx.doi.org/10.1152/ajprenal.00077.2021.

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Kidney transport and other renal functions are regulated by multiple G protein-coupled receptors (GPCRs) expressed along the renal tubule. The rapid, recent appearance of comprehensive unbiased gene expression data in the various renal tubule segments, chiefly RNA sequencing and protein mass spectrometry data, has provided a means of identifying patterns of GPCR expression along the renal tubule. To allow for comprehensive mapping, we first curated a comprehensive list of GPCRs in the genomes of mice, rats, and humans ( https://hpcwebapps.cit.nih.gov/ESBL/Database/GPCRs/ ) using multiple online data sources. We used this list to mine segment-specific and cell type-specific expression data from RNA-sequencing studies in microdissected mouse tubule segments to identify GPCRs that are selectively expressed in discrete tubule segments. Comparisons of these mapped mouse GPCRs with other omics datasets as well as functional data from isolated perfused tubule and micropuncture studies confirmed patterns of expression for well-known receptors and identified poorly studied GPCRs that are likely to play roles in the regulation of renal tubule function. Thus, we provide data resources for GPCR expression across the renal tubule, highlighting both well-known GPCRs and understudied receptors to provide guidance for future studies.

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Luo, Jiaqian, i Fa-Xing Yu. "GPCR-Hippo Signaling in Cancer". Cells 8, nr 5 (8.05.2019): 426. http://dx.doi.org/10.3390/cells8050426.

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The Hippo signaling pathway is involved in tissue size regulation and tumorigenesis. Genetic deletion or aberrant expression of some Hippo pathway genes lead to enhanced cell proliferation, tumorigenesis, and cancer metastasis. Recently, multiple studies have identified a wide range of upstream regulators of the Hippo pathway, including mechanical cues and ligands of G protein-coupled receptors (GPCRs). Through the activation related G proteins and possibly rearrangements of actin cytoskeleton, GPCR signaling can potently modulate the phosphorylation states and activity of YAP and TAZ, two homologous oncogenic transcriptional co-activators, and major effectors of the Hippo pathway. Herein, we summarize the network, regulation, and functions of GPCR-Hippo signaling, and we will also discuss potential anti-cancer therapies targeting GPCR-YAP signaling.

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Rozprawy doktorskie na temat "GPCR function and regulation"

Dromey, Jasmin Rachel. "Elucidating novel aspects of hypothalamic releasing hormone receptor regulation". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0133.

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[Truncated abstract] G-protein coupled receptors (GPCRs) form one of the largest superfamilies of cell-surface receptors and respond to a vast range of stimuli including light, hormones and neurotransmitters. Although structurally similar, GPCRs are regulated by many diverse proteins, which allow the specific functions of each receptor to be carried out. This thesis focussed on two well-documented GPCRs, the thyrotropin releasing hormone receptor (TRHR) and gonadotrophin-releasing hormone receptor (GnRHR), which control the thyroid and reproductive endocrine pathways respectively. Although each of these anterior pituitary receptors is responsible for distinct physiological responses, both are integral to normal development and homeostasis. This thesis focused on three areas of GPCR regulation: ?-arrestin recruitment, transcription factor regulation and receptor up-regulation. The role of the cytoplasmic protein, ?-arrestin, has perhaps been previously underestimated in GPCR regulation, but it is now increasingly apparent that ?-arrestins not only inhibit further G-protein activation and assist in GPCR internalisation but also act as complex scaffolding platforms to mediate and amplify downstream signalling networks for hours after initial GPCR activation. It is therefore becoming increasingly important to be able to monitor such complexes in live cells over longer time-frames. ... Members of the E2F transcription family have been previously identified by this laboratory as potential GnRHR interacting proteins, via a yeast-2-hybrid screen and BRET. This thesis further investigated the role of E2F family members and demonstrates that a range of GPCRs are able to activate E2F transcriptional activity when stimulated by agonist. However, despite GnRHR displaying robust E2F transcriptional activation upon agonist stimulation, this did not result in any conclusive evidence for functional regulation, although it is possible E2F may modulate and assist in GnRHR trafficking. Furthermore it is apparent that E2F family members are highly redundant, as small effects in GnRHR binding and cell growth were only observed when protein levels of both E2F4 and E2F5 were altered. During the course of the investigation into the effect of E2F transcription on GPCR function, it was evident that long-term agonist stimulation of GnRHR had a profound effect on its expression. As this was explored further, it became clear that this agonist-induced up-regulation was both dose- and time-dependent. Furthermore, altering levels of intracellular calcium and receptor recycling/synthesis could modulate GnRHR up-regulation. In addition, an extremely sensitive CCD camera has been used for the first time to visualise the luciferase activity attributed to GnRHR up-regulation. Overall, this thesis demonstrates the complex nature of GPCR regulation. For the first time, long-term BRET analysis on ?-arrestin interactions with both classes of GPCRs has been examined in a variety of cellular formats. This has given valuable insights into the roles of phosphorylation and internalisation on ?-arrestin interaction. Additionally, this thesis has revealed that prolonged agonist exposure increases receptor expression levels, which has major implications for drug therapy regimes in the treatment of endocrine-related disorders and tumours.

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Jama, Abdirahman Mohamud. "Functional regulation of kisspeptin receptor by calmodulin and Ca2+/calmodulin-dependent protein kinase II". Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15914.

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The kisspeptin receptor (KISS1R), functioning as a metastasis suppressor and gatekeeper of GnRH neurons, is a potent activator of intracellular Ca2+. The surge in cytoplasmic Ca2+ mediates the exocytosis of GnRH from GnRH neurons. However, the regulatory processes which enable KISS1R to sense increasing intracellular Ca2+ and avoid Ca2+ excitotoxicity via a signalling off-switch mechanism remain unclear. This thesis provides evidence for the interaction between KISS1R and the Ca2+ regulated proteins of calmodulin (CaM), and αCa2+/CaM-dependent-protein kinase II (α-CaMKII). Binding of CaM to KISS1R was shown with three independent approaches. Firstly, cell-free spectrofluorimeter assays showed that CaM selectively binds to intracellular loop (IL) 2 and IL3 of the KISS1R. Secondly, KISS1R co-immunoprecipitation experiments identified ligand/Ca2+-dependent binding of KISS1R to HEK-293 endogenous CaM. Thirdly, confocal experiments showed CFPCaM co-localises with YFP-KISS1R. The functional relevance of CaM binding was examined with alanine substitution of critical residues of the CaM binding motifs in IL2 and IL3 of KISS1R. This approach revealed that the receptor activity (relative maximum responsiveness) was increased in the mutated residues of the juxtamembrane regions of IL3 and the N-terminus of IL2 relative to wild-type KISS1R. The Ca2+/CaM regulated αCaMKII was also found to interact with KISS1R by selectively phosphorylating T77 of IL1. Phosphomimetic mutations of T77 into E or D created a receptor that was unable to elicit inositol phosphate production upon ligand stimulation. Finally, in vivo studies using ovariectomised rats that were intracerebroventricularly administered with a cell-permeable αCaMKII inhibitor augmented the effects of kisspeptin ligand stimulation of plasma luteinizing hormone levels. Taken together, this thesis demonstrates that the KISS1R-G protein coupling is regulated by Ca2+-dependent CaM binding and αCaMKII-mediated KISS1R phosphorylation.

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Åkerberg, Helena. "Functional Studies of the Neuropeptide Y System : Receptor-Ligand Interaction and Regulation of Food Intake". Doctoral thesis, Uppsala universitet, Institutionen för neurovetenskap, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9533.

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The members of the mammalian neuropeptide Y family, i.e. the peptides neuropeptide Y (NPY), peptide YY (PYY) and pancreatic polypeptide (PP), are all involved in regulation of food intake. In human and most other mammals they act via receptors Y1, Y2, Y4 and Y5. NPY is released in the hypothalamus and is one of the strongest appetite-stimulating neurotransmitters whereas PP and PYY are secreted from gut endocrine cells after meals and function as appetite-reducing hormones. This thesis describes studies of the NPY system at both the molecular and the physiological level. The first part describes two investigations of receptor-ligand interactions with the human Y1 and Y2 receptors. The results clarify the importance of several amino-acid residues of the human Y1 receptor. Three amino acids previously suggested by others to form a binding pocket for the carboxy-terminus of the peptide were confirmed to be crucial for interaction with peptide ligands. However, they were found to be too distantly located from each other to be able to form a binding pocket. Further investigation of the three corresponding positions in the human Y2 receptor showed that only one of the positions was important for interaction with full-length peptides. The results indicate overlapping but, surprisingly, non-identical binding of the different peptides to human Y1 and Y2 receptors, despite the fact that the two receptors share a common ancestor. The second part of the thesis describes an investigation of the effect of PP on food intake in six beagle dogs and a test for personality characteristics in dogs (TFPC). Treatment with physiological doses of PP decreased both the appetitive and the consummatory drive but had no effect on the amount food consumed. The TFPC protocol was used to map individual behavioral differences in a population of sixteen beagle dogs. The test, which included several situations that may appear in an experimental study, revealed considerable inter-individual differences in behavioral responses despite the fact that the dogs were born and housed in the same animal facility in constant controlled conditions. These results demonstrate that PP can influence food intake in distantly related mammals and emphasize the importance of considering differences in personality in experimental animals.

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Richardson, Kathryn. "Mechanisms of GPCR signal regulation in fission yeast". Thesis, University of Warwick, 2014. http://wrap.warwick.ac.uk/63554/.

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Cells communicate with each other and respond to environmental cues by sending and receiving signals. Many external signals (ligands) are detected through G protein-coupled receptors (GPCRs), a major class of transmembrane proteins. GPCRs transduce these external signals into appropriate intracellular responses, enabling the cell to adapt to its environment. Malfunctions in these signalling pathways can lead to a range of human diseases and hence GPCRs have become attractive candidates for pharmacological design. The activation of a single receptor has the ability to induce numerous intracellular responses. Coupling this with the great number of different GPCR-types expressed in human cells means that understanding the basic principles of signal transduction and termination in humans is complicated. This study utilises the more simplistic eukaryotic yeast Schizosaccharomyces pombe (S. pombe) to overcome this complexity, as it contains only two GPCR types and hence the cross-talk between pathways is greatly reduced, whilst the structure and signalling functions of GPCRs are often evolutionarily conserved between yeast and humans. Mathematical modelling was used to aid the understanding of GPCR signalling in S. pombe and to inform experimental design. Speci�cally, an ordinary differential equation model �rst developed by Croft et al. (2013) was extended to include all known downstream signal transduction, regulation and termination events. This model is the �rst of its kind to describe a whole GPCR signalling pathway within S. pombe. Although it accurately predicts the cellular response to GPCR signalling it could only reproduce the biological plateau in temporal response with the addition of a 'yet unknown mechanism' GPCR degradation term. This motivated the investigation of how GPCRs in S. pombe are internalised from the plasma membrane in response to ligand stimulation. The primary mechanism for signal termination is via internalisation of the GPCR. This study identi�ed three potential casein kinases (Cki1, Cki2 and Cki3) that promote internalisation of the S. pombe GPCR Mam2. Microscopy analyses in combination with quantitative transcriptional, cell growth and cell cycle position assays uncovered a novel role for these kinases: that Cki2 regulates cell size during vegetative growth, Cki1 and Cki3 regulate the GPCR-response pathway and that Cki3 is essential for completing cytokinesis in S. pombe that have already undergone formation of a conjugation tube in response to ligand. Confocal microscopy of uorescent labelled Mam2 indicated a role for Cki2 in the internalisation and hence termination of the GPCR-response pathway. These findings add to the growing body of evidence that casein kinases are implicated in GPCR desensitisation.

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Ranganathan, Anirudh. "The impact of GPCR structures on understanding receptor function and ligand binding". Doctoral thesis, Stockholms universitet, Institutionen för biokemi och biofysik, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-129879.

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G protein-coupled receptors (GPCRs) form the largest superfamily of eukaryotic membrane proteins and are responsible for the action of nearly 30% of all marketed drugs. For a long period, efforts to study these receptors were limited by the paucity of atomic-resolution structural information. Numerous receptors spread across the GPCR superfamily have recently been crystallized, revealing crucial clues about receptor function and ligand recognition. The work in this thesis has primarily focused on using computational techniques to capitalize on this increasing amount of structural information. In papers I, II, and III protocols were developed to identify novel ligands for pharmaceutically important targets from in silico screens of large chemical libraries. In these papers, the fragment-based lead discovery (FBLD) approach was evaluated for GPCR targets using molecular docking screens. The high hit-rates obtained in these studies indicate promise for the use of computational approaches for fragment screening. In paper IV, molecular dynamics was used to identify a possible role for a conserved ionizable residue (Asp792.50) as a protonation switch during the activation process of the β2 adrenergic receptor. Analyses from this paper indicated that this residue could also perform a similar function in other class A GPCRs. Papers V and VI detail the modeling strategy followed during the GPCR Dock 2013 assessment to blindly predict the structure of two serotonin receptor subtypes (5-HT1B and 5-HT2B) bound to ergotamine. The developed ligand-steered homology modeling protocol was largely successful resulting in the best-ranked predictions for the 5-HT1B subtype. It is hoped that the work described in this thesis has highlighted the potential for structure-based computational approaches to identify novel ligands for important pharmaceutical targets and improve understanding of GPCR function.

At the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 3: Manuscript.

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Hillier, Stephen Gilbert. "Regulation of ovarian function". Thesis, University of Edinburgh, 1992. http://hdl.handle.net/1842/26607.

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(i) Basic Experimental studies Publications 1-35 deal mainly with the use of cultured rat and marmoset monkey granulosa cells to study endocrine and paracrine mechanisms underlying gonadotrophin action on the ovaries. Primary cell cultures were used to define the roles of FSH and LH in controlling granulosa cell function and to assess the intrafollicular functions of sex steroids and putative nonsteroidal regulatory factors, such as inhibin. A particular contribution was the demonstration that androgens produced by thecal cells exert specific (receptor-mediated) modulation of granulosa cell differentiation - notably expression of aromatase, the enzyme uniquely responsible for oestrogen synthesis. Synthesis of inhibin and expression of messenger RNA species encoding inhibin and activin subunits in granulosa cells were also shown to be under gonadotrophic control and modulated by sex steroids, leading to the suggestion that the androgen/oestrogen and inhibin/activin axes of the ovarian paracrine system are functionally interlinked. (ii) Basic Clinical Studies Publications 36-56 are concerned with in vitro research on 'normal' ovarian tissues obtained from women undergoing elective surgical procedures. Techniques and experience acquired from experimental work on animal ovarian tissues were used to study the regulation of steroid hormone synthesis in human follicular and luteal cells. This work demonstrated that granulosa cells are primary cellular sites of oestradiol biosynthesis in the human ovary. It also confirmed the potential that theca-derived androgens have to modulate FSH-induced granulosa cell function, including aromatase activity and inhibin production. Conversely, androgen production by thecal cells was shown to be promoted by inhibin. Based on these findings it is postulated that an intrafollicular positive feedback loop exists mediated by theca-derived androgen and granulosa-derived inhibin, which may underpin preovulatory follicular 'selection' and oestrogen synthesis in the human menstrual cycle.

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Bittencourt, Fabiola M. "Examination of the Function of the Murine Cytomegalovirus Encoded G Protein-Coupled Receptor M33 in vivo". University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1397234044.

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Munjal, Akankshi. "Regulation of a bio-mechanical network driving shape changes during tissue morphogenesis". Thesis, Aix-Marseille, 2015. http://www.theses.fr/2015AIXM4038/document.

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Forces requises pour les changements de forme au cours de la morphogenèse des tissus sont générés par d’actine et de myosine. Durant ma thèse, je étudié le rôle de la réglementation MyoII par la voie Rho1-Rok durant l’élongation de l’ectoderme ventro-latéral par intercalation cellulaire. Les pulsations de MyoII médio-apicale se déplacent de manière anisotrope vers les jonctions parallèles avec l’axe dorso-ventral (ou jonctions verticales). Ceci provoque le rétrécissement graduel des jonctions qui sont stabilisées par une population de MyoII polarisée dans le plan du tissu et enrichie au niveau de ces jonctions. Les mécanismes cellulaires qui régulent la pulsatilité, la stabilité et la polarité de la myosine II restent à élucider. J’ai identifié deux propriétés cruciales de la dynamique de la myosine II régie par phospho- à savoir la cinétique d’échange gouvernée par les cycles de phosphorylation-déphosphorylation des chaines légères régulatrices de la MyoII (RLC) et l’advection due à la contraction des moteurs sur le réseau de F-actine. Contrôle spatial sur le chiffre d'affaires MyoII établit 2 régimes stables des taux élevés et faibles dissociation résultant dans MyoII polarité. Pulsatilité est un comportement auto-organisé qui émerge à taux de dissociation intermédiaires permettant d'advection MyoII et les régulateurs en amont. Dans la deuxième partie de ma thèse, je l'ai montré que la protéine GPCR- GRsmog et la brume, et la voie G-protéines en aval permettent l'activation progressive des MyoII, établissant pulsatilité et de la stabilité pour produire des déformations de forme polarisées cours de la morphogenèse
Forces required to power shape changes during tissue morphogenesis are generated by non-muscle MyosinII (MyoII) pulling filamentous actin. During my PhD, I investigated the role of MyoII regulation through the conserved Rho1-Rok pathway during Drosophila germband extension. The morphogenetic process is powered by cell intercalation involving shrinkage of junctions in the dorsal-ventral axis (‘vertical junctions’) followed by junction extension in the anterior-posterior axis. Advances in light microscopy revealed that the actomyosin networks exhibit pulsed contractions to power junction shrinkage, and alternate with steps of stabilization by MyoII enriched on vertical junctions (planar-polarity) to result in irreversible shape changes. Although described in many different contexts, the underlying mechanisms of this ratchet-like behavior remained unclear. Using genetic and biophysical tools, quantitative imaging and subtle perturbations, I identified 2 critical properties underlying MyoII dynamics- turnover governed by phospho-cycling of the MyoII Regulatory Light Chain, and advection due to contraction of the motors on actin networks. Spatial control over MyoII turnover establishes 2 stable regimes of high and low dissociation rates resulting in MyoII planar polarity. Pulsatility is a self-organized behavior that emerges at intermediate dissociation rates enabling advection of MyoII and upstream regulators. In the second part of my thesis, I showed that G protein coupled receptors- GRsmog and Mist, and the downstream G-protein pathway allow step-wise activation of MyoII, establishing pulsatility and stability, to drive polarized shape deformations during morphogenesis

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Clay, L. "CDC20 function, regulation and proteolysis". Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597750.

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The destruction of mitotic cyclins and other key regulators uses ubiquitin mediated proteolysis controlled via the activation of the ubiquitin ligase the Anaphase Promoting Complex/Cyclosome (APC/C), and its adaptor proteins Cdc20 and Cdh1. The spindle assembly checkpoint coordinates the APC/C with microtubule attachment and sets the timing from NEBD to anaphase. Cdc20 is inactivated by the spindle assembly checkpoint to prevent premature anaphase onset. Once the spindle assembly checkpoint is satisfied, Cdc20 can be released and activate the APC/C. However, cyclin A is degraded independently of the spindle assembly checkpoint before cyclin B1 and the anaphase inhibitor Securin. How Cdc20 can target different substrates for degradation at different times during mitosis is not yet clear. Using live-cell imaging and RNA interference and immunofluorescence techniques, I have studied the degradation of endogenous and ectopicly expressed APC/C substrates in cells with reduced Cdc20 levels. In this dissertation, I show that cyclin A degradation strongly depends on Cdc20, whereas cyclin B1 and Securin degradation do not. I identified the region of Cdc20 required for cyclin A binding and by mutating this site, I found that Cdc20 was no longer properly localised. I also show that Cdc20 proteolysis in human somatic cells does not require the KEN motif and gone on to find the motif required for Cdc20 degradation. I also show that the function of Cdc20 in the spindle assembly checkpoint can be influenced by the serine/threonine kinase Aurora A. Co-expression of a fluorescently tagged Cdc20 and Aurora A in human somatic cells causes an accelerated progression through mitosis and premature substrate degradation.

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Brandao, Haga Raquel. "Function and regulation of RhoBTB1". Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/function-and-regulation-of-rhobtb1(0904ff24-d566-4987-8c61-440c09854eeb).html.

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Rho GTPases are a family of proteins known to be involved in cytoskeletal regulation and are important for several processes including cell migration, cell polarity, vesicle trafficking and cytokinesis. RhoBTB1 is an atypical member of the Rho GTPase family. It consists of a non-functional GTP-binding domain followed by a proline-rich region and two tandem BTB domains. The only known interacting partner for RhoBTB1 is cullin3, a scaffold protein in ubiquitin ligase complexes. So far RhoBTB1 has not been shown to affect the cytoskeleton and it has no known cellular function. Most Rho GTPases are regulated by GEFs, GAPs, RhoGDIs and post-translational lipid modifications at the C-terminus. However, RhoBTB1 is not regulated by any of these mechanisms. RhoBTB1 has additional domains that could be involved in protein-protein interaction, leading to an alternative mechanism for RhoBTB1 regulation. This project has shown that RhoBTB1 can interact with RhoA and ROCK1 as well as cullin3. The interaction between RhoA and RhoBTB1 was explored since RhoBTB1 has the potential to recruit substrates for ubiquitination by cullin3 complexes. The region of interaction between RhoA and RhoBTB1 was mapped and RhoBTB1 influenced the protein level of RhoA, suggesting that it inhibits RhoA degradation by the proteasome. RhoBTB1 was found to localise diffusely in the cytoplasm or to punctate structures. Knockdown of RhoBTB1 led to a change in cell morphology in a 3D Matrigel matrix, indicating that it influences cell shape in 3D, although it did not alter cell shape on 2D substrata. RhoBTB1 can be phosphorylated by ROCK1 in vitro and the region of interaction between RhoBTB1 and ROCK1 was mapped using ROCK1 deletion mutants. I hypothesize that RhoBTB1 interacts with RhoA to affect its ubiquitination and degradation and hence affects cell morphology in a 3D matrix, and that RhoBTB1 activity is regulated by ROCK1-mediated phosphorylation.

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Książki na temat "GPCR function and regulation"

C, Froehner Stanley, i Bennett Vann, red. Cytoskeletal regulation of membrane function. New York: Rockefeller University Press, 1997.

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Maki, Nina Diana. LUCA-15 function and regulation. Sudbury, Ont: Laurentian University, School of Graduate Studies, 2004.

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Means, Anthony R. Calcium regulation of cellular function. New York: Raven Press, 1995.

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name, No. Neurotransmitter transporters: Structure, function, and regulation. Wyd. 2. Totowa, NJ: Humana Press, 2002.

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Wolffe, A. Regulation of chromatin structure and function. Austin, TX: R.G. Landes, 1994.

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Deutsch, Andreas, Jonathon Howard, Martin Falcke i Walter Zimmermann, red. Function and Regulation of Cellular Systems. Basel: Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7895-1.

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Bevan, John A., Gabor Kaley i Gabor M. Rubanyi, red. Flow-Dependent Regulation of Vascular Function. New York, NY: Springer New York, 1995. http://dx.doi.org/10.1007/978-1-4614-7527-9.

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Mahesh, Virendra B., Dharam S. Dhindsa, Everett Anderson i Satya P. Kalra, red. Regulation of Ovarian and Testicular Function. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5395-9.

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Deutsch, Andreas. Function and Regulation of Cellular Systems. Basel: Birkhäuser Basel, 2004.

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Naik, Salma Iqbal. Physiological regulation of gonadotroph function in mice. Birmingham: University of Birmingham, 1985.

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Części książek na temat "GPCR function and regulation"

Gimpl, Gerald, i Katja Gehrig-Burger. "Specific and Nonspecific Regulation of GPCR Function by Cholesterol". W Cholesterol Regulation of Ion Channels and Receptors, 205–30. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118342312.ch10.

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Pera, Tonio, i Raymond B. Penn. "Methods to Investigate β-Arrestin-Mediated Regulation of GPCR Function in Human Airway Smooth Muscle". W Beta-Arrestins, 69–82. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_4.

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Bomberger, Jennifer M., Narayanan Parameswaran i William S. Spielman. "Regulation of GPCR Trafficking by RAMPs". W Advances in Experimental Medicine and Biology, 25–37. New York, NY: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2364-5_3.

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Kamimura, Yoichiro, i Masahiro Ueda. "GPCR Signaling Regulation in Dictyostelium Chemotaxis". W Methods in Molecular Biology, 317–36. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1258-3_27.

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Chen, Xi, Wai-Ki Ching i Nam-Kiu Tsing. "Regulation Function". W Encyclopedia of Systems Biology, 1833–34. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_378.

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Alexiev, Ulrike. "Dynamics of Helix 8 in GPCR Function". W Encyclopedia of Biophysics, 549–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-16712-6_787.

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Willets, Jonathon M. "Approaches to Study GPCR Regulation in Native Systems". W Methods in Molecular Biology, 99–112. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-126-0_6.

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Saenz del Burgo, L., i G. Milligan. "Chapter 6. Ligand Regulation of GPCR Quaternary Structure". W Drug Discovery, 111–52. Cambridge: Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/9781849733441-00111.

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Eglen, Richard M., i Terry Reisine. "New Insights into GPCR Function: Implications for HTS". W Methods in Molecular Biology, 1–13. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-317-6_1.

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Ludwig, Marie-Gabrielle, Klaus Seuwen i James P. Bridges. "Adhesion GPCR Function in Pulmonary Development and Disease". W Adhesion G Protein-coupled Receptors, 309–27. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41523-9_14.

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Streszczenia konferencji na temat "GPCR function and regulation"

Bekhouche, Safia, i Yamina Mohamed Ben Ali. "Optimizing the identification of GPCR function". W SMC '19: The Second Conference of the Moroccan Classification Society. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3314074.3314082.

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Haak, A., D. Jones i D. J. Tschumperlin. "Epigenetic Regulation of Myofibroblast GPCR Landscape Mediates Antifibrotic Efficacy". W American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4057.

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Romao, Luiz Melo, i Julio Cesar Nievola. "Predicting GPCR and enzymes function with a global approach based on LCS". W 2012 IEEE 12th International Conference on Bioinformatics & Bioengineering (BIBE). IEEE, 2012. http://dx.doi.org/10.1109/bibe.2012.6399665.

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Ren, Yong, i Qian Wang. "Physics-Informed Gaussian Process Based Optimal Control of Laser Powder Bed Fusion". W ASME 2020 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/dscc2020-3197.

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Abstract Regulating the melt-pool size to a constant reference value during the build process is a challenging task in Laser Powder Bed Fusion additive manufacturing (LPBF-AM). This paper considers adjusting laser power to achieve a constant melt-pool volume during laser processing of a multi-track build under LPBF-AM. First, a Gaussian Process Regression (GPR) is applied to model the variation of the melt-pool volume along the deposition distance, with physics-informed input features. Then a constrained finite-horizon optimal control problem is formulated, with a quadratic cost function defined to minimize the difference between the melt-pool volume and a reference value. A projected gradient descent algorithm is applied to compute the sequence of laser power in the proposed optimal control problem. The GPR modeling of melt-pool dynamics is trained and tested using simulated data sets generated from a commercial finite-element based AM software, and the same commercial AM software is used to evaluate the control performance. Simulation results demonstrate the effectiveness of the proposed GPR modeling and optimal control in regulating melt-pool volume for building multi-track parts with LPBF-AM.

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Zhu, Yuncheng, i Okita Hideki. "Traffic management using value function-based regulation". W 2017 19th Asia-Pacific Network Operations and Management Symposium (APNOMS). IEEE, 2017. http://dx.doi.org/10.1109/apnoms.2017.8094197.

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Arakaki, Aleena K. S., Wen-An Pan, Helen Wedegaertner i JoAnn Trejo. "Abstract A16: The α-arrestin ARRDC3 functions as a metastasis suppressor by regulating GPCR activation of the Hippo pathway". W Abstracts: AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; May 8-11, 2019; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-a16.

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Sokol, Nicholas. "Regulation and function oflet-7-ComplexmicroRNAs inDrosophila melanogaster". W 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.82459.

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Muslim, Shohib, Hudriyah Mundzir i Ane Fany Novitasari. "Regulation on Independent Function of Financial Services Authority". W 1st Annual Management, Business and Economic Conference (AMBEC 2019). Paris, France: Atlantis Press, 2020. http://dx.doi.org/10.2991/aebmr.k.200415.009.

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Kumar, Vineet. "On the regulation and transfer function of photon". W ADVANCES IN BASIC SCIENCE (ICABS 2019). AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5122367.

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Wan, Qingfeng, i Wenbin Zhang. "Study of Cellular Immune Function and Regulation Measurement". W 2016 6th International Conference on Machinery, Materials, Environment, Biotechnology and Computer. Paris, France: Atlantis Press, 2016. http://dx.doi.org/10.2991/mmebc-16.2016.450.

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Raporty organizacyjne na temat "GPCR function and regulation"

Treistman, Steven N. Regulation of Voltage-Dependent Channel Function. Fort Belvoir, VA: Defense Technical Information Center, sierpień 1988. http://dx.doi.org/10.21236/ada200375.

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Tublitz, Nathan. Neural Regulation Of Chromatophore Function In Cephalopods. Fort Belvoir, VA: Defense Technical Information Center, maj 2015. http://dx.doi.org/10.21236/ada619935.

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Starczynowski, Daniel. Regulation and Function of TIFAB in Myelodysplastic Syndrome. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2014. http://dx.doi.org/10.21236/ada613223.

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Kotwaliwale, Chitra, i Sue Biggins. Regulation and Function of the Ipl1/Aurora Kinase. Fort Belvoir, VA: Defense Technical Information Center, maj 2004. http://dx.doi.org/10.21236/ada432454.

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Starczynowski, Daniel. Regulation and Function of TIFAB in Myelodysplastic Syndrome. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2012. http://dx.doi.org/10.21236/ada567467.

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Starczynowski, Daniel. Regulation and Function of TIFAB in Myelodysplastic Syndrome. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2013. http://dx.doi.org/10.21236/ada585851.

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Balk, Steven P. Regulation of AR Degradation and Function by Ubiquitylation. Fort Belvoir, VA: Defense Technical Information Center, październik 2014. http://dx.doi.org/10.21236/ada615205.

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Doi, Roy H. Structure, Function and Regulation of the Clostridium cellulovorans Cellulosome. Office of Scientific and Technical Information (OSTI), czerwiec 2008. http://dx.doi.org/10.2172/951625.

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Surls, Jacqueline D. Regulation of CD4+ T-Cell Function by Membrane Cholesterol. Fort Belvoir, VA: Defense Technical Information Center, luty 2012. http://dx.doi.org/10.21236/ad1013280.

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Bhowmick, Neil A. Regulation and Function of Cytokines that Predict Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2012. http://dx.doi.org/10.21236/ada569356.

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