Relevant bibliographies by topics / Regulation function

Academic literature on the topic 'Regulation function'

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Published: 30 May 2022
Last updated: 31 May 2022

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Journal articles on the topic "Regulation function"

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Pandit, Abha, and Abhay Kumar Pandey. "Glycaemic regulation and metabolic syndrome: A reference to thyroid function state." Scholars Journal of Applied Medical Sciences 4, no. 6 (June 2016): 1906–8. http://dx.doi.org/10.21276/sjams.2016.4.6.7.

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Nakamura, Ichiro, Naoyuki Takahashi, Eijiro Jimi, Nobuyuki Udagawa, and Tatsuo Suda. "Regulation of osteoclast function." Modern Rheumatology 22, no. 2 (April 2012): 167–77. http://dx.doi.org/10.3109/s10165-011-0530-8.

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Luo, T., and J. V. Garcia. "Regulation of Nef function." Research in Virology 148, no. 1 (January 1997): 64–68. http://dx.doi.org/10.1016/s0923-2516(97)81916-4.

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Noonan, Emily, Robert Place, Charles Giardina, and Lawrence Hightower. "Hsp70B' Regulation and Function." Cell Stress & Chaperones preprint, no. 2007 (2005): 1. http://dx.doi.org/10.1379/csc-278.

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Noonan, Emily J., Robert F. Place, Charles Giardina, and Lawrence E. Hightower. "Hsp70B′ regulation and function." Cell Stress & Chaperones 12, no. 3 (2007): 219. http://dx.doi.org/10.1379/csc-278.1.

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Noonan, Emily J., Robert F. Place, Charles Giardina, and Lawrence E. Hightower. "Hsp70B′ regulation and function." Cell Stress & Chaperones 12, no. 4 (2007): 393. http://dx.doi.org/10.1379/csc-278e.1.

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Suda, Tatsuo, Ichiro Nakamura, Eijiro Jimi, and Naoyuki Takahashi. "Regulation of Osteoclast Function." Journal of Bone and Mineral Research 12, no. 6 (June 1, 1997): 869–79. http://dx.doi.org/10.1359/jbmr.1997.12.6.869.

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Zajac, J. D. "Regulation of parathyroid function." Bone 27, no. 4 (October 2000): 7. http://dx.doi.org/10.1016/s8756-3282(00)80017-4.

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Marcu, Kenneth B., Steven A. Bossone, and Amanda J. Patel. "myc Function and Regulation." Annual Review of Biochemistry 61, no. 1 (June 1992): 809–58. http://dx.doi.org/10.1146/annurev.bi.61.070192.004113.

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Woods, Douglas B., and Karen H. Vousden. "Regulation of p53 Function." Experimental Cell Research 264, no. 1 (March 2001): 56–66. http://dx.doi.org/10.1006/excr.2000.5141.

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Dissertations / Theses on the topic "Regulation function"

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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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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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Berry, David (David A. ). "Glycosaminoglycan regulation of cell function." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/34153.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Biological Engineering Division, 2005.
Includes bibliographical references (p. 252-285).
Glycosaminoglycans (GAGs) are complex polysaccharides that exist both on the cell surface and free within the extracellular matrix. The intrinsic sequence variety stemming from the large number of building blocks that compose this biopolymer leads to substantial information density as well as to the ability to regulate a wide variety of important biological processes. With the recent and progressive emergence of biochemical and analytical tools to probe GAG structure and function, efforts can be taken to understand the role of GAGs in cell biology and in disease in the various physiological locations where GAGs can exist. As a first step to probe the functions of GAGs, the heparin/heparan sulfate-GAG (HSGAG)-fibroblast growth factor (FGF) system was examined. Understanding the role of HSGAGs in inducing FGF2 dimerization led to the development of a novel engineered protein that was found to be effective at promoting functional recovery in stroke. Subsequently, methods to isolate HSGAGs from the cell surface were optimized and the ability of HSGAGs to support FGF signaling was investigated. Cell surface HSGAGs can define the responsiveness of a given cell to FGF1 and FGF2 through multiple receptor isoforms. Stromal cell derived HSGAGs were also identified as critical regulators of tumor cell growth and metastasis, effecting not only FGF2., but also 1-integrin signaling.
(cont.) Other GAGs, including dermatan sulfates, were characterized as modulators of FGFs and vascular endothelial growth factors. Finally, FGFs and HSGAGs were found to have important roles in maintaining epithelial monolayer integrity, with syndecan-l serving as a critical factor in inflammatory bowel disease. In addition to understanding HSGAGs in their normal physiological settings, techniques to internalize them were developed. Poly(3-amino ester)s were found to condense heparin and enable its endocytosis into cells. Internalized heparin is preferentially taken up by cancer cells, which often have a faster endocytic rate than non-transformed cells, and promotes apoptotic cell death. Internalized heparin can also be used as a tool to probe cell function. In Burkitt's lymphoma, poly(3-amino ester)-heparin conjugates served to identify cell surface HSGAGs as an important modulator of cell growth that can be harnessed to inhibit growth. Finally, studies that sought to broaden the scope of GAG biology were undertaken. Cell surface HSGA(:is were identified as mediators of vascular permeability. Furthermore a novel technique to immobilize GAGs was employed. The interactions between GAG and substrate were via hydrogen bonding. Immobilization of GAGs alters their properties, such that they can affect cells in ways distinct from GAGs free in the ECM.
(cont.) Furthermore, immobilized GAGs can regulate cancer cell adhesion, growth and progression, and may offer a new way to regulate the activity of cancer cells. In addition to directly providing new potential therapeutics and drug targets, these studies represent a foundation to enable additional studies of GAG function. Future work harnessing the techniques presented may open new avenues of research and facilitate the development of novel GAG-based therapeutics.
by David Berry.
Ph.D.
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Vespoli, Jessica L. "Genomic Regulation of Clock Function." Kent State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=kent1449500602.

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Tran, Stella Lê Minh. "Foxl2 regulation and function in gonadotropes." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116978.

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Pituitary follicle-stimulating hormone (FSH) is crucial for mammalian reproduction; it regulates gametogenesis and gonadal function. We know that impaired FSH production may leads to infertility, yet the mechanisms controlling FSH synthesis are poorly understood. Intra-pituitary activins stimulate FSHβ subunit (Fshb) gene transcription in gonadotrope cells, the rate-limiting step in FSH hormone synthesis. Studies conducted in immortalized gonadotrope cells indicate that activin A-stimulated Fshb gene transcription is dependent on homologs of Drosophila mothers against decapentaplegic (SMAD) proteins. More recently, the transcription factor forkhead box L2 (FOXL2) was reported to stimulate SMAD/activin A-induced Fshb transcription. Here, I focused on elucidating the mechanisms underlying Foxl2 regulation and function in gonadotrope cells. First, I demonstrated that overexpression of FOXL2 and SMAD 2, 3, and 4 confers activin-responsiveness to the murine Fshb promoter in heterologous cells. Upon activin A induction, FOXL2 synergizes with SMAD proteins to activate the Fshb promoter; this cooperation requires binding of both FOXL2 and SMAD3 (or SMAD4) to DNA. I showed that SMAD3-induction of the Fshb transcript is dependent on endogenous FOXL2 in homologous cells. I identified a proximal putative forkhead binding elements (FBE) and an adjacent SMAD binding element (SBE), that are crucial for FOXL2/SMAD3 induction of murine Fshb promoter-reporter activity. Based on previous data and my results, I propose a model where activins stimulate formation of FOXL2-SMAD2/3/4 complexes that drive murine Fshb transcription by binding to a conserved composite SBE/FBE element within the proximal promoter. FOXL2 plays a critical role in activin A-stimulated murine Fshb transcription in vitro. Next I tested the hypothesis that FOXL2 is required for FSH synthesis in vivo. Using a Cre/lox approach, I generated a conditional knockout (cKO) mouse where Foxl2 is selectively ablated in the anterior pituitary gonadotrope cells. I observed that cKO mice are hypogonadal and sub-fertile in adulthood. I showed that cKO mice exhibit impaired spermatogenesis and folliculogenesis. Indeed, cKO males have decreased sperm counts, whereas cKO females ovulate fewer oocytes during natural estrous cycles. I demonstrated that both male and female cKO mice are FSH-deficient, secondary to diminished pituitary Fshb mRNA production. In Foxl2-depleted primary pituitary cultures, both basal and activin A-stimulated Fshb expression is impaired. These results indicate that gonadotrope-specific FOXL2 is required for selective induction of FSH production in vivo. Besides its role in gonadotrope cells, FOXL2 is also expressed in the pituitary thyrotropes, the perioptic mesenchyme of the developing eyelid and the ovarian granulosa cells. However the mechanisms governing this selective expression have not been described. In order to study Foxl2 transcription, I cloned the murine promoter region of Foxl2. Next, I demonstrated a correlation between promoter CpG methylation status and gene expression, whereby methylation may repress Foxl2 expression in some heterologous cell lines. Our results indicate that Foxl2 is not regulated by its promoter sequence alone and unveil a possible role for CpG methylation in mediating Foxl2 cell-specific gene expression in the mouse. In summary, my thesis work defined a necessary role for pituitary FOXL2 in FSH synthesis and reproduction in vivo. The FSH deficiency observed in our gonadotrope-specific cKO mice is in agreement with the mechanisms describing a role for endogenous FOXL2 in murine Fshb transcription. Collectively, my research on pituitary FOXL2 is part of our unrelenting efforts to investigate the many factors implicated in FSH regulation, and ultimately required for normal reproductive function. This, in turn, may help identify causes of idiopathic infertility or novel drug targets for infertility and contraceptive treatments.
L'hormone folliculo-stimulante de l'hypophyse (FSH) est cruciale car elle régule gamétogenèse et fonction gonadique chez les mammifères. Une diminution dans la production de FSH peut mener à l'infertilité, mais les mécanismes contrôlant la synthèse de FSH demeurent incompris. Les activines de l'hypophyse stimulent la transcription du gène FSH sous-unité β (Fshb) dans les cellules gonadotropes; ceci est l'étape limitante dans la synthèse de l'hormone FSH. Les résults provenant de lignée gonadotrope immortalisée indiquent que la transcription de Fshb est stimulée par l'activine A; ceci est dépend des protéines homologues de Drosophila mothers against decapentaplegic (SMAD). Récemment, Forkhead box L2 (FOXL2) a été décrite comme étant un facteur-clé dans la stimulation de la transcription de Fshb induite par les SMADs et l'activine A. Ici, je dissèque les mécanismes expliquant la régulation et fonction de Foxl2 dans les cellules gonadotropes. Tout d'abord, la surexpression de FOXL2 et SMAD 2, 3, et 4 confère une réactivité à l'activine au promoteur du gène murin Fshb dans les cellules hétérologues. Sous stimulation par l'activine A, FOXL2 coopère de façon synergétique avec les SMADs pour activer le promoteur Fshb; cela nécessite que FOXL2 et SMAD3 (ou SMAD4) lient l'ADN. L'l'induction via SMAD3 du gène Fshb dépend de FOXL2 endogène dans les cellules homologues. Un élément proximal forkhead binding element (FBE) et un élément adjacent SMAD binding element (SBE) sont essentiels pour l'induction de l'activité du promoteur-reporter Fshb par FOXL2/SMAD3. Basé sur ces résultats, je propose un modèle où les activines stimulent la formation de complexes FOXL2-SMAD2/3/4 induisant la transcription du gène murinFshb via liaison à un élément SBE/FBE conservé du promoteur proximal. J'ai ensuite testé l'hypothèse que FOXL2 est nécessaire pour la synthèse de FSH in vivo en utilisant une approche Cre/lox: j'ai généré une souris knock-out conditionnelle (cKO) où Foxl2 est sélectivement absent dans les cellules gonadotropes. J'ai observé que les souris cKO sont hypogonadiques et souffrent d'une baisse de fertilité à l'âge adulte. J'ai démontré que la spermatogenèse et la folliculogénèse sont altérées chez les souris cKO. En effet, les cKO mâles ont un nombre diminué de spermatozoïdes, tandis que femelles cKO ovulent moins d'ovocytes pendant leur cycle oestral. J'ai démontré que cKO mâles et femelles sont déficientes en FSH, découlant d'une diminution d'ARN Fshb dans l'hypophyse. Les cultures primaires de cellules hypophysaires où Foxl2 est absent ne réagissent pas à l'activine A : Fshb est diminuée, tant au niveau basal que dans sa réponse au ligand. Ces résultats indiquent que l'expression de Foxl2 dans les gonadotropes est requise pour l'induction sélective de la production de FSH in vivo. Outre son rôle dans les gonadotropes, FOXL2 est également détecté dans les cellules thyrotropes de l'hypophyse, dans la paupière en développement et les cellules granuleuses de l'ovaire. Cependant les mécanismes qui régissent cette expression sélective n'ont pas encore été décrits. Afin d'étudier ce qui contrôle la transcription de Foxl2, j'ai cloné la région du promoteur murin de Foxl2. Ensuite, j'ai démontré une corrélation entre l'état de méthylation des CpGs du promoteur et l'expression des gènes, par lequel la méthylation exerce une inhibition sur le gène Foxl2 dans certaines cellules hétérologues. Mes résultats indiquent que Foxl2 n'est pas seulement contrôlé par la séquence de son promoteur et dévoilent un rôle possible pour la méthylation des CpGs dans la régulation de l'expression spécifique de Foxl2 chez la souris. En résumé, ma thèse définit un rôle nécessaire pour FOXL2 exprimé dans les gonadotropes pour la synthèse de Fshb et FSH, ainsi que la reproduction in vivo. Collectivement, mes recherches sur FOXL2 hypophysaire contribueront à identifier des causes de l'infertilité idiopathique ou encore trouver de nouvelles cibles pharmacologiques.
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Cheng, C. W. "Regulation of endothelial and endometrial function." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597573.

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Angiogenesis is highly regulated during reproduction, as vessel growth, maturation and regression are observed in cyclic endometrium. This thesis investigates the possible regulation of endothelial and endometrial function, mainly focused on Wnt signalling, in angiogenesis and the female reproductive tract. The transcript profiles in a murine model of menstruation were also studied using two independent microarray experiments and platforms, which provide a broader view of molecular processes during menstruation. The major findings of this thesis include: 1) mRNAs encoding many Wnt signalling-related molecules are present in human umbilical vein endothelial cells and female reproductive tissues. 2) Wnt signalling has a role in endothelial cell growth control and this is mediated through cell-cell contact. 3) Wnt signalling is tightly regulated in endothelial cells and endometrium through the balance of positive and negative regulators of Wnt signalling pathway. There is also a tight balance between the canonical pathway and the non-canonical pathway. 4) Transcript levels of genes involved in many molecular processes changed during the time-course of a murine model of menstruation, suggesting that these molecule processes, including immune response, cell growth and maintenance, metabolism, transport and cell-cell interaction, are regulated during menstruation and participate in regulating endometrial function. These results provide further insights into the complexity of endometrial function and offer new therapeutic possibilities for the treatment of gynaecological disease.
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English, Jane Louise. "Cellular regulation of matrix metalloproteinase function." Thesis, University of East Anglia, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247107.

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Raghavan, Srikala. "Connectin function and regulation in Drosophila." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624670.

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BERCLAZ, PIERRE-YVES. "REGULATION OF ALVEOLAR MACROPHAGE IMMUNE FUNCTION." University of Cincinnati / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1022869185.

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Books on the topic "Regulation function"

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C, Froehner Stanley, and Bennett Vann, eds. 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. 2nd ed. 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, and Walter Zimmermann, eds. 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, and Gabor M. Rubanyi, eds. 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, and Satya P. Kalra, eds. 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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Book chapters on the topic "Regulation function"

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Chen, Xi, Wai-Ki Ching, and Nam-Kiu Tsing. "Regulation Function." In 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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Bonavida, Ben, and Elizabeth Simpson. "Function of Effector T Cells." In Immune Regulation, 363–67. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-4996-2_43.

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Sugino, Norihiro, Isao Tamura, Ryo Maekawa, and Kosuke Jozaki. "Decidualization and Epigenetic Regulation." In Uterine Endometrial Function, 125–37. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55972-6_8.

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McNaughton, L., A. Radomski, G. Sawicki, and Marek W. Radomski. "Regulation of Platelet Function." In Nitric Oxide, 235–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57077-3_11.

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Okada, Hidetaka, Tomoko Tsuzuki, Hiromi Murata, Atsushi Kasamatsu, Tomoo Yoshimura, and Hideharu Kanzaki. "Regulation of Angiogenesis in the Human Endometrium." In Uterine Endometrial Function, 83–103. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55972-6_6.

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Cerottini, J. C., H. R. MacDonald, J. Lowenthal, and R. Shimonkevitz. "Non Antigen-Specific Surface Molecules Involved in T Lymphocyte Function." In Immune Regulation, 27–38. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-4996-2_3.

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Riedl, Stefan J., and Fiona L. Scott. "Caspases: Activation, Regulation, and Function." In Essentials of Apoptosis, 3–24. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-381-7_1.

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van Wimersma Greidanus, T. B., and A. B. Grossman. "Opioid Regulation of Pituitary Function." In Progress in Sensory Physiology, 1–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75964-2_1.

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Kirchheim, H. R. "Baroreceptor Regulation of Renal Function." In Baroreceptor Reflexes, 181–208. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76366-3_7.

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Baslé, Arnaud, and Anne H. Delcour. "Regulation of Bacterial Porin Function." In Bacterial and Eukaryotic Porins, 79–98. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527603875.ch5.

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Conference papers on the topic "Regulation function"

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Karkanaki, Artemis. "SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTION AND REPRODUCTIVE MEDICINE: CURRENT PROBLEMS." In MODERN PROBLEMS IN SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTIONS. NPG Publishing, 2019. http://dx.doi.org/10.24108/5-2019-confnf-2.

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Shukurova, P., Kh Babayev, S. Gasanova, and G. Gasimova. "EXPERIMENTAL EVALUATION OF THE SAFFRON (CROCUS SATIVUS L. İRIDACEAE) ON THE ANIMALS REPRODUCTIVE FUNCTION." In MODERN PROBLEMS IN SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTIONS. NPG Publishing, 2019. http://dx.doi.org/10.24108/5-2019-confnf-84.

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Zhu, Yuncheng, and Okita Hideki. "Traffic management using value function-based regulation." In 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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Sokol, Nicholas. "Regulation and function oflet-7-ComplexmicroRNAs inDrosophila melanogaster." In 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, and Ane Fany Novitasari. "Regulation on Independent Function of Financial Services Authority." In 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." In ADVANCES IN BASIC SCIENCE (ICABS 2019). AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5122367.

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Wan, Qingfeng, and Wenbin Zhang. "Study of Cellular Immune Function and Regulation Measurement." In 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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Yang, Yizeng, Taicheng Zhou, Zhen Zong, Gwen Lomberk, Raul Urrutia, and Jonathan Katz. "Abstract 2087: Regulation of p53 function by KLF5." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2087.

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"Update status of mouse resources for studies of gene function and disease at RIKEN BRC." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-248.

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Velontrasina, Irène, Denis Payet, and Rémy Courdier. "Regulation Function for Agent Adaptation Issues in Ambient Environment." In the 11th International Conference. New York, New York, USA: ACM Press, 2019. http://dx.doi.org/10.1145/3307363.3307376.

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Reports on the topic "Regulation function"

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

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Meidan, Rina, and Robert Milvae. Regulation of Bovine Corpus Luteum Function. United States Department of Agriculture, March 1995. http://dx.doi.org/10.32747/1995.7604935.bard.

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The main goal of this research plan was to elucidate regulatory mechanisms controlling the development, function of the bovine corpus luteum (CL). The CL contains two different sterodigenic cell types and therefore it was necessary to obtain pure cell population. A system was developed in which granulosa and theca interna cells, isolated from a preovulatory follicle, acquired characteristics typical of large (LL) and small (SL) luteal cells, respectively, as judged by several biochemical and morphological criteria. Experiments were conducted to determine the effects of granulosa cells removal on subsequent CL function, the results obtained support the concept that granulosa cells make a substaintial contribution to the output of progesterone by the cyclic CL but may have a limited role in determining the functional lifespan of the CL. This experimental model was also used to better understand the contribution of follicular granulosa cells to subsequent luteal SCC mRNA expression. The mitochondrial cytochrome side-chain cleavage enzyme (SCC), which converts cholesterol to pregnenolone, is the first and rate-limiting enzyme of the steroidogenic pathway. Experiments were conducted to characterize the gene expression of P450scc in bovine CL. Levels of P450scc mRNA were higher during mid-luteal phase than in either the early or late luteal phases. PGF 2a injection decreased luteal P450scc mRNA in a time-dependent manner; levels were significantly reduced by 2h after treatment. CLs obtained from heifers on day 8 of the estrous cycle which had granulosa cells removed had a 45% reduction in the levels of mRNA for SCC enzymes as well as a 78% reduction in the numbers of LL cells. To characterize SCC expression in each steroidogenic cell type we utilized pure cell populations. Upon luteinization, LL expressed 2-3 fold higher amounts of both SCC enzymes mRNAs than SL. Moreover, eight days after stimulant removal, LL retained their P4 production capacity, expressed P450scc mRNA and contained this protein. In our attempts to establish the in vitro luteinization model, we had to select the prevulatory and pre-gonadotropin surge follicles. The ratio of estradiol:P4 which is often used was unreliable since P4 levels are high in atretic follicles and also in preovulatory post-gonadotropin follicles. We have therefore examined whether oxytocin (OT) levels in follicular fluids could enhance our ability to correctly and easily define follicular status. Based on E2 and OT concentrations in follicular fluids we could more accurately identify follicles that are preovulatory and post gonadotropin surge. Next we studied OT biosynthesis in granulosa cells, cells which were incubated with forskolin contained stores of the precursor indicating that forskolin (which mimics gonadotropin action) is an effective stimulator of OT biosynthesis and release. While studying in vitro luteinization, we noticed that IGF-I induced effects were not identical to those induced by insulin despite the fact that megadoses of insulin were used. This was the first indication that the cells may secrete IGF binding protein(s) which regonize IGFs and not insulin. In a detailed study involving several techniques, we characterized the species of IGF binding proteins secreted by luteal cells. The effects of exogenous polyunsaturated fatty acids and arachidonic acid on the production of P4 and prostanoids by dispersed bovine luteal cells was examined. The addition of eicosapentaenoic acid and arachidonic acid resulted in a dose-dependent reduction in basal and LH-stimulated biosynthesis of P4 and PGI2 and an increase in production of PGF 2a and 5-HETE production. Indomethacin, an inhibitor of arachidonic acid metabolism via the production of 5-HETE was unaffected. Results of these experiments suggest that the inhibitory effect of arachidonic acid on the biosynthesis of luteal P4 is due to either a direct action of arachidonic acid, or its conversion to 5-HETE via the lipoxgenase pathway of metabolism. The detailed and important information gained by the two labs elucidated the mode of action of factors crucially important to the function of the bovine CL. The data indicate that follicular granulosa cells make a major contribution to numbers of large luteal cells, OT and basal P4 production, as well as the content of cytochrome P450 scc. Granulosa-derived large luteal cells have distinct features: when luteinized, the cell no longer possesses LH receptors, its cAMP response is diminished yet P4 synthesis is sustained. This may imply that maintenance of P4 (even in the absence of a Luteotropic signal) during critical periods such as pregnancy recognition, is dependent on the proper luteinization and function of the large luteal cell.
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Tublitz, Nathan. Neural Regulation Of Chromatophore Function In Cephalopods. Fort Belvoir, VA: Defense Technical Information Center, May 2015. http://dx.doi.org/10.21236/ada619935.

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Lers, Amnon, and Pamela J. Green. LX Senescence-Induced Ribonuclease in Tomato: Function and Regulation. United States Department of Agriculture, September 2003. http://dx.doi.org/10.32747/2003.7586455.bard.

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Natural leaf senescence, which occurs even when growth conditions are near optimal, has a negative influence on yield. Postharvest induced senescence contributes to the losses of quality in flowers, foliage, and vegetables. Strategies designed to control the senescence process in crop plants could therefore have great applied significance. However, the successful design of such strategies requires a better insight into the senescence machinery and control in higher plants. A main feature of senescence is the hydrolysis of macromolecules by hydrolases of various types such as ribonucleases (RNases) and proteases. Previously we had identified and characterized the tomato LX RNase gene demonstrating its transcript to be highly and specifically induced during senescence. This reported study was focused on LX but also had broadened our research to other senescence-associated nucleic acids degrading enzymes to learn about their function and the regulation of their encoding genes. Beside tomato we used parsley and Arabidopsis for the study of: the bi-functional nuclease which has a role in senescence. The study of different senescence- associated nucleases in few plant systems will allow a more general view on function and regulation of these enzymes in senescence. The specific original proposed objectives included: 1. Study the consequences of alterations in LX RNase level on tomato leaf senescence and general development; 2. Analyze stimuli which may participate in senescence-specific activation of the LX gene; 3. Clone the senescence-associated BFNI nuclease gene homologue from tomato. 4. Further characterize the sequences required for senescence-specific gene expression. Homozygous transgenic plants in which LX gene was either inhibited or over-expressed were generated. In both of these LX mutated plants no major phenotypic consequences were observed, which may suggests that LX is not essential for plant growth under optimal growth conditions. Lack of any abnormalities in the LX over-expressing lines suggests that special system exist to allow function of the RNase only when needed. Detailed analyses of growth under stress and consequences to RNA metabolism are underway. We have analyzed LX expression on the protein level demonstrating that it is involved also in petal senescing. Our results suggest that LX is responding to complex regulation involving developmental, organ dependent factors and responds differently to hormonal or environmental stimuli in the different plant organs. The cloned 1.4 kb promoter was cloned and its analysis revealed that probably not all required elements for senescence induction are included. Biochemical analysis of senescence-associated be-functional nucleases in the different plants, tomato, parsley and Arabidopsis, suggests they belong to a sub-class within the type I plant nucleases. The parsley PcNUC1/2 nuclease protein was purified from senescing leaves its and activity was studied in vitro revealing endo-, double strand, nucleolytic activity and exo-nucleolytic activity. Its encoding gene was cloned and found to be induced on the mRNA level. The promoter of the related Arabidopsis BFNI nuclease was shown in both tomato and Arabidopsis to be able and direct senescence-specific expression suggesting that, at least part, the gene is regulated on the transcriptional level and that the mechanism for this senescence-specific regulation is conserved between different plants. Few plants in which the BFNI gene is mutated were identified which are subjected now to detailed analysis. Our results suggest that the senescence-related nucleic acid degrading enzymes share similarities in both function and regulation between different plants and possibly have important functions in processes un-related to senescence. Still, the function of these enzymes, at least in some cases is not essential to plant development under optimal growth conditions. We are now at the stage which permits in depth investigation of the specific functions and mode of molecular regulation of senescence-associated nucleases with the aid of the research tools developed. The isolated senescence-specific promoter, shown to be active in heterologous plant system, could be utilized in agricultural-related biotechnological applications for retardation of senescence.
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Starczynowski, Daniel. Regulation and Function of TIFAB in Myelodysplastic Syndrome. Fort Belvoir, VA: Defense Technical Information Center, August 2014. http://dx.doi.org/10.21236/ada613223.

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Kotwaliwale, Chitra, and Sue Biggins. Regulation and Function of the Ipl1/Aurora Kinase. Fort Belvoir, VA: Defense Technical Information Center, May 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, June 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, June 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, October 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), June 2008. http://dx.doi.org/10.2172/951625.

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