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Journal articles on the topic 'Negative regulators'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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11

ELLIS, R. "Negative regulators of programed cell death." Current Biology 2, no. 9 (September 1992): 486. http://dx.doi.org/10.1016/0960-9822(92)90671-v.

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12

Hilton, D. J. "Negative regulators of cytokine signal transduction." Cellular and Molecular Life Sciences (CMLS) 55, no. 12 (October 2, 1999): 1568–77. http://dx.doi.org/10.1007/s000180050396.

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13

Graham, Gerard J., and Ian B. Pragnell. "Negative regulators of haemopoiesis—Current advances." Progress in Growth Factor Research 2, no. 3 (January 1990): 181–92. http://dx.doi.org/10.1016/0955-2235(90)90004-4.

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14

Iwamoto, Rina, Masanori Koide, Nobuyuki Udagawa, and Yasuhiro Kobayashi. "Positive and Negative Regulators of Sclerostin Expression." International Journal of Molecular Sciences 23, no. 9 (April 28, 2022): 4895. http://dx.doi.org/10.3390/ijms23094895.

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Sclerostin is secreted from osteocytes, binds to the Wnt co-receptor Lrp5/6, and affects the interaction between Wnt ligands and Lrp5/6, which inhibits Wnt/β-catenin signals and suppresses bone formation. Sclerostin plays an important role in the preservation of bone mass by functioning as a negative regulator of bone formation. A sclerostin deficiency causes sclerosteosis, which is characterized by an excess bone mass with enhanced bone formation in humans and mice. The expression of sclerostin is positively and negatively regulated by many factors, which also govern bone metabolism. Positive and negative regulators of sclerostin expression and their effects are introduced and discussed herein based on recent and previous findings, including our research.

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15

Huang, Shujun, Wayne Xu, Pingzhao Hu, and Ted M. Lakowski. "Integrative Analysis Reveals Subtype-Specific Regulatory Determinants in Triple Negative Breast Cancer." Cancers 11, no. 4 (April 10, 2019): 507. http://dx.doi.org/10.3390/cancers11040507.

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Different breast cancer (BC) subtypes have unique gene expression patterns, but their regulatory mechanisms have yet to be fully elucidated. We hypothesized that the top upregulated (Yin) and downregulated (Yang) genes determine the fate of cancer cells. To reveal the regulatory determinants of these Yin and Yang genes in different BC subtypes, we developed a lasso regression model integrating DNA methylation (DM), copy number variation (CNV) and microRNA (miRNA) expression of 391 BC patients, coupled with miRNA–target interactions and transcription factor (TF) binding sites. A total of 25, 20, 15 and 24 key regulators were identified for luminal A, luminal B, Her2-enriched, and triple negative (TN) subtypes, respectively. Many of the 24 TN regulators were found to regulate the PPARA and FOXM1 pathways. The Yin Yang gene expression mean ratio (YMR) and combined risk score (CRS) signatures built with either the targets of or the TN regulators were associated with the BC patients’ survival. Previously, we identified FOXM1 and PPARA as the top Yin and Yang pathways in TN, respectively. These two pathways and their regulators could be further explored experimentally, which might help to identify potential therapeutic targets for TN.

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16

CHAN, YVONNE C., YUEWEI HU, SORAYA CHATURONGAKUL, KALI D. FILES, BARBARA M. BOWEN, KATHRYN J. BOOR, and MARTIN WIEDMANN. "Contributions of Two-Component Regulatory Systems, Alternative σ Factors, and Negative Regulators to Listeria monocytogenes Cold Adaptation and Cold Growth." Journal of Food Protection 71, no. 2 (February 1, 2008): 420–25. http://dx.doi.org/10.4315/0362-028x-71.2.420.

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The ability of Listeria monocytogenes to grow at refrigeration temperatures is critical for transmission of this foodborne pathogen. We evaluated the contributions of different transcriptional regulators and two-component regulatory systems to L. monocytogenes cold adaptation and cold growth. L. monocytogenes parent strain 10403S and selected isogenic null mutants in genes encoding four alternative σ factors (sigB, sigH, sigC, and sigL), two regulators of σB (rsbT and rsbV), two negative regulators (ctsR and hrcA), and 15 two-component response regulators were grown in brain heart infusion broth at 4°C with (i) a high-concentration starting inoculum (108 CFU/ml), (ii) a low-concentration starting inoculum (102 CFU/ml), and (iii) a high-concentration starting inoculum of cold-adapted cells. With a starting inoculum of 108 CFU/ml, null mutants in genes encoding selected alternative σ factors (ΔsigH, ΔsigC, and ΔsigL), a negative regulator (ΔctsR), regulators of σB (ΔrsbT and ΔrsbV), and selected two-component response regulators (ΔlisR, Δlmo1172, and Δlmo1060) had significantly reduced growth (P < 0.05) compared with the parent strain after 12 days at 4°C. The growth defect for ΔsigL was limited and was not confirmed by optical density (OD600) measurement data. With a starting inoculum of 102 CFU/ml and after monitoring growth at 4°C over 84 days, only the ΔctsR strain had a consistent but limited growth defect; the other mutant strains had either no growth defects or limited growth defects apparent at only one or two of the nine sampling points evaluated during the 84-day growth period (ΔsigB, ΔsigC, and Δlmo1172). With a 108 CFU/ml starting inoculum of cold-adapted cells, none of the mutant strains that had a growth defect when inoculation was performed with cells pregrown at 37°C had reduced growth as compared with the parent strain after 12 days at 4°C, suggesting a specific defect in the ability of these mutant strains to adapt to 4°C after growth at 37°C. Our data indicate (i) selected σ factors and two-component regulators may contribute to cold adaptation even though two-component regulatory systems, alternative σ factors, and the negative regulators CtsR and HrcA appear to have limited contributions to L. monocytogenes growth at 4°C in rich media, and (ii) inoculum concentration and pregrowth conditions affect the L. monocytogenes cold-growth phenotype.

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17

Clark, Alistair. "The relationship between political parties and their regulators." Party Politics 23, no. 6 (November 9, 2015): 646–56. http://dx.doi.org/10.1177/1354068815616027.

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Political parties are in a unique situation, being able to change electoral rules and regulations to minimise any potential negative effects on their electoral prospects. Attempts to influence regulators, however, can be complex and include voicing concerns, public pressure and the regulatory capture of electoral regulators. Little is known about this relationship between parties and their regulators. This article focuses on this crucial electoral relationship through a study of political parties’ relations with the UK Electoral Commission. The first section addresses the background to the legal regulation of political parties. The second section proposes a framework through which parties’ reactions to regulation may be understood. The third part introduces the British case, providing evidence to demonstrate the broad utility of the framework. The final section analyses the issues that parties have raised with their regulators.

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18

Hyytiäinen, Heidi, Marcos Montesano, and E. Tapio Palva. "Global Regulators ExpA (GacA) and KdgR Modulate Extracellular Enzyme Gene Expression Through the RsmA-rsmB System in Erwinia carotovora subsp. carotovora." Molecular Plant-Microbe Interactions® 14, no. 8 (August 2001): 931–38. http://dx.doi.org/10.1094/mpmi.2001.14.8.931.

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The production of the main virulence determinants, the extracellular plant cell wall-degrading enzymes, and hence virulence of Erwinia carotovora subsp. carotovora is controlled by a complex regulatory network. One of the global regulators, the response regulator ExpA, a GacA homolog, is required for transcriptional activation of the extracellular enzyme genes of this soft-rot pathogen. To elucidate the mechanism of ExpA control as well as interactions with other regulatory systems, we isolated second-site transposon mutants that would suppress the enzyme-negative phenotype of an expA (gacA) mutant. Inactivation of kdgR resulted in partial restoration of extracellular enzyme production and virulence to the expA mutant, suggesting an interaction between the two regulatory pathways. This interaction was mediated by the RsmA-rsmB system. Northern analysis was used to show that the regulatory rsmB RNA was under positive control of ExpA. Conversely, the expression of rsmA encoding a global repressor was under negative control of ExpA and positive control of KdgR. This study indicates a central role for the RsmA-rsmB regulatory system during pathogenesis, integrating signals from the ExpA (GacA) and KdgR global regulators of extracellular enzyme production in E. carotovora subsp. carotovora.

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19

Greenberg, M. L., P. L. Myers, R. C. Skvirsky, and H. Greer. "New positive and negative regulators for general control of amino acid biosynthesis in Saccharomyces cerevisiae." Molecular and Cellular Biology 6, no. 5 (May 1986): 1820–29. http://dx.doi.org/10.1128/mcb.6.5.1820-1829.1986.

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The biosynthesis of most amino acids in Saccharomyces cerevisiae is coregulated. Starvation for a single amino acid results in the derepression of amino acid biosynthetic enzymes in many unrelated pathways. This phenomenon, known as general control, is mediated by both positive (GCN) and negative (GCD) regulatory genes. In this paper we describe the identification and characterization of several new regulatory genes for this system, GCN6, GCN7, GCN8, GCN9, and GCD5. A mutation in the negative regulator GCD5 was isolated on the basis of its suppression of a gcn2 mutation. The effect of gcd5 is a posttranscriptional increase in histidine biosynthetic enzyme activity. Suppressors of gcd5 which are deficient in derepression were in turn isolated. Eight such mutations, defining four new positive regulatory genes (GCN6 through GCN9), were obtained. These mutations are recessive, confer sensitivity to multiple amino acid analogs, and result in decreased mRNA levels for genes under general control. The GCN6 and GCN7 gene products were shown to be positive regulators for transcription of the GCN4 gene, the most direct-acting positive regulator thus far identified. The interaction of GCN6 and GCN7 with GCN4 is fundamentally different from that of previously isolated GCN genes. It should also be noted that these gcn selections gave a completely different nonoverlapping set of mutations from earlier selections which relied on analog sensitivity. Thus, we may have identified a new class of GCN genes which are functionally distinct from GCN1 through GCN5.

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20

Greenberg, M. L., P. L. Myers, R. C. Skvirsky, and H. Greer. "New positive and negative regulators for general control of amino acid biosynthesis in Saccharomyces cerevisiae." Molecular and Cellular Biology 6, no. 5 (May 1986): 1820–29. http://dx.doi.org/10.1128/mcb.6.5.1820.

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The biosynthesis of most amino acids in Saccharomyces cerevisiae is coregulated. Starvation for a single amino acid results in the derepression of amino acid biosynthetic enzymes in many unrelated pathways. This phenomenon, known as general control, is mediated by both positive (GCN) and negative (GCD) regulatory genes. In this paper we describe the identification and characterization of several new regulatory genes for this system, GCN6, GCN7, GCN8, GCN9, and GCD5. A mutation in the negative regulator GCD5 was isolated on the basis of its suppression of a gcn2 mutation. The effect of gcd5 is a posttranscriptional increase in histidine biosynthetic enzyme activity. Suppressors of gcd5 which are deficient in derepression were in turn isolated. Eight such mutations, defining four new positive regulatory genes (GCN6 through GCN9), were obtained. These mutations are recessive, confer sensitivity to multiple amino acid analogs, and result in decreased mRNA levels for genes under general control. The GCN6 and GCN7 gene products were shown to be positive regulators for transcription of the GCN4 gene, the most direct-acting positive regulator thus far identified. The interaction of GCN6 and GCN7 with GCN4 is fundamentally different from that of previously isolated GCN genes. It should also be noted that these gcn selections gave a completely different nonoverlapping set of mutations from earlier selections which relied on analog sensitivity. Thus, we may have identified a new class of GCN genes which are functionally distinct from GCN1 through GCN5.

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21

Krebs, Danielle L., and Douglas J. Hilton. "SOCS Proteins: Negative Regulators of Cytokine Signaling." Stem Cells 19, no. 5 (September 2001): 378–87. http://dx.doi.org/10.1634/stemcells.19-5-378.

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22

Kincade, P. W., K. L. Medina, and G. Smithson. "Sex Hormones as Negative Regulators of Lymphopoiesis." Immunological Reviews 137, no. 1 (February 1994): 119–34. http://dx.doi.org/10.1111/j.1600-065x.1994.tb00661.x.

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23

Franklin, RA, and JA McCubrey. "Kinases: positive and negative regulators of apoptosis." Leukemia 14, no. 12 (December 2000): 2019–34. http://dx.doi.org/10.1038/sj.leu.2401967.

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24

Akira, Shizuo, Tatsuya Saitoh, Kazufumi Matsushita, and Osamu Takeuchi. "Negative Regulators in Toll-like Receptor Responses." Cornea 29 (November 2010): S13—S19. http://dx.doi.org/10.1097/ico.0b013e3181ea4834.

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25

Stefanini, L., and W. Bergmeier. "Negative regulators of platelet activation and adhesion." Journal of Thrombosis and Haemostasis 16, no. 2 (December 26, 2017): 220–30. http://dx.doi.org/10.1111/jth.13910.

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26

Simpson, Pat. "Positive and negative regulators of neural fate." Neuron 15, no. 4 (October 1995): 739–42. http://dx.doi.org/10.1016/0896-6273(95)90163-9.

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27

SUL, H., C. SMAS, and N. MOUSTAID. "Positive and negative regulators of adipocyte differentiation☆." Journal of Nutritional Biochemistry 4, no. 10 (October 1993): 554–62. http://dx.doi.org/10.1016/0955-2863(93)90023-p.

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28

Fath, Thomas, Robert S. Fischer, Leif Dehmelt, Shelley Halpain, and Velia M. Fowler. "Tropomodulins are negative regulators of neurite outgrowth." European Journal of Cell Biology 90, no. 4 (April 2011): 291–300. http://dx.doi.org/10.1016/j.ejcb.2010.10.014.

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29

Soysa, Niroshani Surangika, and Neil Alles. "Positive and negative regulators of osteoclast apoptosis." Bone Reports 11 (December 2019): 100225. http://dx.doi.org/10.1016/j.bonr.2019.100225.

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30

Lock, Rebecca, and Karen Cichowski. "Loss of negative regulators amplifies RAS signaling." Nature Genetics 47, no. 5 (April 28, 2015): 426–27. http://dx.doi.org/10.1038/ng.3299.

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31

Kuwana, M. "Dysregulated negative immune regulators in immune thrombocytopenia." ISBT Science Series 9, no. 1 (July 2014): 217–22. http://dx.doi.org/10.1111/voxs.12065.

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32

Taylor, Andrew W., and Tat Fong Ng. "Negative regulators that mediate ocular immune privilege." Journal of Leukocyte Biology 103, no. 6 (February 12, 2018): 1179–87. http://dx.doi.org/10.1002/jlb.3mir0817-337r.

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33

Mori, Jun, Zoltan Nagy, Giada Di Nunzio, Christopher W. Smith, Mitchell J. Geer, Rashid Al Ghaithi, Johanna P. van Geffen, et al. "Maintenance of murine platelet homeostasis by the kinase Csk and phosphatase CD148." Blood 131, no. 10 (March 8, 2018): 1122–44. http://dx.doi.org/10.1182/blood-2017-02-768077.

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Key Points Csk and CD148 are nonredundant regulators of SFKs in platelets, and deletion of either induces cell-intrinsic negative feedback mechanisms. Csk is a negative regulator of SFK activity, whereas CD148 is a dual positive and negative regulator of SFK activity in platelets.

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34

Liu, Yao-Hua, I.-Jeng Yeh, Ming-Derg Lai, Kuan-Ting Liu, Po-Lin Kuo, and Meng-Chi Yen. "Cancer Immunotherapy: Silencing Intracellular Negative Immune Regulators of Dendritic Cells." Cancers 11, no. 1 (January 17, 2019): 108. http://dx.doi.org/10.3390/cancers11010108.

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Dendritic cells (DCs) are capable of activating adaptive immune responses, or inducing immune suppression or tolerance. In the tumor microenvironment, the function of DCs is polarized into immune suppression that attenuates the effect of T cells, promoting differentiation of regulatory T cells and supporting tumor progression. Therefore, blocking negative immune regulators in DCs is considered a strategy of cancer immunotherapy. Antibodies can target molecules on the cell surface, but not intracellular molecules of DCs. The delivery of short-hairpin RNAs (shRNA) and small-interfering RNAs (siRNA) should be a strategy to silence specific intracellular targets in DCs. This review provides an overview of the known negative immune regulators of DCs. Moreover, a combination of shRNA/siRNA and DC vaccines, DNA vaccines in animal models, and clinical trials are also discussed.

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35

Gaidenko, Tatiana A., Tae-Jong Kim, Andrea L. Weigel, Margaret S. Brody, and Chester W. Price. "The Blue-Light Receptor YtvA Acts in the Environmental Stress Signaling Pathway of Bacillus subtilis." Journal of Bacteriology 188, no. 17 (September 1, 2006): 6387–95. http://dx.doi.org/10.1128/jb.00691-06.

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ABSTRACT The general stress response of the bacterium Bacillus subtilis is regulated by a partner-switching mechanism in which serine and threonine phosphorylation controls protein interactions in the stress-signaling pathway. The environmental branch of this pathway contains a family of five paralogous proteins that function as negative regulators. Here we present genetic evidence that a sixth paralog, YtvA, acts as a positive regulator in the same environmental signaling branch. We also present biochemical evidence that YtvA and at least three of the negative regulators can be isolated from cell extracts in a large environmental signaling complex. YtvA differs from these associated negative regulators by its flavin mononucleotide (FMN)-containing light-oxygen-voltage domain. Others have shown that this domain has the photochemistry expected for a blue-light sensor, with the covalent linkage of the FMN chromophore to cysteine 62 composing a critical part of the photocycle. Consistent with the view that light intensity modifies the output of the environmental signaling pathway, we found that cysteine 62 is required for YtvA to exert its positive regulatory role in the absence of other stress. Transcriptional analysis of the ytvA structural gene indicated that it provides the entry point for at least one additional environmental input, mediated by the Spx global regulator of disulfide stress. These results support a model in which the large signaling complex serves to integrate multiple environmental signals in order to modulate the general stress response.

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36

Chaturongakul, Soraya, Sarita Raengpradub, M. Elizabeth Palmer, Teresa M. Bergholz, Renato H. Orsi, Yuewei Hu, Juliane Ollinger, Martin Wiedmann, and Kathryn J. Boor. "Transcriptomic and Phenotypic Analyses Identify Coregulated, Overlapping Regulons among PrfA, CtsR, HrcA, and the Alternative Sigma Factors σB, σC, σH, and σLinListeria monocytogenes." Applied and Environmental Microbiology 77, no. 1 (October 29, 2010): 187–200. http://dx.doi.org/10.1128/aem.00952-10.

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ABSTRACTA set of sevenListeria monocytogenes10403S mutant strains, each bearing an in-frame null mutation in a gene encoding a key regulatory protein, was used to characterize transcriptional networks inL. monocytogenes; the seven regulatory proteins addressed include all fourL. monocytogenesalternative sigma factors (σB, σC, σH, and σL), the virulence gene regulator PrfA, and the heat shock-related negative regulators CtsR and HrcA. Whole-genome microarray analyses, used to identify regulons for each of these 7 transcriptional regulators, showed considerable overlap among regulons. Among 188 genes controlled by more than one regulator, 176 were coregulated by σB, including 92 genes regulated by both σBand σH(with 18 of these genes coregulated by σB, σH, and at least one additional regulator) and 31 genes regulated by both σBand σL(with 10 of these genes coregulated by σB, σL, and at least one additional regulator). Comparative phenotypic characterization measuring acid resistance, heat resistance, intracellular growth in J774 cells, invasion into Caco-2 epithelial cells, and virulence in the guinea pig model indicated contributions of (i) σBto acid resistance, (ii) CtsR to heat resistance, and (iii) PrfA, σB, and CtsR to virulence-associated characteristics. Loss of the remaining transcriptional regulators (i.e.,sigH,sigL, orsigC) resulted in limited phenotypic consequences associated with stress survival and virulence. Identification of overlaps among the regulons provides strong evidence supporting the existence of complex regulatory networks that appear to provide the cell with regulatory redundancies, along with the ability to fine-tune gene expression in response to rapidly changing environmental conditions.

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37

Baltrus, David A., Kevin Dougherty, Beatriz Diaz, and Rachel Murillo. "Evolutionary Plasticity of AmrZ Regulation in Pseudomonas." mSphere 3, no. 2 (April 18, 2018): e00132-18. http://dx.doi.org/10.1128/msphere.00132-18.

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ABSTRACT amrZ encodes a master regulator protein conserved across pseudomonads, which can be either a positive or negative regulator of swimming motility depending on the species examined. To better understand plasticity in the regulatory function of AmrZ, we characterized the mode of regulation for this protein for two different motility-related phenotypes in Pseudomonas stutzeri. As in Pseudomonas syringae, AmrZ functions as a positive regulator of swimming motility within P. stutzeri, which suggests that the functions of this protein with regard to swimming motility have switched at least twice across pseudomonads. Shifts in mode of regulation cannot be explained by changes in AmrZ sequence alone. We further show that AmrZ acts as a positive regulator of colony spreading within this strain and that this regulation is at least partially independent of swimming motility. Closer investigation of mechanistic shifts in dual-function regulators like AmrZ could provide unique insights into how transcriptional pathways are rewired between closely related species. IMPORTANCE Microbes often display finely tuned patterns of gene regulation across different environments, with major regulatory changes controlled by a small group of “master” regulators within each cell. AmrZ is a master regulator of gene expression across pseudomonads and can be either a positive or negative regulator for a variety of pathways depending on the strain and genomic context. Here, we demonstrate that the phenotypic outcomes of regulation of swimming motility by AmrZ have switched at least twice independently in pseudomonads, so that AmrZ promotes increased swimming motility in P. stutzeri and P. syringae but represses this phenotype in Pseudomonas fluorescens and Pseudomonas aeruginosa. Since examples of switches in regulatory mode are relatively rare, further investigation into the mechanisms underlying shifts in regulator function for AmrZ could provide unique insights into the evolution of bacterial regulatory proteins.

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38

Matsui, Mari, Akiko Takaya, and Tomoko Yamamoto. "σ32-Mediated Negative Regulation of Salmonella Pathogenicity Island 1 Expression." Journal of Bacteriology 190, no. 20 (August 22, 2008): 6636–45. http://dx.doi.org/10.1128/jb.00744-08.

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ABSTRACT Salmonella pathogenicity island 1 (SPI1) enables infecting salmonellae to invade the intestinal epithelium and induce a proinflammatory response and macrophage cell death. SPI1 expression is controlled by a complex cascade with several transcriptional regulators within the island and global regulators outside it. Previously, we reported that DnaK-depleted salmonellae could neither invade epithelial cells nor secrete SPI1-encoded proteins, suggesting that DnaK is involved in the expression of SPI1. Here, we found that DnaK is involved in SPI1 expression through inhibition of σ32 protein, which directs the transcription of a group of genes in response to various global stresses. Overproduction of σ32 resulted in decreased levels of the SPI1-specific transcriptional regulators HilD and HilA. Further analysis demonstrated that the σ32-mediated system negatively regulates HilD and HilA at the posttranslational and transcriptional levels, respectively. The executioner of this negative regulation was shown to be a σ32-induced protein ATP-dependent Lon protease, which specifically degrades HilD. Since HilD can activate hilA transcription, is at the top of the hierarchical SPI1 regulatory loop, and has a dominant role, the posttranslational control of HilD by Lon is critically important for precise expression of SPI1. Consequently, we suggest that SPI1 expression is controlled by the feedback regulatory loop in which σ32 induces Lon to control turnover of HilD, and DnaK, which inhibits σ32 function, leading to the modulation of lon expression. This regulation in response to a specific combination of environmental signals would ensure that SPI1 expression is restricted to a few specific locations in the host.

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39

To, Jennifer P. C., Georg Haberer, Fernando J. Ferreira, Jean Deruère, Michael G. Mason, G. Eric Schaller, Jose M. Alonso, Joseph R. Ecker, and Joseph J. Kieber. "Type-A Arabidopsis Response Regulators Are Partially Redundant Negative Regulators of Cytokinin Signaling." Plant Cell 16, no. 3 (February 18, 2004): 658–71. http://dx.doi.org/10.1105/tpc.018978.

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40

Gulati, Nicholas, Mayte Suárez-Fariñas, Joel Correa da Rosa, and James G. Krueger. "Psoriasis is characterized by deficient negative immune regulation compared to transient delayed-type hypersensitivity reactions." F1000Research 4 (June 11, 2015): 149. http://dx.doi.org/10.12688/f1000research.6581.1.

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Diphencyprone (DPCP) is a hapten that causes delayed-type hypersensitivity (DTH) reactions in human skin, and is used as a topical therapeutic for alopecia areata, warts, and cutaneous melanoma metastases. We examined peak DTH reactions induced by DPCP (3 days post-challenge) by comprehensive gene expression and histological analysis. To better understand how these DTH reactions naturally resolve, we compared our DPCP biopsies to those from patients with psoriasis vulgaris, a chronic inflammatory disease that does not resolve. By both microarray and qRT-PCR, we found that psoriasis lesional skin has significantly lower expression of many negative immune regulators compared to peak DPCP reactions. These regulators include: interleukin-10, cytotoxic T lymphocyte-associated 4 (CTLA4), programmed cell death 1 (PD1), programmed cell death 1 ligand 1 (PDL1), programmed cell death 1 ligand 2 (PDL2), and indoleamine 2,3-dioxygenase (IDO1). Their decreased expression was confirmed at the protein level by immunohistochemistry. To more completely determine the balance of positive vs. negative immune regulators in both DPCP reactions and psoriasis, we developed one comprehensive gene list for positive regulatory (inflammatory) genes, and another for negative regulatory (immunosuppressive) genes, through Gene Ontology terms and literature review. With this approach, we found that DPCP reactions have a higher ratio of negative to positive regulatory genes (both in terms of quantity and expression levels) than psoriasis lesional skin. These data suggest that the disease chronicity that distinguishes psoriasis from transient DTH reactions may be related to absence of negative immune regulatory pathways, and induction of these is therefore of therapeutic interest. Further study of these negative regulatory mechanisms that are present in DPCP reactions, but not in psoriasis, could reveal novel players in the pathogenesis of chronic inflammation. The DPCP system used here thus provides a tractable model for primary discovery of pathways potentially involved in immune regulation in peripheral tissues.

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Stec, Wojciech J., and Martin P. Zeidler. "Drosophila SOCS Proteins." Journal of Signal Transduction 2011 (December 13, 2011): 1–8. http://dx.doi.org/10.1155/2011/894510.

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The importance of signal transduction cascades such as the EGFR and JAK/STAT pathways for development and homeostasis is highlighted by the high levels of molecular conservation maintained between organisms as evolutionary diverged as fruit flies and humans. This conservation is also mirrored in many of the regulatory mechanisms that control the extent and duration of signalling in vivo. One group of proteins that represent important physiological regulators of both EGFR and JAK/STAT signalling is the members of the SOCS family. Only 3 SOCS-like proteins are encoded by the Drosophila genome, and despite this low complexity, Drosophila SOCS proteins share many similarities to their human homologues. SOCS36E is both a target gene and negative regulator of JAK/STAT signalling while SOCS44A and SOCS36E represent positive and negative regulators of EGFR signalling. Here we review our current understanding of Drosophila SOCS proteins, their roles in vivo, and future approaches to elucidating their functions.

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Okinaga, Toshinori, Guoqing Niu, Zhoujie Xie, Fengxia Qi, and Justin Merritt. "The hdrRM Operon of Streptococcus mutans Encodes a Novel Regulatory System for Coordinated Competence Development and Bacteriocin Production." Journal of Bacteriology 192, no. 7 (January 29, 2010): 1844–52. http://dx.doi.org/10.1128/jb.01667-09.

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ABSTRACT The Streptococcus mutans hdrRM operon encodes a novel two-gene regulatory system induced by high cell density. Previous studies identified hdrM as the only known negative regulator of competence development in S. mutans. In the present study, we demonstrated that the HdrRM system bypasses the prototypical competence gene regulators ComC and ComDE in the transcriptional regulation of the competence-specific sigma factor comX and the late competence genes. Similarly, the HdrRM system can abrogate the requirement for ComE to produce the bacteriocin mutacin IV. To further probe the regulatory mechanism of hdrRM, we created an hdrR overexpression strain and showed that it could reproduce each of the hdrM competence and mutacin phenotypes, indicating that HdrM acts as a negative regulator of HdrR activity. Using a mutacin IV-luciferase reporter, we also demonstrated that the hdrRM system utilizes the same promoter elements recognized by ComE and thus appears to comprise a novel regulatory pathway parallel to ComCDE.

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Wu, Moli, Danyang Song, Hui Li, Yang Yang, Xiaodong Ma, Sa Deng, Changle Ren, and Xiaohong Shu. "Negative regulators of STAT3 signaling pathway in cancers." Cancer Management and Research Volume 11 (May 2019): 4957–69. http://dx.doi.org/10.2147/cmar.s206175.

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Neumann, Carl. "Hedgehogs as Negative Regulators of the Cell Cycle." Cell Cycle 4, no. 9 (July 8, 2005): 1139–40. http://dx.doi.org/10.4161/cc.4.9.1999.

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Zhou, Xiang, Bo Cao, and Hua Lu. "Negative auto-regulators trap p53 in their web." Journal of Molecular Cell Biology 9, no. 1 (January 24, 2017): 62–68. http://dx.doi.org/10.1093/jmcb/mjx001.

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Galeev, Roman, Aurelie Baudet, Anders Kvist, Therese Törngren, Shamit Soneji, Åke Borg, and Jonas Larsson. "Cohesin Genes Are Negative Regulators of HSC Renewal." Blood 124, no. 21 (December 6, 2014): 605. http://dx.doi.org/10.1182/blood.v124.21.605.605.

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Abstract The molecular principles regulating hematopoietic stem cells (HSCs) remain incompletely defined. To gain deeper insights into the mechanisms underlying renewal and differentiation of hematopoietic stem and progenitor cells (HSPCs), we have developed global RNAi screens targeted to human cord blood derived CD34+ cells. In previous work such screens have allowed us to identify novel druggable targets to facilitate ex vivo expansion of HSPCs. Recently, we employed a near genome-wide screen (targeting 15 000 genes) to identify genes with an impact on renewal/differentiation of HSPCs, in a completely unbiased manner. Among the most prominent hits from this screen were many transcription factors and epigenetic modifiers and we found a strong enrichment of genes known to be recurrently mutated in hematopoietic neoplasms. A striking finding, was the identification of several members of the cohesin complex (STAG2, RAD21, STAG1 and SMC3) among our top hits (top 0.5%). Cohesin is a multimeric protein complex that mediates adhesion of sister chromatids as well as long-range interactions of chromosomal elements to regulate transcription. Recent large-scale sequencing studies have identified recurrent mutations in the cohesin genes in myeloid malignancies. Upon individual validation and targeting of the cohesin genes by lentiviral shRNA in human CD34+ cells, we found that their knockdown by independent shRNAs led to an immediate and profound expansion of primitive hematopoietic CD34+CD90+ cells in vitro. A similar expansion phenotype was observed in vivo following transplantation to primary and secondary immundeficient mice. Transplantation of CD34+CD38lowCD90+CD45RA- cells transduced with shRNA targeting STAG2 (the cohesin component with the strongest in vitro phenotype) into NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ (NSG) mice resulted in a significant increase in human reconstitution in the bone marrow 16 weeks post-transplantation compared to controls (31.3±4.4% vs 11.6±2.8% p=0.001). The engrafted mice showed a marked skewing towards the myeloid lineage as analyzed by CD33/CD15 expression in bone marrow (27.0±5.0% vs 13.0±2.6% p=0.013), as well as an increase in the more primitive CD34+CD38- population (2.8±0.6% vs 1.3±0.4% p=0.036). In secondary transplanted mice, 3/6 recipients in the STAG2 group maintained detectable levels of human chimerism while no engraftment was detected in the control group, indicating an increased expansion of HSPCs in vivo upon knockdown of STAG2. Global transcriptome analysis of cohesin deficient CD34+ cells 36 hours post shRNA transduction showed a distinct up-regulation of HSC specific genes coupled with down-regulation of genes specific for more downstream progenitors, demonstrating an immediate shift towards a more stem-like gene expression signature upon cohesin deficiency. This observation was consistent for all cohesin genes tested (STAG2, RAD21, STAG1 and SMC3). Our findings implicate cohesin as a novel major player in regulation of human HSPCs and, together with the recent discovery of recurrent mutations in myeloid malignancies, point toward a direct role of perturbed cohesin function as a true driver event in myeloid leukemogenesis. Our findings illustrate how global RNAi screens targeted to primary human HSPCs can identify novel modifiers of cell fate and may complement genome-wide sequencing approaches to guide the identification of functionally relevant disease-related genes in hematopoietic malignancies. Disclosures No relevant conflicts of interest to declare.

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T. Cornell, Timothy. "Negative Regulators of the Host Response in Sepsis." Open Inflammation Journal 4, no. 1 (October 7, 2011): 61–66. http://dx.doi.org/10.2174/1875041901104010061.

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Chung, Myung-Chul, Scott Dean, Ekaterina S. Marakasova, Albert O. Nwabueze, and Monique L. van Hoek. "Chitinases Are Negative Regulators of Francisella novicida Biofilms." PLoS ONE 9, no. 3 (March 24, 2014): e93119. http://dx.doi.org/10.1371/journal.pone.0093119.

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Rodriguez, Eleazar, Hassan El Ghoul, John Mundy, and Morten Petersen. "Making sense of plant autoimmunity and ‘negative regulators’." FEBS Journal 283, no. 8 (December 21, 2015): 1385–91. http://dx.doi.org/10.1111/febs.13613.

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Larraguibel, Jahdiel, Alexander R. E. Weiss, Daniel J. Pasula, Rasmeet S. Dhaliwal, Roman Kondra, and Terence J. Van Raay. "Wnt ligand–dependent activation of the negative feedback regulator Nkd1." Molecular Biology of the Cell 26, no. 12 (June 15, 2015): 2375–84. http://dx.doi.org/10.1091/mbc.e14-12-1648.

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Misregulation of Wnt signaling is at the root of many diseases, most notably colorectal cancer, and although we understand the activation of the pathway, we have a very poor understanding of the circumstances under which Wnt signaling turns itself off. There are numerous negative feedback regulators of Wnt signaling, but two stand out as constitutive and obligate Wnt-induced regulators: Axin2 and Nkd1. Whereas Axin2 behaves similarly to Axin in the destruction complex, Nkd1 is more enigmatic. Here we use zebrafish blastula cells that are responsive Wnt signaling to demonstrate that Nkd1 activity is specifically dependent on Wnt ligand activation of the receptor. Furthermore, our results support the hypothesis that Nkd1 is recruited to the Wnt signalosome with Dvl2, where it becomes activated to move into the cytoplasm to interact with β-catenin, inhibiting its nuclear accumulation. Comparison of these results with Nkd function in Drosophila generates a unified and conserved model for the role of this negative feedback regulator in the modulation of Wnt signaling.

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