Relevant bibliographies by topics / Negative regulators

Academic literature on the topic 'Negative regulators'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Negative regulators.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Negative regulators"

1

Thomson, Christopher W., Boris P. L. Lee, and Li Zhang. "Double-Negative Regulatory T Cells: Non-conventional Regulators." Immunologic Research 35, no. 1-2 (2006): 163–78. http://dx.doi.org/10.1385/ir:35:1:163.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Massagué, Joan, and Robert A. Weinberg. "Negative regulators of growth." Current Opinion in Genetics & Development 2, no. 1 (February 1992): 28–32. http://dx.doi.org/10.1016/s0959-437x(05)80317-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Pouwels, J., J. Nevo, T. Pellinen, J. Ylanne, and J. Ivaska. "Negative regulators of integrin activity." Journal of Cell Science 125, no. 14 (July 15, 2012): 3271–80. http://dx.doi.org/10.1242/jcs.093641.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Frank, Steven A., and Paul Schmid-Hempel. "Evolution of negative immune regulators." PLOS Pathogens 15, no. 8 (August 1, 2019): e1007913. http://dx.doi.org/10.1371/journal.ppat.1007913.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Kile, Benjamin T., Nicos A. Nicola, and Warren S. Alexander. "Negative Regulators of Cytokine Signaling." International Journal of Hematology 73, no. 3 (April 2001): 292–98. http://dx.doi.org/10.1007/bf02981953.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Monticelli, Silvia, and Federica Sallusto. "Negative regulators take center stage." Nature Immunology 13, no. 8 (July 19, 2012): 719–20. http://dx.doi.org/10.1038/ni.2377.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Johnson, Terry C. "Negative regulators of cell proliferation." Pharmacology & Therapeutics 62, no. 1-2 (January 1994): 247–65. http://dx.doi.org/10.1016/0163-7258(94)90013-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Wang, John L., and Yen-Ming Hsu. "Negative regulators of cell growth." Trends in Biochemical Sciences 11, no. 1 (January 1986): 24–26. http://dx.doi.org/10.1016/0968-0004(86)90227-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

HARDT, S. "Negative regulators of cardiac hypertrophy." Cardiovascular Research 63, no. 3 (August 2004): 500–509. http://dx.doi.org/10.1016/j.cardiores.2004.03.015.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Ellis, Ronald E. "Negative regulators of programed cell death." Current Opinion in Genetics & Development 2, no. 4 (January 1992): 635–41. http://dx.doi.org/10.1016/s0959-437x(05)80184-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Negative regulators"

1

Lively, Julie C. (Julie Christina) 1971. "Beta 3 integrins : negative regulators of angiogenesis." Thesis, Massachusetts Institute of Technology, 2002. http://hdl.handle.net/1721.1/8386.

Full text
Abstract:
Thesis (Ph.D.)--Massachusetts Institute of Technology, Dept. of Biology, 2002.
Includes bibliographical references (leaves 199-219).
A method was developed to isolate and purify primary murine endothelial cells from lung tissue (MLEC). The cells generated by this method were characterized by immuno-fluorescence detection and FACS analysis and expressed specific antigens including PECAM-1, ICAM-1, ICAM-2, VCAM-1 and VE-cadherin. Using this method, cells from wild-type and beta 3-integrin-deficient animals were purified and used to determine the specificity of a novel potential anti-angiogenic drug. This study shows that tumstatin, a fragment of the alpha 3 chain of collagen IV, inhibits proliferation, inhibits total protein synthesis and specifically inhibits CAP-dependent protein synthesis in MLEC. These effects do not occur when beta 3-null MLEC are treated with tumstatin or any of its derivatives. Nor do they occur in mouse embryonic fibroblasts which do express beta 3 integrin. The inhibition by tumstatin also occurs in in vivo angiogenesis assayed using a Matrigel plug insert. Similarly to in vitro assays, tumstatin failed to inhibit angiogenesis in beta 3 integrin-deficient animals. These results suggest that avf33 integrin is necessary but not sufficient for the activity of tumstatin. Further studies are required to identify avf33 integrin-associated factors in endothelial cells which determine tumstatin's endothelial cell specificity. Matrigel plug assays were also used to demonstrate that the loss of beta-3 integrin enhanced VEGF-induced angiogenesis. Results also show that VEGF-induced angiogenesis was enhanced in aortic ring explants from beta 3-null animals. These data suggest a new role for beta 3 integrin as a negative regulator of angiogenesis, both as a receptor for an endogenous inhibitory molecule and as an inhibitor of VEGF-induced angiogenesis.
by Julie C. Lively.
Ph.D.
APA, Harvard, Vancouver, ISO, and other styles
2

Kearns, Jeffrey D. "Distinct functions of negative regulators of NF-kappaB." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p3360060.

Full text
Abstract:
Thesis (Ph. D.)--University of California, San Diego, 2009.
Title from first page of PDF file (viewed August 11, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 197-205).
APA, Harvard, Vancouver, ISO, and other styles
3

Datar, Ila. "Positive and negative regulators of tumorigenesis and/or metastasis." University of Toledo Health Science Campus / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=mco1438962728.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Subedee, Ashim. "Molecular Determinants and Transcriptional Regulators in Triple Negative Breast Cancer." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:23845415.

Full text
Abstract:
Breast cancer is a highly heterogeneous disease with differences in histopathological and biological characteristics, variable prognoses, and response to therapy. Clinically, breast tumors are classified based on the expression of hormone receptors (ER and PR) and HER2 as hormone receptor positive (ER+, PR+), HER2+, and triple negative (ER-, PR-, HER2-). Based on gene expression profiling, breast cancers have been classified into luminal (luminal A and B), HER2+, basal-like and claudin-low subtypes. Knowledge of the molecular properties of luminal and HER2+ subtypes has led to the development of endocrine and HER2-targeted therapies. However, the molecular determinants and transcriptional regulators of basal-like tumors that constitute the majority of triple negative breast cancer (TNBC) are poorly understood. In this dissertation, we have defined some of the molecular characteristics of the basal-like breast cancer phenotype and also identified multiple transcriptional regulators specific to TNBCs. By using three different reprogramming approaches – somatic cell fusion, nuclear reprogramming, and transcription factor transduction, we showed that the basal-like breast cancer phenotype is generally dominant and is largely defined by epigenetic repression of luminal transcription factors. We found that luminal breast cancers share a common core epigenetic program, whereas basal-like breast cancers are highly heterogeneous. We demonstrated that protein extracts of basal-like breast cancer cells can reprogram a subset of luminal breast cancer cells to a basal-like state. Additionally, we identified three transcription factors, EN1, TBX18, and TCF4, the overexpression of which induced the repression of some luminal features in luminal breast cancer cells. We also performed a targeted cellular viability screen for selected transcription factors differentially expressed between triple negative and other breast cancer subtypes and identified multiple factors essential for TNBCs including EN1 and TRIP13. We found that downregulation of EN1 and TRIP13 preferentially and significantly reduce cellular viability, colony formation, and in vivo tumorigenicity of TNBC cell lines. We demonstrated that downregulation of EN1 induces an arrest in the G1 phase of the cell cycle and apoptosis. By analyzing the gene expression and histone H3 lysine 27 acetylation (H3K27ac) profiles of TNBC cell lines following downregulation of EN1, we found that EN1 regulates genes involved in angiogenesis, neurogenesis, cell matrix interactions, and WNT signaling pathways. We also performed ChIP-seq for exogenously expressed HA-tagged EN1 to identify its genomic targets. Lastly, we showed that the expression of EN1 correlates with shorter overall survival among patients with basal-like breast tumors. Similarly, by analyzing the gene expression profiles of TNBC cell lines following downregulation of TRIP13, we found that TRIP13 regulates genes involved in IL6 signaling, cell proliferation, and angiogenesis; in line with this we confirmed reduced levels of JAK2 and phospho-STAT3 following TRIP13 downregulation. In summary, we have unraveled some of the molecular mechanisms of basal-like and luminal breast cancer cell phenotypes and identified factors that might repress luminal differentiation programs in basal-like breast tumors. We have also identified multiple triple negative breast cancer specific transcription regulators. We believe these studies have increased our molecular understanding of basal-like and triple negative breast cancers and have provided potential therapeutic targets for these breast tumors.
Medical Sciences
APA, Harvard, Vancouver, ISO, and other styles
5

Carlsson, Emil Karl Viktor. "Biochemical, molecular and cellular studies on negative regulators of TLR-signalling." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/38528.

Full text
Abstract:
Toll-like receptors (TLRs) recognise pathogenic microorganisms through conserved pathogen associated molecular patterns, which activates the innate immune response. TLR signalling is mediated by cytoplasmic adaptor proteins via Toll/interleukin-1 receptor (TIR) domains. Sterile α- and armadillo-motif-containing protein (SARM) is the fifth TLR adaptor protein identified in humans and has been described as a negative regulator of the innate immune response. Several pathogenic bacteria are also known to express proteins with TIR- domains, which are believed to be involved in disruption of TLR signalling. This raises the question of whether SARM functions in a similar manner, as phylogenetic studies have shown that SARM is closely related to bacterial proteins. In this project, functional characterisation of SARM and a bacterial TIR domain protein from Bacillus anthracis (BaTdp) have been performed using both recombinantly expressed and purified proteins, as well as cellular assays. The TIR domains of both SARM and BaTdp were found to form heterotypic TIR-TIR interactions with multiple human TLR adaptors, including Myeloid differentiation factor 88 (MyD88). SARM and MyD88 both localised to mitochondria when overexpressed in mammalian cells, and SARM overexpression was associated with a reduction of TLR2-, TLR4- and MyD88- induced cytokine activation. A single amino acid residue in the SARM BB-loop motif, G601, was also identified as being critical for SARM's anti-inflammatory effect. A short peptide derived from this motif was able to target MyD88 in vitro and slightly reduce TLR4-mediated cytokine activation. Overexpression of BaTdp in mammalian cells had no significant effect on TLR-mediated cytokine activation. Instead, the protein targeted microtubular networks in the cell and BaTdp expression was associated with a significant increase in cellular autophagy activity. The findings further enhance our understanding of the underlying mechanisms by which SARM suppress the innate immune response, and also describe previously unknown functions of BaTdp.
APA, Harvard, Vancouver, ISO, and other styles
6

Spencer, William John. "Negative regulators of chromosome replication in the dimorphic bacterium Caulobacter crescentus." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103183.

Full text
Abstract:
Caulobacter crescentus provides an accessible system for investigating the regulation of chromosome replication and cellular development. The Caulobacter cell cycle produces a free-swimming swarmer cell and a sessile stalk cell. In swarmer cells, chromosome replication is selectively repressed while stalk cells are committed to chromosome replication.
In Caulobacter, chromosome replication is repressed, in part, by the binding of the response regulator CtrA to five binding sites (a-e) within the Caulobacter origin of replication (Cori ). Periodic phosphorylation of CtrA stimulates binding to the consensus sequence TTAA-N7-TTAA (N= any nucleotide) found in Cori and many cell-cycle regulated genes. This thesis presents an alternate mode of CtrA binding, namely, that phosphorylation does not stimulate binding to a specific class of CtrA-regulated promoters. This work shows that CtrA and CtrA-phosphate bind to two ctrA promoters with equal and weak affinity. As well, in vivo binding assays reveal that a non-proteolyzable CtrA allele (CtrADelta3) can occupy the ctrA promoters continuously without altering the temporal regulation of these promoters. The data suggest phosphorylation, while not increasing affinity for weak CtrA binding sites, provides allosteric signals that permit the recruitment of components required for transcription.
The proposed allosteric mechanism of CtrA-regulated transcription may also be important for CtrA-mediated repression of chromosome replication. Chromatin Immunoprecipitation assays (ChIP) allow for the sensitive detection of specific protein/DNA complexes in vivo. ChIP reveals that CtrA binds to Cori in swarmers but not in stalk cells when chromosome replication commences. The protein chaperone, ClpX, was recruited to Cori prior to the start of S-phase and correlates with the loss of CtrA binding to Cori. Expression of a non-proteolyzable CtrADelta3 allele showed increased affinity for Cori DNA. The increase in CtrADelta3 binding stimulated a corresponding increase in C1pX binding to Cori. This evidence suggests that C1pX recruitment to Cori is likely CtrA-dependant. The absence of CtrA binding in stalk cells suggests other mechanisms may be required to prevent re-replication in stalk cells.
An analysis of the Caulobacter genome identifies two DnaA-like genes. The first, cdl-1, is a homolog of the E. coli hda gene, a protein essential for regulated inactivation of DnaA (RIDA). The second, cdl-2, is a novel gene restricted to the alpha-proteobacteria group and whose function is unknown. Overexpression of either gene in Caulobacter produced filamentous cells that could not divide. DNA synthesis in these cells is also impaired and suggests the intracellular concentrations of these two proteins are important for coordinating proper cell cycle progression.
APA, Harvard, Vancouver, ISO, and other styles
7

Hooker, Erika. "Negative regulators of the Src family kinases in renal epithelial cells." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116932.

Full text
Abstract:
The Src kinases are non-receptor tyrosine kinases involved in many epithelial processes in both normal and injured cells. Src was originally identified as a viral oncogene and has since been characterized as an important regulator of cellular proliferation, differentiation, and motility. Our lab has previously demonstrated that the Src kinases are important modifiers of gene expression in tubule cells of the kidney during ischemia-reperfusion injury. The signalling events that control and mediate the Src kinase transcriptional response in renal epithelial cells are not well understood. In this thesis, I have identified two novel negative regulators of the Src transcriptional response in renal epithelial cells. In Manuscript I and II, I demonstrate that the adapter protein Dok-4 can act as an inhibitor of Src-mediated transcription. Unlike most other adapter proteins, several members of the Dok family are primarily characterized by their inhibitory actions downstream of active tyrosine kinases. Despite being the most ubiquitously expressed Dok family member, Dok-4 function has remained elusive as few interacting proteins have been identified. In Manuscript I, we found that the previously defined boundaries of the Dok-4 PTB domain needed to be extended for proper function. We demonstrate that the PTB domain of Dok-4 contains an extended C-terminal alpha helix critical for canonical PTB-mediated interaction and identified the lipid phosphatase Ship1 as a novel partner of this redefined Dok-4 PTB domain. This interaction is greatly increased in the presence of active Src kinases and occurs through a canonical NPXpY motif present in the C-terminal region of Ship1. In contrast to the Dok-4-Ship1 interaction, in Manuscript II we present a non-canonical PTB-mediated interaction between Dok-4 and the nuclear transcription factor, Elk4. This interaction leads to relocalization of Elk4 from the nucleus to the cytoplasm and degradation of full-length Elk4. In renal cells, Dok-4 inhibits Src-mediated activation of Elk4 and represses expression of the immediate early genes, such as egr-1 and fos1, as well as some of their transcriptional targets. In agreement with this data, knock-down of Dok-4 was associated with increased proliferation of renal epithelial cells. During renal ischemia-reperfusion injury, where upregulation of immediate early genes is known to occur, we have for the first time detected a strong activation of the Src kinases and a delayed upregulation of Elk4, suggesting that Elk4 may be not only highly expressed, but also highly active. Dok-4, which is expressed in the kidney, may be essential for limiting damage to the kidney caused by Elk4-induced expression of the immediate early genes. In addition to activating transcription of the immediate early genes, we have previously shown that the Src kinases are responsible for transcriptionally upregulating the receptor tyrosine kinase, EphA2, during renal ischemia-reperfusion injury. In the preliminary manuscript presented here, we observed that while the Src kinases are highly active, the Stat proteins, downstream effectors of the Jak kinases, are dephosphorylated and inactive. As a corollary of this observation, overexpression of all three ubiquitous Jak family members, Jak1, Jak2 and Tyk2 could attenuate Src-mediated activation of the EphA2 promoter. Inhibition of endogenous Jak kinase by siRNA-mediated knock-down or incubation with the pharmacological inhibitor, Jak inhibitor I also activated EphA2 transcription. Surprisingly, Jak-mediated inhibition of EphA2 expression occurs independently of the Stat family and the cytokine receptors. Collectively, this thesis identifies two novel regulators of the Src kinase family in renal epithelial cells, the Dok-4 adapter protein and the family of Jak kinases.
Les kinases Src sont des tyrosine-kinases cytosoliques qui sont impliquées dans multiples processus dans les cellules épithéliales et autres. Originalement identifiée comme un oncogène viral, la kinase Src est maintenant caractérisée comme une régulatrice de la prolifération, la différenciation et la motilité cellulaire. Nous avons précédemment montré que les kinases Src sont capables de modifier l'expression génique dans les tubules des reins durant le domage rénal par ischémie et réperfusion. Cependant, les mécanismes de signalisation qui contrôle la réponse transcriptionelle des kinases Src ne sont pas bien compris. La présente thèse décrit deux nouveaux inhibiteurs endogènes de la famille de kinases Src dans les cellules rénale épithéliales.Les deux premiers manuscrits établissent que la protéine adaptatrice Dok-4 fonctionne comme un inhibiteur des kinases Src. Contrairement à la plus part de protéines adaptatrices, la famille Dok est caractérisée par des actions inhibitrices durant la signalisation par les tyrosines kinases. Malgré que Dok-4 soit le membre de la famille Dok exprimé de manière la plus ubiquitaire, sa fonction est encore mal connue. Le premier manuscrit que je présente (Manuscrit I) décrit le domaine PTB de Dok-4. On y a démontré que le domaine PTB contient une extension C-terminal consistant probablement en une hélice alpha et que celle-ci est essentielle pour les interactions canoniques du domaine PTB de Dok-4. De plus, nous avons identifié la phosphatase lipidique Ship1 comme un nouveau partenaire de ce domaine PTB redéfini. Cette interaction est augmentée quand les kinases Src sont actives et elle implique un motif NPXpY dans la région C-terminale de Ship1. Contrairement à l'interaction entre Dok-4 et Ship1, l'interaction décrite dans le deuxième manuscrit (Manuscrit II) entre Dok-4 et le facteur de transcription, Elk4, implique le domaine PTB, mais se fait dans une manière atypique. L'interaction entre Dok-4 et Elk4 induit la relocalisation d'Elk4 du noyau au cytoplasme et cause la dégradation de la protéine Elk4. Dans les cellules rénales, Dok-4 inhibe l'activation d'Elk4 par les kinases Src et réprime l'expression des gènes de réponse précoce ("immediate early genes"), comme egr-1 et fos, et quelques cibles transcriptionelles de ces gènes. En accord avec ces données, suppression de Dok-4 est associée avec une augmentation de prolifération. En utilisant un modèle in vivo d'ischémie-reperfusion rénale, où la surexpression de gène de réponse précoce a déjà été démontrée, nous avons détecté une forte activation des kinases Src suivie d'une augmentation retardée de l'expression d'Elk4 dans les lysates de reins. Ces données suggèrent que dans ce modèle Dok-4 pourrait être critique pour limiter les dommages aux reins causé par l'induction des gènes de réponse précoce par Elk4. En plus d'activer l'expression des gènes de réponse précoce, nous avons précédemment montré que les kinases Src sont impliquées dans l'induction transcriptionnelle du récepteur tyrosine-kinase, EphA2, durant l'ischémie-reperfusion rénale. Dans le manuscrit préliminaire que je présente, nous avons noté que dans un modèle de déplétion et réplétion d'ATP, les kinases Src sont activées et les protéines Stat, des effecteurs des kinases Jak, sont déphsophorylés et inactives. Comme corollaire de cette observation, la surexpression de trois membres de de la famille Jak inhibent l'activation du promoteur d'EphA2 par les Src kinases. En plus, l'inhibition des kinases Jak endogènes par traitement aux siRNA ou par un inhibiteur pharmacologique, Jak Inhibitor I, active le promoteur d'EphA2. Étonnement, l'inhibition de l'expression d'EphA2 par les kinases Jak se fait indépendamment des protéines Stat et les récepteurs à cytokines. Mises ensemble, les données de cette thèse démontrent deux nouveaux inhibiteurs de la famille Src dans les cellules rénales épithéliales, la protéine adaptatrice, Dok-4 et les kinases, Jak1 et Jak2.
APA, Harvard, Vancouver, ISO, and other styles
8

Evans, Abigail Alexandra. "An analysis of selected negative regulators of growth in breast cancer." Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287979.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Gadbois, Ellen L. (Ellen Louise) 1968. "Functional antagonism of the RNA polymerase II holoenzyme by negative regulators." Thesis, Massachusetts Institute of Technology, 1997. http://hdl.handle.net/1721.1/43553.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Miller, Allan. "Negative regulators of gene expression in yeast : a1/α2 and SIR." Thesis, University of Cambridge, 1987. https://www.repository.cam.ac.uk/handle/1810/270426.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Negative regulators"

1

McPhee, Jennifer. ID-1 and GDF-8 as negative regulators of skeletal muscle mass. Sudbury, Ont: Laurentian University, Behavioural Neuroscience Program, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Beth, McNeil, and Johnson Denise J, eds. Patron behavior in libraries: A Handbook of Positive Approaches to Negative Situations. Chicago: American Library Association, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Retnakaran, Ravi. Identification of RVR, a novel orphan nuclear receptor that acts as a negative regulator of transcription. Ottawa: National Library of Canada, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

ek, Slavoj Z. iz. Tarrying with the negative: Kant, Hegel, and the critique of ideology. Durham: Duke University Press, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Li, Georgia Xiaojie. Both positive and negative regulatory elements may be required for the expression of the human VAMP-1 gene. Ottawa: National Library of Canada, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Philippines. Foreign Investments Act of 1991, R.A. 7042: As amended by R.A. 8179 : implementing rules and regulations : second regular foreign investment negative list. [Makati, Metro Manila, Philippines: Dept. of Trade and Industry, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Grafkina, Marina. Labor protection. ru: INFRA-M Academic Publishing LLC., 2021. http://dx.doi.org/10.12737/1173489.

Full text
Abstract:
The textbook contains information on the legal, regulatory, organizational, and technical bases of labor protection; on the identification of dangerous and harmful factors; and on the impact of various negative factors on human health. Methods and means of protecting a person from the effects of harmful and dangerous industrial factors are disclosed. Meets the requirements of the federal state educational standards of secondary vocational education of the latest generation, approximate educational programs (in terms of the discipline "Labor Protection") in the specialties 15.02.15 "Technology of metalworking production"; 15.02.11 "Technical operation and maintenance of robotic production"; 15.02.14 " Equipment with automation tools for technological processes and production (by industry)". It is intended for students of secondary vocational educational institutions, and can also be used when conducting classes for university students in the main educational programs of the bachelor's degree in the discipline "Labor Protection".
APA, Harvard, Vancouver, ISO, and other styles
8

United States. Congress. House. Committee on Banking, Finance, and Urban Affairs. Subcommittee on Financial Institutions Supervision, Regulation, and Deposit Insurance. Agency actions to reduce the negative impact of regulations on credit availability: Hearing before the Subcommittee on Financial Institutions Supervision, Regulation, and Deposit Insurance of the Committee on Banking, Finance, and Urban Affairs, House of Representatives, One Hundred Third Congress, first session, June 29, 1993. Washington: U.S. G.P.O., 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Suryawan, Agus. Positive and negative regulators of adipocyte differentiation in primary culture. 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Negative regulators of hematopoiesis: Studies on their nature, action, and potential role in cancer therapy. New York, N.Y: New York Academy of Sciences, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Negative regulators"

1

Suchting, Steven, Catarina Freitas, Ferdinand le Noble, Rui Benedito, Christiane Bréant, Antonio Duarte, and Anne Eichmann. "Negative Regulators of Vessel Patterning." In Vascular Development, 77–86. Chichester, UK: John Wiley & Sons, Ltd, 2007. http://dx.doi.org/10.1002/9780470319413.ch7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Campion, Dennis R., and William Kelly Jones. "Regulation of Growth by Negative Growth Regulators." In Animal Growth Regulation, 123–40. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-8872-2_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Zimmermann, Wolfgang, and Robert Kammerer. "Negative Regulators in Cancer Immunology and Immunotherapy." In Experimental and Applied Immunotherapy, 229–49. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-980-2_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Henriksen, Melissa A., and Aurel Betz. "Negative Regulators of STAT Function in Drosophila." In Signal Transducers and Activators of Transcription (STATs), 609–21. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-3000-6_38.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Smolinski, Kara N., and Stephen J. Meltzer. "Inactivation of Negative Growth Regulators During Neoplastic Transformation." In The Molecular Basis of Human Cancer, 81–111. Totowa, NJ: Humana Press, 2002. http://dx.doi.org/10.1007/978-1-59259-125-1_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Wang, Helen Y., and Rong-Fu Wang. "Innate Immune Signaling and Negative Regulators in Cancer." In Innate Immune Regulation and Cancer Immunotherapy, 61–88. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9914-6_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Wright, E. G., and I. B. Pragnell. "The Stem Cell Compartment: Assays and Negative Regulators." In Current Topics in Microbiology and Immunology, 137–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76912-2_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Peluso, J. J. "Steroids as Negative Regulators of Granulosa Cell Proliferation and Differentiation." In Cell Culture in Pharmaceutical Research, 215–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-662-03011-0_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Murphy, Caroline, and Luke A. J. O’Neill. "Negative Regulators of NF-κB Activation and Type I Interferon Pathways." In Innate Immune Regulation and Cancer Immunotherapy, 267–87. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9914-6_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Saxena, Amit, and Nikolaos G. Frangogiannis. "Negative Regulators of Inflammation as Endogenous Protective Mechanisms in Postinfarction Remodeling." In Cardiac Remodeling, 313–30. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5930-9_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Negative regulators"

1

Kong, Moufu, Bin Wang, BingKe Zhang, Ke Huang, Jiaxin Guo, and Jiawei Xu. "Novel CMOS Positive and Negative Voltage Mutual Conversion Circuits and Regulators." In 2020 IEEE 15th International Conference on Solid-State & Integrated Circuit Technology (ICSICT). IEEE, 2020. http://dx.doi.org/10.1109/icsict49897.2020.9278190.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Hailemichael, Yared, Glenn Winn, and Michael Davies. "914 Regulating negative immune regulators to enhance immune checkpoint blockade antitumor potential." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0914.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Burnett, Joseph Patrick, Garrett Johnson, Nathan Truchan, Michael Brooks, Max S. Wicha, and Duxin Sun. "Abstract 500: Discovering epigenetic regulators of cells states in triple negative breast cancers." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-500.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Jizhen Fu, Zhiliang Zhang, W. Eberle, Yan-Fei Liu, and P. C. Sen. "A high efficiency current source driver with negative gate voltage for buck voltage regulators." In 2009 IEEE Energy Conversion Congress and Exposition. ECCE 2009. IEEE, 2009. http://dx.doi.org/10.1109/ecce.2009.5316231.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Hancock, BA, Y.-H. Chen, JP Solzak, MN Ahmad, DC Wedge, D. Brinza, C. Scafe, et al. "Abstract P2-07-04: Molecular regulators of resistance and relapse in chemorefractory triple-negative breast cancers." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-p2-07-04.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Гинда, Елена, and Наталья Трескина. "Использование регуляторов роста растений для реализации продуктивного потенциала столового сорта винограда велика в зависимости от гидротермических условий периода вегетации." In VIIth International Scientific Conference “Genetics, Physiology and Plant Breeding”. Institute of Genetics, Physiology and Plant Protection, Republic of Moldova, 2021. http://dx.doi.org/10.53040/gppb7.2021.37.

Full text
Abstract:
In field experience, the influence of two-fold processing of table grape plants was studied by the Gibber-ellin, Zircon and Epin extra growth regulators on the structure of the bunch, yield and saccharinity of berry juice depending on the hydrothermal conditions of the growing season. It was established that the treatment of grape plants of the Great variety by growth regulators allows to reduce the negative influence of adverse ex-ternal factors and increase the productivity and quality of grape berries. Under more humidified conditions, treatment of Epin Extra plants (3.2 ml/l) contributes to an increase in yield by 82%, in dry conditions - Zir-conom (0.6 ml/l) by 1.5 times compared to control. The use of growth regulators contributes to a greater ac-cumulation of sugar in the juice of berries.
APA, Harvard, Vancouver, ISO, and other styles
7

Lee, E., K. Ito, HY Irie, and J. Zhu. "Abstract P5-08-02: Identify key regulators to modulate chemo-sensitivity of triple negative breast cancer by integrative analysis." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-p5-08-02.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Worsham, MJ, KM Chen, I. Datta, JK Stephen, D. Chitale, and G. Divine. "Abstract P1-04-06: Network integration of epigenomic data: Leveraging the concept of master regulators in ER negative breast cancer." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p1-04-06.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Lee-Verges, Eriong, Arnau Montraveta, Magda Pinyol, Pedro Jares, Cristina Arimany-Nardi, Marta Aymerich, Neus Villamor, et al. "Abstract 993: Upregulation of B-cell activation genes and negative regulators of apoptosis determines resistance to bendamustine in chronic lymphocytic leukemia cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-993.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Worsham, Maria J., Kang Mei Chen, Indrani Datta, Josena K. Stephen, Dhananjay Chitale, and George Divine. "Abstract 4484: Differentially methylation between ER negative and ER positive breast cancer identifies master regulators to expose potential epigenetic drivers of aggressive disease." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4484.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Negative regulators"

1

Li, Luyuan. A Novel Negative Regulator of Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada390998.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Li, Luyuan. A Novel Negative Regulator of Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada391074.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Oviedo, Daniel, Daniel Perez Jaramillo, and Mariajosé Nieto. Governance and Regulation of Ride-hailing Services in Emerging Markets: Challenges, Experiences and Implications. Inter-American Development Bank, August 2021. http://dx.doi.org/10.18235/0003579.

Full text
Abstract:
This paper seeks to shed some light on the different considerations for regulation and governance of ride-hailing platforms in emerging markets, highlighting their positive and negative externalities. Building on an extensive review of the literature and secondary sources, we outline Ride-hailing's identified and potential effects on users (providers and consumers), incumbents, and society. Based on the welfare impacts structure, we identify the significant challenges that regulators face in understanding, monitoring, evaluating, and regulating this type of transportation innovation. Finally, the paper proposes a framework for approaching such mobility innovations from governance and regulation perspectives. In a context of exponential growth in research and innovation in urban mobility in general and Ride-hailing, a rigorous review of the literature and a critical framework for understanding governance and regulation in such services in rapidly changing contexts is a timely contribution.
APA, Harvard, Vancouver, ISO, and other styles
4

Galili, Gad, Harry J. Klee, and Asaph Aharoni. Elucidating the impact of enhanced conversion of primary to secondary metabolism on phenylpropanoids secondary metabolites associated with flavor, aroma and health in tomato fruits. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7597920.bard.

Full text
Abstract:
• Targeted manipulating Phenylalanine (Phe) synthesis is one of the most powerful strategies to boost the biologically and economically important secondary metabolites, including phenylpropaniods, aromatic volatiles and specialized secondary metabolites. • Over-expression of the petunia MYB transcript factor, ODORANT1 (ODO1), results in significant alterations of the levels of specific phenylpropanoid compounds in plants. • Our previous studies indicated that ectopic expression of the feedback-insensitive AroG could break the bottleneck between primary and secondary metabolisms in tomato, thereby aiding in producing new tomato composition and identifying the unknown roles of multiple key regulators in specialized metabolism. Therefore, combining the AroG and ODO1 is of particular interest for elucidating the combined regulatory role of both of these genes in the Phe metabolic pathway, as well as generating tomato fruits that contain higher levels of secondary metabolites. • Here, we performed the LC-MS and GC-MS analyses on fruits of four tomato genotypes, namely, wild type tomato fruits as well as tomato fruits expressing the AroG, ODO1 and the combination of AroG plus ODO1 (AO) genotypes. Our results elaborated that the levels of many of the Phe-derived metabolites were predominately altered in fruits of the AO genotype, compared to tomato fruits expressing either AroG or ODO1 individually. The levels of most of these metabolites were significantly stimulated, such as Tyrosine (Tyr), coumaric acid and ferulic acid derived metabolites, but the levels of some important secondary metabolites were reduced in the AO transgenic genotypes as compared to either AroG or ODO1 lines. Nevertheless, our results also revealed that the levels of aromatic volatiles were obviously down regulated in the AO, compared to that in AroG transgenic fruits, but were boosted while compared to the wild type and ODO1 transgenic fruits. • Our results suggest that ODO1 expression may also have a negative effect on the production of some of the aromatic volatiles in tomato fruits, indicating that ODO1 acts as an important regulator of the shikimate pathway, which leads to the production of the aromatic amino acids and secondary metabolites derived from them. Key words: AroG, ODO1, tomato, metabolism, shikimate pathway
APA, Harvard, Vancouver, ISO, and other styles
5

Andoniou, Christopher E. The Target Sites on EGF Receptor for CBL Its Negative Regulator. Fort Belvoir, VA: Defense Technical Information Center, April 1999. http://dx.doi.org/10.21236/ada367438.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Andoniou, Christopher E., and Hamid Band. The Target Sites on EGF Receptor for Cbl, It's Negative Regulator. Fort Belvoir, VA: Defense Technical Information Center, April 2000. http://dx.doi.org/10.21236/ada384088.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Barash, Itamar, and Robert Rhoads. Translational Mechanisms Governing Milk Protein Levels and Composition. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7696526.bard.

Full text
Abstract:
Original objectives: The long-term goal of the research is to achieve higher protein content in the milk of ruminants by modulating the translational apparatus of the mammary gland genetically, nutritionally, or pharmacologically. The short-term objectives are to obtain a better understanding of 1) the role of amino acids (AA) as regulators of translation in bovine and mouse mammary epithelial cells and 2) the mechanism responsible for the synergistic enhancement of milk-protein mRNA polyadenylation by insulin and prolactin. Background of the topic: In many cell types and tissues, individual AA affect a signaling pathway which parallels the insulin pathway to modulate rates and levels of protein synthesis. Diverse nutritional and hormonal conditions are funneled to mTOR, a multidomain serine/threonine kinase that regulates a number of components in the initiation and elongation stages of translation. The mechanism by which AA signal mTOR is largely unknown. During the current grant period, we have studied the effect of essential AA on mechanisms involved in protein synthesis in differentiated mammary epithelial cells cultured under lactogenic conditions. We also studied lactogenic hormone regulation of milk protein synthesis in differentiated mammary epithelial cells. In the first BARD grant (2000-03), we discovered a novel mechanism for mRNA-specific hormone-regulated translation, namely, that the combination of insulin plus prolactin causes cytoplasmic polyadenylation of milk protein mRNAs, which leads to their efficient translation. In the current BARD grant, we have pursued the signaling pathways of this novel hormone action. Major conclusions/solutions/achievements: The positive and negative signaling from AA to the mTOR pathway, combined with modulation of insulin sensitization, mediates the synthesis rates of total and specific milk proteins in mammary epithelial cells. The current in vitro study revealed cryptic negative effects of Lys, His, and Thr on cellular mechanisms regulating translation initiation and protein synthesis in mammary epithelial cells that could not be detected by conventional in vivo analyses. We also showed that a signaling pathway involving Jak2 and Stat5, previously shown to lead from the prolactin receptor to transcription of milk protein genes, is also used for cytoplasmic polyadenylation of milk protein mRNAs, thereby stabilizing these mRNAs and activating them for translation. Implications: In vivo, plasma AA levels are affected by nutritional and hormonal effects as well as by conditions of exercise and stress. The amplitude in plasma AA levels resembles that applied in the current in vitro study. Thus, by changing plasma AA levels in the epithelial cell microenvironment or by sensitizing the mTOR pathway to their presence, it should be possible to modulate the rate of milk protein synthesis. Furthermore, knowledge that phosphorylation of Stat5 is required for enhanced milk protein synthesis in response to lactogenic opens the possibility for pharmacologic approaches to increase the phosphorylation of Stat5 and, thereby, milk protein production.
APA, Harvard, Vancouver, ISO, and other styles
8

Marsden, Eric. Risk regulation, liability and insurance: literature review of their influence on safety management. Fondation pour une culture de sécurité industrielle, September 2014. http://dx.doi.org/10.57071/337rrl.

Full text
Abstract:
This document provides a short literature review on the complementarity (and antagonisms) between liability rules, safety regulation and insurance and their effect on safety management. It draws on a range of disciplines, with a focus on economic analysis of law and regulation theory. Some of the issues discussed are rather complex; this document attempts to provide simple explanations together with references to the professional literature for the interested reader. Some issues are the subject of ongoing debate between scholars; in such situations, we have attempted to present the various points of view. The document provides background information concerning the topics discussed during the NeTWork’2012 workshop, and draws on some of the contributions of workshop participants and the rich discussion which took place during the three days. The first chapter presents issues related to regulation, starting with the classical economic justifications for state intervention (presence of externalities, information failures and moral hazard). A number of obstacles to the effectiveness of safety regulation are presented. Finally, some alternatives or complements to regulation, including self-regulation, are briefly discussed. Chapter 2 presents an overview of liability law, starting with some introductory definitions. Factors which weaken the effectiveness of liability as an incentive to invest in prevention are discussed, as are negative effects of liability regimes on safety management. A number of case studies illustrating the liability of regulators are briefly presented. Chapter 3 discusses the impact of insurance and reinsurance on firms’ and individuals’ safety management. The last chapter briefly analyzes firms’ and individuals’ sources of motivation to take care.
APA, Harvard, Vancouver, ISO, and other styles
9

Huang, Ran, and Stacy Lee. Perceived Deception or Perceived Relevance? The Role of Self-Regulatory Focus in Processing Negative Online Reviews. Ames (Iowa): Iowa State University. Library, January 2019. http://dx.doi.org/10.31274/itaa.8459.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Yalovsky, Shaul, and Julian Schroeder. The function of protein farnesylation in early events of ABA signal transduction in stomatal guard cells of Arabidopsis. United States Department of Agriculture, January 2002. http://dx.doi.org/10.32747/2002.7695873.bard.

Full text
Abstract:
Loss of function mutations in the farnesyltransferase β subunit gene ERA1 (enhanced response to abscisic acid), cause abscisic acid hypersensitivity in seedlings and in guard cells. This results in slowed water loss of plants in response to drought. Farnesyltransferase (PFT) catalyses the attachment of the 15-carbon isoprenoid farnesyl to conserved cysteine residues located in a conserved C-terminal domain designated CaaX box. PFT is a heterodimeric protein comprised of an a and b sununits. The a subunit is shared between PFT and geranylgeranyltransferase-I (PGGTI) which catalyses the attachemt of the 20-carbon isoprenoid geranylgeranyl to CaaX box proteins in which the last amino acid is almost always leucine and in addition have a polybasic domain proximal to the CaaL box. Preliminary data presented in the proposal showed that increased cytoplasmic Ca2+ concentration in stomal guard cells in response to non-inductive ABA treatements. The goals set in the proposal were to characterize better how PFT (ERA1) affects ABA induced Ca2+ concentrations in guard cells and to identify putative CaaX box proteins which function as negative regulators of ABA signaling and which function is compromised in era1 mutant plants. To achieve these goals we proposed to use camelion Ca2+ sensor protein, high throughput genomic to identify the guard cell transcriptome and test prenylation of candidate proteins. We also proposed to focus our efforts of RAC small GTPases which are prenylated proteins which function in signaling. Our results show that farnesyltransferaseprenylates protein/s that act between the points of ABA perception and the activation of plasma membrane calcium influx channels. A RAC protein designated AtRAC8/AtRop10 also acts in negative regulation of ABA signaling. However, we discovered that this protein is palmitoylated and not prenylated although it contains a C-terminal CXXX motif. We further discovered a unique C-terminal sequence motif required for membrane targeting of palmitoylatedRACs and showed that their function is prenylation independent. A GC/MS based method for expression in plants, purification and analysis of prenyl group was developed. This method would allow highly reliable identification of prenylated protein. Mutants in the shared α subunit of PFT and PGGT-I was identified and characterized and was shown to be ABA hypersensitive but less than era1. This suggested that PFT and PGGT-I have opposing functions in ABA signaling. Our results enhanced the understanding of the role of protein prenylation in ABA signaling and drought resistance in plants with the implications of developing drought resistant plants. The results of our studies were published 4 papers which acknowledge support from BARD.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Negative regulators' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography