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Автор: Grafiati
Опубліковано: 11 вересня 2023

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Статті в журналах з теми "MODULATING RESPONSES"

1

Hariri, Ahmad R., Susan Y. Bookheimer, and John C. Mazziotta. "Modulating emotional responses." NeuroReport 11, no. 1 (January 2000): 43–48. http://dx.doi.org/10.1097/00001756-200001170-00009.

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2

Leder, Christoph, Melanie Ziegler, and Meinrad Gawaz. "Modulating Immune Responses and Inflammation." Seminars in Thrombosis and Hemostasis 36, no. 02 (March 2010): 219–22. http://dx.doi.org/10.1055/s-0030-1251507.

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3

Wen, Ya-Chien, and Chen-Gia Tsai. "The effect of harmonization on cortical magnetic responses evoked by music of rapidly changing tonalities." Psychology of Music 45, no. 1 (July 7, 2016): 22–35. http://dx.doi.org/10.1177/0305735616639386.

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The act of shifting from one key to another is termed tonal modulation, which has been used to articulate emotion expressions and formal structures in Western music. The present study recorded cortical activity to examine how the auditory-evoked magnetic fields are affected by harmonizing music of rapidly changing tonalities. Participants were asked to covertly sing the pitch names of well-learned modulating melodies along with the harmonized or unharmonized melodies. In our musical stimuli, three flats were added to the key signature for every four beats. Such a rapid modulation is achieved by a chromatic inflection of the submediant tone between the third and fourth beats. Tonal modulations with such chromatic progressions are termed chromatic modulations. A major finding was that the amplitude of N1m (neuromagnetic response at approximately 110 ms after the onset of a stimulus) was significantly reduced by harmonization only when a modulation occurred. We also observed that harmonization enhanced the P2m (neuromagnetic response at approximately 200 ms after the onset of a stimulus) amplitude. The results provide evidence of the impacts of harmonization on attention efforts and pitch categorization.
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4

Matsuzaki, Takeshi, and James Chin. "Modulating immune responses with probiotic bacteria." Immunology and Cell Biology 78, no. 1 (February 2000): 67–73. http://dx.doi.org/10.1046/j.1440-1711.2000.00887.x.

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5

Batty, Matthew J., Gwladys Chabrier, Alanah Sheridan, and Matthew C. Gage. "Metabolic Hormones Modulate Macrophage Inflammatory Responses." Cancers 13, no. 18 (September 17, 2021): 4661. http://dx.doi.org/10.3390/cancers13184661.

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Macrophages are phagocytotic leukocytes that play an important role in the innate immune response and have established roles in metabolic diseases and cancer progression. Increased adiposity in obese individuals leads to dysregulation of many hormones including those whose functions are to coordinate metabolism. Recent evidence suggests additional roles of these metabolic hormones in modulating macrophage inflammatory responses. In this review, we highlight key metabolic hormones and summarise their influence on the inflammatory response of macrophages and consider how, in turn, these hormones may influence the development of different cancer types through the modulation of macrophage functions.
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6

Radtke, Franziska A., Gareth Chapman, Jeremy Hall, and Yasir A. Syed. "Modulating Neuroinflammation to Treat Neuropsychiatric Disorders." BioMed Research International 2017 (2017): 1–21. http://dx.doi.org/10.1155/2017/5071786.

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Neuroinflammation is recognised as one of the potential mechanisms mediating the onset of a broad range of psychiatric disorders and may contribute to nonresponsiveness to current therapies. Both preclinical and clinical studies have indicated that aberrant inflammatory responses can result in altered behavioral responses and cognitive deficits. In this review, we discuss the role of inflammation in the pathogenesis of neuropsychiatric disorders and ask the question if certain genetic copy-number variants (CNVs) associated with psychiatric disorders might play a role in modulating inflammation. Furthermore, we detail some of the potential treatment strategies for psychiatric disorders that may operate by altering inflammatory responses.
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7

Kasahara, S., H. Wago, and E. L. Cooper. "Dissociation of Innate and Adaptive Immunity by UVB Irradiation." International Journal of Immunopathology and Pharmacology 15, no. 1 (January 2002): 1–11. http://dx.doi.org/10.1177/039463200201500101.

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Increasing ultraviolet-B irradiation (UVB) resulting from diminution of stratospheric ozone is becoming a serious international problem. UVB irradiation exerts not only carcinogenic effects on animals but also causes them to become vulnerable to infections by modulating their immune responses. UVB irradiation suppresses innate immune functions of cells such as macrophages, neutrophils, Langerhans cells, dendritic cells, and the serum component, complement. UVB irradiation also causes changes in cytokine profiles, represented by the induction of a paradigm switch involving Th1/Th2 phenotypes. According to earlier studies, Th1 responses are suppressed, whereas Th2 activities are augmented by UVB irradiation. These immune modulations are caused by several pathways via cytokines and neuropeptides, and eventually may lead to increasing incidences of infection, allergy, and cancer. We have reviewed reports concerning UVB-irradiation induced immune modulation from the viewpoint of risks for human diseases and, in addition, for ecosystems and immunity of lower animals.
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8

Warren, Daniel, Christopher Simpkins, Matthew Cooper, and Robert Montgomery. "Modulating Alloimmune Responses with Plasmapheresis and IVIG." Current Drug Target -Cardiovascular & Hematological Disorders 5, no. 3 (June 1, 2005): 215–22. http://dx.doi.org/10.2174/1568006054064735.

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9

Ringertz, BO. "NEUTROPHIL AGGREGATION - FACTORS MODULATING STIMULUS-SPECIFIC RESPONSES." Acta Pathologica Microbiologica Scandinavica Series C: Immunology 94C, no. 1-6 (August 15, 2009): 1–9. http://dx.doi.org/10.1111/j.1699-0463.1986.tb02082.x.

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10

Menon, Ashwathi Puravankara, Beatriz Moreno, Daniel Meraviglia-Crivelli, Francesca Nonatelli, Helena Villanueva, Martin Barainka, Angelina Zheleva, Hisse M. van Santen, and Fernando Pastor. "Modulating T Cell Responses by Targeting CD3." Cancers 15, no. 4 (February 13, 2023): 1189. http://dx.doi.org/10.3390/cancers15041189.

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Harnessing the immune system to fight cancer has become a reality with the clinical success of immune-checkpoint blockade (ICB) antibodies against PD(L)-1 and CTLA-4. However, not all cancer patients respond to ICB. Thus, there is a need to modulate the immune system through alternative strategies for improving clinical responses to ICB. The CD3-T cell receptor (TCR) is the canonical receptor complex on T cells. It provides the “first signal” that initiates T cell activation and determines the specificity of the immune response. The TCR confers the binding specificity whilst the CD3 subunits facilitate signal transduction necessary for T cell activation. While the mechanisms through which antigen sensing and signal transduction occur in the CD3–TCR complex are still under debate, recent revelations regarding the intricate 3D structure of the CD3–TCR complex might open the possibility of modulating its activity by designing targeted drugs and tools, including aptamers. In this review, we summarize the basis of CD3–TCR complex assembly and survey the clinical and preclinical therapeutic tools available to modulate CD3–TCR function for potentiating cancer immunotherapy.
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Дисертації з теми "MODULATING RESPONSES"

1

Roey, Griet Van. "Modulating mucosal immune responses to HIV." Thesis, St George's, University of London, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589775.

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Development of a successful vaccine against HIV is likely to require the induction of strong and long-lasting humoral immune responses at the mucosal portals of virus entry. One approach to achieve this is the direct immunisation of mucosal sites. However, there is a need for potent and safe adjuvants that work at mucosal surfaces. A number of cytokines have recently been identified that specifically activate B-cells including BAFF, APRIL and TSLP. The hypothesis of this thesis is that these cytokines will act as adjuvants to boost antibody responses to mucosally delivered HIV antigen. Following immunisation of mice, serum and vaginal samples were tested for gp140-specific IgA and IgG responses. Splenocytes were assessed for T-cell proliferation and gp140-specific IgA and IgG antibody secreting cells. Cytokine production by T-cells after in vitro stimulation with CN54gp140 peptides was also assessed. TSLP, but not APRIL or BAFF, induced strong immune responses after nasal " immunisation, comparable to those seen with cholera toxin. Responses were still detected 4 months after the last boost, indicating a long lasting response. TSLP also induced T -cell proliferative responses to gp 140 after nasal immunisation and induced a T H2 type immune response but without induction of an allergic response. Due to cost limitations on the mass production of protein for use as an adjuvant, it was also tested whether TSLP could be delivered in the form of a plasmid DNA adjuvant. These studies demonstrated limited efficacy. In conclusion, the study demonstrated that B-cell activating cytokine TSLP, but not BAFF and APRIL can work as a mucosal adjuvant. It is notable that there was no significant development of allergic responses following administration of TSLP. This is 4 , the first time that TSLP has been demonstrated to have a positive effect as a mucosal adjuvant, and specifically promoting mucosal and systemic responses to HIV gp140.
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2

Kannan, Yashaswini. "Functional Characterization Of Human IkappaBzeta In Modulating Inflammatory Responses." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1314564642.

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3

Lay, Abigail C. "Understanding and modulating insulin responses of the glomerular podocyte." Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.684357.

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Podocytes are highly specialised epithelial cells, located on the urinary side of the glomerular filtration barrier. Disruptions to podocyte structure and function results in a disruption to the filtration process and proteinuria. Therefore, an understanding of factors that influence podocyte biology is desirable. Podocytes respond to insulin both in vitro and in vivo and the podocyte-specific knock-down of the insulin receptor results in a glomerular pathology with features characteristic of diabetic nephropathy. There is also evidence that podocyte insulin signalling is disrupted in models of insulin resistance and diabetes. The aim of this thesis was to investigate how both positive and negative modulators of insulin signalling specifically influence podocyte responses in vitro. Initial work was undertaken to characterise the responses of a recently developed mouse podocyte cell line. These cells express the insulin and insulin-like growth factor {IGF)-I receptors, and the phosphorylation of these proteins is evident following insulin stimulation. Downstream of receptor activation, increased phosphorylation of insulin receptor substrate (IRS) proteins and activation of phosphoinositide 3-kinase {PI3K)/Akt and MEK/ERK mitogen activated protein kinase (MAPK) cascades is observed . Furthermore, these cells activate glucose transport pathways following insulin stimulation. The effects of the anti-diabetic agent metformin and the selective chemical inhibition of protein tyrosine phosphatase 1B (PTP1B) were next examined, as potential enhancers of podocyte insulin signalling. Data herein demonstrates that these chemicals have direct effects on mouse podocytes in vitro and influence cellular glucose uptake. The modulation of podocyte signalling by diabetic factors, specifically the chronic exposure to high insulin, high glucose and inflammatory cytokines, was also investigated. Data reveals that the exposure of podocytes to a combination of these diabetic factors disrupts the activation of insulinstimulated signalling and glucose uptake. Individually, these factors exert their effects at different points within the signalling network. Quantitative peR arrays were also performed to identify changes at the mRNA level. Interestingly, the mRNA encoding the neurotransmitter Neuropeptide Y (NPY) was down regulated by 7-fold following cytokine exposure. Further investigation demonstrates that this peptide signals to both human and mouse podocytes in vitro stimulating the phosphorylation of Akt and ERK1/2, as well as influencing calcium signalling. Overall, work within this thesis demonstrates both the positive and negative modulation of podocyte insulin signalling in vitro and identifies a novel role for NPY in podocyte biology.
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4

Salazar, F. "The role of indoleamine 2,3-dioxygenase in modulating allergic responses." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/33071/.

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Dendritic cells (DCs) are key players in the induction and re-elicitation of T helper (Th) 2 immune responses to allergens. Recent data by our group have shown that different C-type lectin receptors (CLRs) on DCs play a major role in allergen recognition and uptake. Particularly, mannose receptor (MR), through modulation of Toll-like receptor (TLR) 4 signalling pathway, can regulate indoleamine 2,3 dioxygenase (IDO) activity favouring Th2 responses. IDO is the rate limiting enzyme involved in tryptophan (TRP) catabolism and it is well known for its role in modulating immune responses through TRP depletion and generation of immune-regulatory metabolites known as kynurenines (KYN). Interestingly, another CLR named dendritic cell-specific intracellular adhesion molecule 3-grabbing non-integrin (DC-SIGN) has been suggested to support Th1 responses; however, the mechanisms involved are unknown. Therefore, the main objective of this project was to evaluate the role of CLRs, with focus on MR and DC-SIGN, and TLRs in modulating the IDO pathway in order to understand their involvement in regulating Th2 immune responses. In addition, it was aimed to study how regulation of IDO levels could impact immune responses in order to understand the signalling pathways involved in this process. The data show that mannosylated allergens can down-regulate TLR4-induced IDO1 and IDO2 expressions as well as IDO activity in human DCs, most likely through binding to the MR. This correlates with data showing increased IDO activity in MRlow-DCs (generated by gene silencing) stimulated with mannan compared with control-DCs (CT-DCs). Conversely, DC-SIGN could exert a differential regulation on IDO levels depending on the antigen’s sugar moieties. Mannosylated ligands could up-regulate TLR4-induced IDO activity through DC-SIGN as evidence by a significant reduction in IDO activity in DC-SIGNlow-DCs upon stimulation with mannan compared with CT-DCs. In contrast, DC-SIGN-specific fucosylated ligands, such as Lewis-X (LeX), can down-regulate IDO activity in a TLR4-dependent manner. It was also found that allergens from diverse source can down-regulate IL-12p70 production by DC, which can further impact T helper cell polarization by reducing IFN-γ production by T cells in autologous co-cultures. Moreover, mannan was also shown to decrease CD86 expression in human DCs, which might impact the IDO pathway, as CD86 is one of the B7 family molecules involved in IDO induction. Furthermore, it was found that the LeX can potentially down-regulate IL-6 production by DCs. In addition, DCs stimulated with LeX and LPS induce lower levels of IFN-γ production by autologous T cells than DCs stimulated with LPS only. This effect was reversed in the presence of KYN, showing that the IDO pathway can regulates T helper cell polarization. TLR4 signalling and LPS exposure have been shown to play a pivotal role in Th2-mediated inflammation and asthma. In addition, it is known that CLRs can modulate TLR-induced responses in an allergy context. Therefore, we further study the role of the TLR signalling pathway in modulating IDO levels in human DCs. TLR4 engagement on human DCs was shown to induce high levels of both IDO isoforms. DCs primed with LPS induce much higher levels of IDO than single LPS controls, inducing a cellular re-programing. This was characterized by an induction of anti-inflammatory mediators such as IL-10 and the transcription factor aryl-hydrocarbon receptor (AhR); the last has been previously linked with the IDO pathway in mouse DCs. Intriguingly, TLR9 engagement with synthetic cytosine-phosphate guanosine (CpG) A motifs was able to down-regulate IDO and induce a pro-inflammatory phenotype in human DCs. Future studies should aim at evaluating their implications in immune responses under tolerance and during infection. Finally, the study was aimed at elucidating the intracellular molecules involved in IDO regulation in human DCs. The analysis was first focused on AhR, a ligand-dependent transcription factor that have been suggested to modulate IDO levels in mouse DCs. It was shown for the first time that TLR4 induction of IDO was dependent on AhR in human DCs. In addition, AhR gene expression as well as AhR activity were reduced in DCs stimulated with mannan and LPS compared with LPS only controls. This data suggest that MR can regulate IDO levels by interfering with AhR expression. Furthermore, it was shown that the NF-κB pathway is key in regulating IDO levels through CLRs and TLRs in human DCs. Particularly, RelB, a member of the non-canonical pathway, expression correlates with the levels of AhR, suggesting that a functional and/or physical association between them might be involved in regulating IDO levels in human DCs. Future studies should aim at elucidating such interactions. To sum up, this project has shown the pivotal role of CLRs and TLRs in modulating the IDO pathway in human DCs, which can affect DC phenotype and function and impact immune responses. In addition, we have gained some understanding into the molecular mechanisms of IDO modulation which might involve cooperation between different transcription factors such as AhR and RelB. These data give new insights into how glycosylated allergens can induce Th2 immune responses, which can pave the way to develop better therapeutic strategies to fight back allergy related diseases.
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5

Chute, Christopher. "Decoding Neural Circuits Modulating Behavioral Responses to Aversive Social Cues." Digital WPI, 2018. https://digitalcommons.wpi.edu/etd-dissertations/496.

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Understanding how the human brain functions on a molecular and cellular level is nearly impossible with current technology and ethical considerations. Utilizing the small nematode, Caenorhabditis elegans, and its innate behavioral responses to olfactory social cues, we can begin to unravel the mechanisms underlying social behavior. This is made possible given that innate behaviors are crucial for survival, and therefore hardwired into the genome of organisms. This allows for genetic-level analysis of neural circuitries driving behavior. Studying the neuronal mechanisms underlying C. elegans’ behavioral responses to social cues will not only assist in our overall understanding of how the brain perceives stimuli to enact a behavioral response at the cellular and molecular level, but also our understanding as to how the nervous system properly integrates information to enact social behavioral responses: mis-integration and social abnormalities are commonalities seen in many neuropsychiatric disorders, and these studies will provide fruitful insights into the defects observed in these disorders. Lastly, by comparing the perception of several different types of social chemicals, we can further our understanding of neural coding strategies for the various behaviors crucial for survival. Chapter One of this thesis orients the reader to social, innate behavior, and the usefulness of C. elegans as a tool for understanding behavioral coding. Chapter Two explores and establishes the required components of a socially aversive pheromone, providing insight into signaling evolution and co-option of biological machineries. Chapter Three examines how multiple, competing stimuli are integrated to modulate behavioral output, furthering our understanding of molecular and cellular integration and decision making within the nervous system. Chapter Four highlights the importance of predator pressure, and provides insights into circuit strategies of redundant and promiscuous networks of threat detection. Lastly, Chapter Five considers the implications of these findings as a whole, in the perspective of evolutionary strategies leading to neuronal coding of different behavioral outputs. Taken together, this dissertation aimed to fill the void in our understanding of social behavior neural circuitries, and how integration governed at the molecular and cellular level of the nervous system affects those behaviors.
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6

Suen, Victoria Melissa. "Investigating the role of defined microbes in modulating skin immune responses." Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/investigating-the-role-of-defined-microbes-in-modulating-skin-immune-responses(bb414aa0-66d9-4a4e-8f8b-56a9cc51b7e6).html.

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The skin represents the primary interface between the host and the external environment. It is home to an array of microorganisms that are crucial in maintaining homeostasis and controlling local immunity. Accumulating evidence suggests that skewing of microbial colonisation is critically linked to the development of different skin diseases such as atopic dermatitis (AD) and psoriasis. Among those S. aureus and C. simulans are of special interest for AD and psoriasis respectively, whereas L. crispatus appears to be relevant for healthy skin. However, little is known about how host-microbe interactions can trigger or regulate inflammatory processes in the skin. Dendritic cells (DCs) play a pivotal role in immunological responses and were therefore used in this study to explore the effect of key microbes on skin immunity. The aim of the project was to investigate the direct effects of defined microbes on different DC subsets and their indirect effects on adaptive immune responses. This study demonstrates that different DC subsets in skin exhibit unique immune responses to specific microbes. Langerhans cells were unresponsive to bacterial extracts whereas dermal DCs (DDCs) were more readily matured. Notably, CD141+ DDCs were the only subset to be activated by L. crispatus and produced a range of cytokines after bacterial stimulation. Next it was shown that DC priming with specific microbes, such as L. crispatus-primed CD141+ DDC-like DCs, could induce a distinct population of CD25+ FoxP3hi-expressing T cells, which was impaired in psoriasis patients. Despite phenotypic resemblance to T regulatory (Treg) cells, these cells failed to exhibit suppressive function. Functional specialisation of DC subsets could account for the compartmentalised host regulation of immunogenic or tolerogenic responses to skin microbes. Overall, cutaneous immune cells act in a coordinated manner with specific microbes to calibrate immune status with profound implications for homeostasis and skin disease.
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7

Ebner, Friederike. "The role of microglia phenotypes in modulating CD4 + T cell responses." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2014. http://dx.doi.org/10.18452/16882.

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Die Invasion von Leukozyten in das zentrale Nervensystem (ZNS) ist ein wesentlicher Bestandteil bei der Pathogenese von Hirnverletzungen sowie akuten und chronischen Entzündungsvorgängen im Gehirn. Mikrogliazellen, die überwiegende Population immunkompetenter Zellen des ZNS, stellen die erste Verteidigungslinie im Hinblick auf Verletzungen und Erkrankungen des Gehirns dar. Im Rahmen vieler neurodegenerativer Erkrankungen wird die Zerstörung von Neuronen, aber auch die kollaterale Gewebsschädigung auf die Aktivierung der Mikrogliazellen zurückgeführt. Die vorliegende Arbeit beschreibt erstmalig einen regulatorischen Aktivierungszustand der Mikroglia (CD40dimCD86dimIL-10high), der zur Induktion regulatorischer Foxp3+ T-Zellen (Treg) führt. Die Stabilität und funktionelle Aktivität Mikroglia-induzierter Treg konnte sowohl in vitro als auch in vivo gezeigt werden. In vitro inhibierten sie die Proliferation antigen-spezifischer Effektorzellen, in vivo führte ein adoptiver Transfer der regulatorischen T-Zellen zur Abmilderung des Krankheitsverlaufes experimentell induzierter, autoimmuner Enzephalomyelitis (EAE). Mikrogliazellen unterstützten sowohl die Proliferation bereits ausgebildeter regulatorischer T-Zellen als auch deren Differenzierung aus naiven T-Zellen. Die Induktion regulatorischer T-Zellen durch Mikroglia war Major Histocompatibility Complex (MHC)-II-abhängig und antigenspezifisch. Für Untersuchungen zur in vivo Relevanz wurden MHC-II-chimäre Mäuse generiert und eine Läsion im entorhinalen Kortex gesetzt. Fehlte MHC-II in ZNS-residenten Zellen, wurden weniger regulatorische T-Zellen pro Leukozyt in die lädierten Hemispheren rekrutiert. Zusammenfassend demonstrieren diese Ergebnisse das Modulationspotential von Mikrogliazellen auf die CD4+ T-Zellantwort. Die Mikroglia-induzierte Differenzierung und Proliferation von Foxp3+ regulatorischen T-Zellen ist ein möglicher Mechanismus der Regulation von Entzündungsvorgängen im ZNS durch Mikrogliazellen.
The invasion of leukocytes into the central nervous system (CNS) is a key event in the pathogenesis of CNS injury and acute or chronic inflammatory neurological diseases. However, regulatory mechanisms of local innate immune responses that limit CNS inflammation are only poorly understood. Microglia are the predominant innate immune cells of the brain and present the first line of defence in CNS injury or disease. In the context of neurodegenerative disease, microglia activation accounts for collateral tissue damage and neurodestruction. This thesis for the first time describes a regulatory microglia phenotype (MHCII+CD40dimCD86dimIL-10high) that induced a strong Foxp3+ regulatory T cell (Treg) response. Microglia-induced Treg cells were stable and functionally active in vitro by inhibiting antigen-specific proliferation of effector T cells and in vivo, by attenuating experimental autoimmune encephalomyelitis (EAE) disease course after adoptive transfer. The data also suggested that regulatory microglia can mediate both, proliferation of Foxp3+ Treg cells and de novo differentiation from naive CD4+ T cells. Microglia-mediated Treg induction was proven to be MHCII and antigen-dependent. Using entorhinal cortex lesion (ECL) as a brain injury mouse model, diminished Foxp3+ Treg cell recruitment per infiltrated leukocyte in chimeric mice lacking MHCII specifically in the CNS was demonstrated, indicating in vivo relevance of antigen presentation by brain resident cells. Taken together, these findings demonstrate that microglial cells can directly modulate CD4+ T cell responses by regulating molecule levels for efficient antigen presentation and levels of secreted cytokines and chemokines. Microglia-mediated differentiation and proliferation of Foxp3+ Treg cells can be one of the mechanisms how microglia contribute to local immune homeostasis and limit CNS inflammation.
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8

El-Yassir, Nada. "The role of different 5-HT receptor subtypes in modulating nociception in the rat." Thesis, University of Edinburgh, 1989. http://hdl.handle.net/1842/30179.

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9

Masri, S. Hajar. "The role of natural killer T cells in modulating antigen-specific immune responses." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497047.

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10

Huang, Huang. "The Role of CD39 in Modulating Effector Immune Responses in Inflammatory Bowel Disease." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17295870.

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Inflammatory bowel disease is associated with excessive inflammation of the bowel and intestinal tissues in genetically susceptible individuals. IBD can manifest in two major forms, ulcerative colitis and Crohn’s disease. T helper type 17 cells (Th17) are effector lymphocytes that have been linked to intestinal inflammation in both mice and humans. Effector Th17 cells and regulatory T cells (Treg) – a subset pivotal to immune-tolerance maintenance – derive from the same CD4 progenitors. Our investigation demonstrates that Th17 cells with suppressor activity (supTh17) can be generated upon induced regulatory T cell (iTreg) exposure to Th17 polarizing conditions. With immune suppressive function that differentiates it from Th17, suppressor Th17 (supTh17) expresses high levels of CD39, a membrane-bound protein that catalyzes conversion of pro-inflammatory extracellular nucleotides into nucleosides, such as adenosine. Interestingly, though supTh17 is detected in the peripheral circulation and lamina propria of healthy subjects, it is diminished in patients with Crohn’s disease. This finding has important clinical implications for the development of innovative therapeutic techniques for targeting inflammation in autoimmune diseases, such as IBD.
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Книги з теми "MODULATING RESPONSES"

1

1954-, Kresina Thomas F., ed. Immune modulating agents. New York: M. Dekker, 1998.

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2

Kuba, Kenji, Haruhiro Higashida, David A. Brown, and Tohru Yoshioka, eds. Slow Synaptic Responses and Modulation. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-66973-9.

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3

United States. National Aeronautics and Space Administration., ed. Modulation of bone remodeling via mechanically activated ion channels: Grant: NASA NAG 2-791 & NAG 2-1049, final technical report covering the period from May 1, 1992 - December 31, 1994. [Washington, DC: National Aeronautics and Space Administration, 1996.

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4

United States. National Aeronautics and Space Administration., ed. Modulation of bone remodeling via mechanically activated ion channels: Grant: NASA NAG 2-791 & NAG 2-1049, final technical report covering the period from May 1, 1992 - December 31, 1994. [Washington, DC: National Aeronautics and Space Administration, 1996.

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Galli, Corrado L., Marina Marinovich, and Alan M. Goldberg, eds. Modulation of Cellular Responses in Toxicity. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79872-6.

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L, Galli C., Marinovich Marina, Goldberg Alan M, North Atlantic Treaty Organization. Scientific Affairs Division., and NATO Advanced Study Institute on the Modulation of Cellular Responses in Toxicity (1994 : Ponte di Legno, Italy), eds. Modulation of cellular responses in toxicity. Berlin: Springer, 1995.

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Susanna, Cunningham-Rundles, ed. Nutrient modulation of the immune response. New York: Dekker, 1993.

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Knight, Louise Alice. Modulating sensitivity and response to DNA damaging cytotoxic drugs. Portsmouth: University of Portsmouth, 2004.

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1964-, Buračas Giedrius T., North Atlantic Treaty Organization. Scientific Affairs Division., and NATO Advanced Study Institute on Modulation of Neurological Responses: Implications for Active Vision (2000 : Nida, Lithuania). Proceedings, eds. Modulation of neuronal responses: Implications for active vision. Amsterdam: IOS Press, 2003.

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S, Mitchell Malcolm, ed. The Modulation of immunity. Oxford [Oxfordshire]: Pergamon, 1985.

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Більше джерел

Частини книг з теми "MODULATING RESPONSES"

1

Arruda, Valder R. "Modulating Immune Responses in Muscle Gene Therapy." In Muscle Gene Therapy, 181–204. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1207-7_11.

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Bjørgo, Elisa, Kristine Moltu, and Kjetil Taskén. "Phosphodiesterases as Targets for Modulating T-Cell Responses." In Phosphodiesterases as Drug Targets, 345–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17969-3_15.

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Boxer, Laurence A. "The Role of Antioxidants in Modulating Neutrophil Functional Responses." In Advances in Experimental Medicine and Biology, 19–33. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0553-8_3.

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D’Avola, Delia, and Bruno Sangro. "Modulating Immune Responses to Overcome Resistance in Hepatocellular Carcinoma." In Resistance to Targeted Anti-Cancer Therapeutics, 25–43. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56197-4_2.

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Gater, P. R., and L. M. Renzetti. "Ro 45-2081, a TNF receptor fusion protein, prevents inflammatory responses in the airways." In Therapeutic Strategies for Modulating the Inflammatory Diseases, 67–71. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8857-8_10.

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Henderson, Brian, and Gerry A. Higgs. "Targets for modulating cytokine responses in inflammatory and infectious diseases." In Novel Cytokine Inhibitors, 1–8. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8450-1_1.

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Galea, Gabriel L., and Lee B. Meakin. "Modulating Skeletal Responses to Mechanical Loading by Targeting Estrogen Receptor Signaling." In Mechanobiology, 115–29. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118966174.ch7.

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Harrington, Kevin J., Charleen M. L. Chan Wah Hak, Antonio Rullan, and Emmanuel Patin. "DNA Repair Mechanisms as a New Target in Head and Neck Cancer." In Critical Issues in Head and Neck Oncology, 23–35. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23175-9_3.

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AbstractUntil recently, radiotherapy was viewed solely from a tumour cell-autonomous perspective, whereby successful therapy resulted from inflicting breaks in nuclear DNA above an unspecified threshold that exceeded the tumour cell’s capacity for repair. Greater understanding of the importance of non-tumour cell-autonomous, immunological aspects of radiation-induced cell death in the context of the tumour micro-environment (TME) has altered this rather narrow perception. We now know that clinical responses to radiotherapy are inextricably linked to the immune system: loco-regional radiotherapy can trigger abscopal, immune-mediated responses at distant unirradiated sites (albeit rarely), while patients who are pathologically or iatrogenically immunosuppressed may derive less benefit from radiotherapy. The intrinsic biology of individual tumours, their associated microenvironments, and the physical characteristics of the delivered radiation, can all influence the immunogenicity of radiotherapy. By understanding and modulating cross-talk between molecular responses to radiation-induced DNA damage, associated mechanisms of cell death and subsequent innate and adaptive immune responses, we may be able to improve clinical outcomes of radiotherapy.In this chapter, the focus will be on mechanisms of DNA damage repair and how tumours exploit alterations in these to enhance their survival. However, tumour cell-intrinsic aberrations in DNA repair can render tumour cells vulnerable to the effects of radiotherapy and this may be enhanced further by rational use of targeted DNA damage-response inhibitors. In particular, we will focus on how disordered DNA repair and its pharmacological modulation through ataxia telangiectasia and Rad3-related kinase inhibition can lead to radiation-induced immunostimulation and how this can be exploited further in the clinic through the use of specific immunotherapies, such as immune checkpoint blockers. As part of the discussion, specific mechanisms of radiation-induced cell death will be discussed, with emphasis on mechanisms of triggering immunologically visible, pro-inflammatory modes of cell death.
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Bisht, Aditi, and Neera Garg. "Significance of Organic Solutes in Modulating Plant Inherent Responses under Heavy Metal Stress." In Organic Solutes, Oxidative Stress, and Antioxidant Enzymes Under Abiotic Stressors, 61–82. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003022879-3.

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Chen, Wang, Leng Xiangpeng, Zhang Wenying, and Fang Jinggui. "The Regulatory and Signaling Roles of Glutathione in Modulating Abiotic Stress Responses and Tolerance." In Glutathione in Plant Growth, Development, and Stress Tolerance, 147–69. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-66682-2_7.

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Тези доповідей конференцій з теми "MODULATING RESPONSES"

1

Weinert, Brian, Tine Hannibal, Preeyam Patel, Evelina Martinenaite, Marion Chapellier, Marco Carretta, Alireza Alavi, Ayako Pedersen, and Muhammad Al-Hajj. "1182 Modulating the tumor microenvironment by a targeting TGFB1 with vaccine-induced immune responses." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1182.

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Khan, Nabiha Haleema, Zachary Schrank, Joseph Kellen, Sanjana Singh, Chike Osude, Neelu Puri, and Gagan Chhabra. "Abstract 1469: T-oligo mediates DNA damage responses by modulating telomere associated proteins and telomerase." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1469.

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Nicholson, Kristen J., Julia C. Quindlen, and Beth A. Winkelstein. "Development of a Duration Threshold for Modulating Evoked Neuronal Responses After Nerve Root Compression Injury." In 55th Stapp Car Crash Conference. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 2011. http://dx.doi.org/10.4271/2011-22-0001.

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Chibaya, Loretah, Hong Zhang, and Stephen N. Jones. "Abstract A23: Mdm2 phosphorylation by Akt is critical for modulating cellular responses to oxidative stress." In Abstracts: AACR Special Conference: Advances in Modeling Cancer in Mice: Technology, Biology, and Beyond; September 24-27, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.mousemodels17-a23.

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Schretter, Colas, and Peter Schelkens. "Sequential Adaptive Scattering-Compensated Holography for Fluorescence Microscopy." In Digital Holography and Three-Dimensional Imaging. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/dh.2022.th2a.8.

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We accelerate the Dynamic Adaptive Scattering Compensation Holography (DASH) method and improve numerical robustness. The algorithm is non-iterative and applies sequential updates of the modulating phase instead of gathering responses for equis-paced modes in K-space.
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Muniz, Luciana Ribeiro, Mansi Saxena, and Nina Bhardwaj. "Abstract B169: Matrix metalloproteinase-2 and Toll-like receptors modulating immune responses in the tumor microenvironment." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b169.

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Muniz-Bongers, Luciana Rebiero, Mansi Saxena, and Nina Bhardwaj. "Abstract A104: Matrix metalloproteinase-2 and Toll-Like receptors modulating immune responses in the tumor microenvironment." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a104.

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D'Alessio, Franco R., Kenji Tsushima, Neil R. Aggarwal, Brian T. Garibaldi, D. Clark Files, Michael T. Crow, and Landon S. King. "Macrophage-inducible Nitric Oxide Resolves Experimental Lung Injury By Modulating Lung Innate And Adaptive Immune Responses." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2720.

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Ahn, Sarah, John Yi, and Subing Cao. "1314 Trilaciclib, an intravenous cyclin-dependent kinase 4/6 inhibitor, enhances antitumor responses by modulating T cells." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1314.

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Coarfa, C., S. L. Grimm, R. E. Stading, M. J. Robertson, T. Gandhi, C. Fu, W. Jiang, and B. Moorthy. "Cytochrome P450 (CYP)1B1 Modulates Hyperoxia Responses in Lung by Modulating Protein and Lipid Metabolism." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2531.

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Звіти організацій з теми "MODULATING RESPONSES"

1

Beg, Amer A. Potentiation of T Lymphocyte Responses by Modulating NF-kB Activity in Dendritic Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada437633.

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Beg, Amer A. Potentiation of T Lymphocyte Responses by Modulating NF - Kappa Beta Activity in Dendritic Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417929.

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Philosoph-Hadas, Sonia, Richard Crain, Shimon Meir, Nehemia Aharoni, and Susan Lurie. Calcium-Mediated Signal Transduction during Leaf Senescence. United States Department of Agriculture, November 1995. http://dx.doi.org/10.32747/1995.7604925.bard.

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We have examined the possibility that modulation of [Ca2+]cyt may represent a signal which induces senescence processes in leaves, through triggering of lipid hydrolysis leading to the cascade of detriorative events. Characterization of the signal transduction components operating during leaf senescence was gained by studying various Ca2+-dependent activities of parsley and chrysanthemum leaves, in relation to several senescence functions, and in response to senescence-modulating hormones (ethylene,ABA, BA and IAA). Some innovative findings regarding the control of senescence processes by [Ca2+]cyt were established: Several Ca2+-or CaM-related compounds were shown to modulate [Ca2+]cyt and action, thereby affecting whole leaf senescence. The involvement of [Ca2+]cyt in mediating the effects of senescence-modulating hormones has been demonstrated. Loss of energized Ca2+-transport capability of PM was found to an early event in leaf senescence, which occurs before changes in senescence parameters are observed, and while other PM ATPase enzymes still retain about 50% of their activities. A general pattern of increased phosphorylation of PM proteins with advanced senescence, which could be modified by plant hormones applied in vivo (BA) or in vitro (ABA), sa found. Taken together, all this indirect evidence indicate that [Ca2+]cyt is elevated due to the senescence-induced decrease in the ability to extrude Ca2+, which results particularly from reduced PM Ca2++-transport capability rather than increased operation of Ca2+ channels or elevated Ins(1,4,5)P3 levels. The direct proof for such a senescence-related elevation in [Ca2+]cyt was provided for the first time by the Ca2+ imaging measures with fura-2, showing a rise in [Ca2+]cyt of mesophyll cells upon senescence induction, which preceeded changes in typical senescence characteristics. This research provides strong evidence for regarding the rise in [Ca2+]cyt as a primary event in induction of the senescence syndrome in detached leaves. The findings have also broad implications for postharvest handling of leafy crops and ornamentals, and open new avenues for employing Ca2+-related inhibitors to delay leaf senescence.
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Olszewski, Neil, and David Weiss. Role of Serine/Threonine O-GlcNAc Modifications in Signaling Networks. United States Department of Agriculture, September 2010. http://dx.doi.org/10.32747/2010.7696544.bard.

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Significant evidence suggests that serine/threonine-O-linked N-acetyl glucosamine0-(GlcNAc) modifications play a central role in the regulation of plant signaling networks. Forexample, mutations in SPINDLY,) SPY (an O-GlcNAc transferase,) OGT (promote gibberellin GA) (signal transduction and inhibit cytokinin responses. In addition, mutating both Arabidopsis OGTsSEC (and SPY) causes embryo lethality. The long-term goal of this research is to elucidate the mechanism by which Arabidopsis OGTs regulate signaling networks. This project investigated the mechanisms of O-GlcNAc regulation of cytokinin and gibberellin signaling, identified additional processes regulated by this modification and investigated the regulation of SEC activity. Although SPY is a nucleocytoplasmic protein, its site of action and targets were unknown. Severalstudies suggested that SPY acted in the nucleus where it modified nuclear components such as the DELLA proteins. Using chimeric GFP-SPY fused to a nuclear-export signal or to a nuclear-import signal, we showed that cytosolic, but not nuclear SPY, regulated cytokinin and GA signaling. We also obtained evidence suggesting that GA and SPY affect cytokinin signaling via a DELLA-independent pathway. Although SEC and SPY were believed to have overlapping functions, the role of SEC in cytokinin and GA signaling was unclear. The role of SEC in cytokinin and GA responses was investigated by partially suppressing SPY expression in secplants using a synthetic Spymicro RNA miR(SPY). The possible contribution of SEC to the regulation of GA and cytokinin signaling wastest by determining the resistance of the miR spy secplants to the GA biosynthesis inhibitor paclobutrazol and to cytokinin. We found that the transgenic plants were resistant to paclobutrazol and to cytokinin, butonlyata level similar to spy. Moreover, expressing SEC under the 35S promoter in spy mutant did not complement the spy mutation. Therefore, we believe that SEC does not act with SPY to regulate GA or cytokinin responses. The cellular targets of Spy are largely unknown. We identified the transcription factor TCP15 in a two-hybrid screen for SPY-interacting proteins and showed that both TCP15 and its closely homolog TCP14 were O-GlcNAc modified by bacterially-produced SEC. The significance of the interaction between SPY and these TCPs was examined by over-expressing the minwild-type and spy-4plants. Overexpression of TCP14 or TCP15 in wild-type background produced phenotypes typical of plants with increased cytokinin and reduced GA signaling. TCP14 overexpression phenotypes were strongly suppressed in the spy background, suggesting that TCP14 and TCP15 affect cytokinin and GA signaling and that SPY activates them. In agreement with this hypothesis, we created a tcp14tcp15 double mutant and found that it has defects similar to spyplants. In animals, O-GlcNAc modification is proposed to regulate the activity of the nuclear pore. Therefore, after discovering that SEC modified a nucleoporinNUP) (that also interacts with SPY, we performed genetic experiments exploring the relationship between NUPs and SPY nupspy double mutants exhibited phenotypes consistent with SPY and NUPs functioning in common processes and nupseeds were resistant to GA biosynthesis inhibitors. All eukaryotic OGTs have a TPR domain. Deletion studies with bacterially-expressed SEC demonstrated SEC'sTPR domain inhibits SEC enzymatic activity. Since the TPR domain interacts with other proteins, we propose that regulatory proteins regulate OGT activity by binding and modulating the inhibitory activity of the TPR domain.
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Sacchi, Nicoletta. Modulation of Breast Tumor Cell Response to Retinoids by Histone Deacetylase Inhibitors. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada417781.

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Usechak, Nicholas G., Michael Pochet, John Schmidt, and Luke Lester. Modulation Response of a Long-Cavity, Gain-Levered Quantum-Dot Semiconductor Laser - Postprint. Fort Belvoir, VA: Defense Technical Information Center, January 2014. http://dx.doi.org/10.21236/ada612528.

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Redmond, Sarah Beth, Rachel Tell, Derrick Coble, Carrie Mueller, Dušan Palić, Claire B. Andreasen, and Susan J. Lamont. Genetic Differences in Chicken Splenic Immune Gene Expression in Response to Dietary Immune Modulation. Ames (Iowa): Iowa State University, January 2010. http://dx.doi.org/10.31274/ans_air-180814-166.

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Chejanovsky, Nor, Diana Cox-Foster, Victoria Soroker, and Ron Ophir. Honeybee modulation of infection with the Israeli acute paralysis virus, in asymptomatic, acutely infected and CCD colonies. United States Department of Agriculture, December 2013. http://dx.doi.org/10.32747/2013.7594392.bard.

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Honey bee (Apis mellifera) colony losses pose a severe risk to the food chain. The IAPV (Israeli acute paralysis virus) was correlated with CCD, a particular case of colony collapse. Honey bees severely infected with IAPV show shivering wings that progress to paralysis and subsequent death. Bee viruses, including IAPV, are widely present in honey bee colonies but often there are no pathological symptoms. Infestation of the beehive with Varroa mites or exposure to stress factors leads to significant increase in viral titers and fatal infections. We hypothesized that the honey bee is regulating/controlling IAPV and viral infections in asymptomatic infections and this control is broken through "stress" leading to acute infections and/or CCD. Our aims were: 1. To discover genetic changes in IAPV that may affect tissue tropism in the host, and/or virus infectivity and pathogenicity. 2. To elucidate mechanisms used by the host to regulate/ manage the IAPV-infection in vivo and in vitro. To achieve the above objectives we first studied stress-induced virus activation. Our data indicated that some pesticides, including myclobutanil, chlorothalonil and fluvalinate, result in amplified viral titers when bees are exposed at sub lethal levels by a single feeding. Analysis of the level of immune-related bee genes indicated that CCD-colonies exhibit altered and weaker immune responses than healthy colonies. Given the important role of viral RNA interference (RNAi) in combating viral infections we investigated if CCD-colonies were able to elicit this particular antiviral response. Deep-sequencing analysis of samples from CCD-colonies from US and Israel revealed high frequency of small interfering RNAs (siRNA) perfectly matching IAPV, Kashmir bee virus and Deformed wing virus genomes. Israeli colonies showed high titers of IAPV and a conserved RNAi pattern of targeting the viral genome .Our findings were further supported by analysis of samples from colonies experimentally infected with IAPV. Following for the first time the dynamics of IAPV infection in a group of CCD colonies that we rescued from collapse, we found that IAPV conserves its potential to act as one lethal, infectious factor and that its continuous replication in CCD colonies deeply affects their health and survival. Ours is the first report on the dominant role of IAPV in CCD-colonies outside from the US under natural conditions. We concluded that CCD-colonies do exhibit a regular siRNA response that is specific against predominant viruses associated with colony losses and other immune pathways may account for their weak immune response towards virus infection. Our findings: 1. Reveal that preventive measures should be taken by the beekeepers to avoid insecticide-based stress induction of viral infections as well as to manage CCD colonies as a source of highly infectious viruses such as IAPV. 2. Contribute to identify honey bee mechanisms involved in managing viral infections.
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Foss, John A., James R. Ison, James P. Torre, Wansack Jr, and Samuel. The Acoustic Startle Response and Disruption of Aiming. 2. Modulation by Forewarning and Preliminary Stimuli. Fort Belvoir, VA: Defense Technical Information Center, November 1989. http://dx.doi.org/10.21236/ada217105.

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Fromm, Hillel, and Joe Poovaiah. Calcium- and Calmodulin-Mediated Regulation of Plant Responses to Stress. United States Department of Agriculture, September 1993. http://dx.doi.org/10.32747/1993.7568096.bard.

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We have taken a molecular approach to clone cellular targets of calcium/calmodulin (Ca2+/CaM). A 35S-labeled recombinant CaM was used as a probe to screen various cDNA expression libraries. One of the isolated clones from petunia codes for the enzyme glutamate decarboxylase (GAD) which catalyzes the conversion of glutamate to g-aminobutyric acid (GABA). The activity of plant GAD has been shown to be dramatically enhanced in response to cold and heat shock, anoxia, drought, mechanical manipulations and by exogenous application of the stress phytohormone ABA in wheat roots. We have purified the recombinant GAD by CaM-affinity chromatography and studied its regulation by Ca2+/CaM. At a physiological pH range (7.0-7.5), the purified enzyme was inactive in the absence of Ca2+ and CaM but could be stimulated to high levels of activity by the addition of exogenous CaM (K0.5 = 15 nM) in the presence of Ca2+ (K 0.5 = 0.8 mM). Neither Ca2+ nor CaM alone had any effect on GAD activity. Transgenic tobacco plants expressing a mutant petunia GAD lacking the CaM-binding domain, or transgenic plants expressing the intact GAD were prepared and studied in detail. We have shown that the CaM-binding domain is necessary for the regulation of glutamate and GABA metabolism and for normal plant development. Moreover, we found that CaM is tightly associated with a 500 kDa GAD complex. The tight association of CaM with its target may be important for the rapid modulation of GAD activity by Ca2+ signaling in response to stresses.
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