Relevant bibliographies by topics / Mediated pathways

Academic literature on the topic 'Mediated pathways'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Mediated pathways"

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ZHU, LING, TIMON CHENG-YI LIU, MIN WU, JIAN-QIN YUAN, and TONG-SHENG CHEN. "EXTRAOCULAR CELLULAR PHOTOTRANSDUCTION." Journal of Innovative Optical Health Sciences 02, no. 01 (January 2009): 93–100. http://dx.doi.org/10.1142/s1793545809000358.

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Photobiomodulation (PBM) is a modulation of monochromatic light or laser irradiation (LI) on biosystems. It is reviewed from the viewpoint of extraocular phototransduction in this paper. It was found that LI can induce extraocular phototransduction, and there may be an exact correspondence relationship of LI at different wavelengths and in different dose zones, and cellular signal transduction pathways. The signal transduction pathways can be classified into two types so that the Gs protein-mediated pathways belong to pathway 1, and the other pathways such as protein kinase Cs -mediated pathways and mitogen-activated protein kinase-mediated pathways belong to pathway 2. Almost all the present pathways found to mediate PBM belong to pathway 2, but there should be a pathway 1-mediated PBM. The previous studies were rather preliminary, and therefore further work should be done.
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Gorvin, Caroline M. "Insights into calcium-sensing receptor trafficking and biased signalling by studies of calcium homeostasis." Journal of Molecular Endocrinology 61, no. 1 (July 2018): R1—R12. http://dx.doi.org/10.1530/jme-18-0049.

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The calcium-sensing receptor (CASR) is a class C G-protein-coupled receptor (GPCR) that detects extracellular calcium concentrations, and modulates parathyroid hormone secretion and urinary calcium excretion to maintain calcium homeostasis. The CASR utilises multiple heterotrimeric G-proteins to mediate signalling effects including activation of intracellular calcium release; mitogen-activated protein kinase (MAPK) pathways; membrane ruffling; and inhibition of cAMP production. By studying germline mutations in the CASR and proteins within its signalling pathway that cause hyper- and hypocalcaemic disorders, novel mechanisms governing GPCR signalling and trafficking have been elucidated. This review focusses on two recently described pathways that provide novel insights into CASR signalling and trafficking mechanisms. The first, identified by studying a CASR gain-of-function mutation that causes autosomal dominant hypocalcaemia (ADH), demonstrated a structural motif located between the third transmembrane domain and the second extracellular loop of the CASR that mediates biased signalling by activating a novel β-arrestin-mediated G-protein-independent pathway. The second, in which the mechanism by which adaptor protein-2 σ-subunit (AP2σ) mutations cause familial hypocalciuric hypercalcaemia (FHH) was investigated, demonstrated that AP2σ mutations impair CASR internalisation and reduce multiple CASR-mediated signalling pathways. Furthermore, these studies showed that the CASR can signal from the cell surface using multiple G-protein pathways, whilst sustained signalling is mediated only by the Gq/11 pathway. Thus, studies of FHH- and ADH-associated mutations have revealed novel steps by which CASR mediates signalling and compartmental bias, and these pathways could provide new targets for therapies for patients with calcaemic disorders.
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Xu, Wen, Bei Wang, Yisong Gao, Yuxuan Cai, Jiali Zhang, Zhiyin Wu, Jiameng Wei, Chong Guo, and Chengfu Yuan. "Alkaloids Exhibit a Meaningful Function as Anticancer Agents by Restraining Cellular Signaling Pathways." Mini-Reviews in Medicinal Chemistry 22, no. 7 (April 2022): 968–83. http://dx.doi.org/10.2174/1389557521666211007114935.

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Abstract: Alkaloids are nitrogen-containing organic compounds widely found in natural products, which play an essential role in clinical treatment. Cellular signaling pathways in tumors are a series of enzymatic reaction pathways that convert extracellular signals into intracellular signals to produce biological effects. The ordered function of cell signaling pathways is essential for tumor cell proliferation, differentiation, and programmed death. This review describes the antitumor progression mediated by various alkaloids after inhibiting classical signaling pathways; related studies are systematically retrieved and collected through PubMed. We selected the four currently most popular pathways for discussion and introduced the molecular mechanisms mediated by alkaloids in different signaling pathways, including the NF-kB signaling pathway, PI3K/AKT signaling pathway, MAPK signaling pathway, and P53 signaling pathway. The research progress of alkaloids related to tumor signal transduction pathwa
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Kamarajan, Pachiyappan, Julius Bunek, Yong Lin, Gabriel Nunez, and Yvonne L. Kapila. "Receptor-interacting Protein Shuttles between Cell Death and Survival Signaling Pathways." Molecular Biology of the Cell 21, no. 3 (February 2010): 481–88. http://dx.doi.org/10.1091/mbc.e09-06-0530.

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Cross-talk between apoptosis and survival signaling pathways is crucial for regulating tissue processes and mitigating disease. We report that anoikis—apoptosis triggered by loss of extracellular matrix contacts—activates a CD95/Fas-mediated signaling pathway regulated by receptor-interacting protein (RIP), a kinase that shuttles between CD95/Fas-mediated cell death and integrin/focal adhesion kinase (FAK)-mediated survival pathways. RIP's death domain was critical for RIP and Fas association to mediate anoikis. Fas or RIP attenuation reduced this association and suppressed anoikis, whereas their overexpression had the reverse effect. Overexpressing FAK restored RIP and FAK association and inhibited anoikis. Thus, RIP shuttles between CD95/Fas death and FAK survival signaling to mediate anoikis.
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Wang, Wen-Horng, Gérald Grégori, Ronald L. Hullinger, and Ourania M. Andrisani. "Sustained Activation of p38 Mitogen-Activated Protein Kinase and c-Jun N-Terminal Kinase Pathways by Hepatitis B Virus X Protein Mediates Apoptosis via Induction of Fas/FasL and Tumor Necrosis Factor (TNF) Receptor 1/TNF-α Expression." Molecular and Cellular Biology 24, no. 23 (December 1, 2004): 10352–65. http://dx.doi.org/10.1128/mcb.24.23.10352-10365.2004.

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ABSTRACT Activation of the cellular stress pathways (c-Jun N-terminal kinase [JNK] and p38 mitogen-activated protein [MAP] kinase) is linked to apoptosis. However, whether both pathways are required for apoptosis remains unresolved. Hepatitis B virus X protein (pX) activates p38 MAP kinase and JNK pathways and, in response to weak apoptotic signals, sensitizes hepatocytes to apoptosis. Employing hepatocyte cell lines expressing pX, which was regulated by tetracycline, we investigated the mechanism of apoptosis by p38 MAP kinase and JNK pathway activation. Inhibition of the p38 MAP kinase pathway rescues by 80% the initiation of pX-mediated apoptosis, whereas subsequent apoptotic events involve both pathways. pX-mediated activation of p38 MAP kinase and JNK pathways is sustained, inducing the transcription of the death receptor family genes encoding Fas/FasL and tumor necrosis factor receptor 1 (TNFR1)/TNF-α and the p53-regulated Bax and Noxa genes. The pX-dependent expression of Fas/FasL and TNFR1/TNF-α mediates caspase 8 activation, resulting in Bid cleavage. In turn, activated Bid, acting with pX-induced Bax and Noxa, mediates the mitochondrial release of cytochrome c, resulting in the activation of caspase 9 and apoptosis. Combined antibody neutralization of FasL and TNF-α reduces by 70% the initiation of pX-mediated apoptosis. These results support the importance of the pX-dependent activation of both the p38 MAP kinase and JNK pathways in pX-mediated apoptosis and suggest that this mechanism of apoptosis occurs in vivo in response to weak apoptotic signals.
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Andriichuk, T. R., N. G. Raksha, and L. I. Ostapchenko. "RADIATION-MEDIATED SIGNALING PATHWAYS." Biological Markers in Fundamental and Clinical Medicine (collection of abstracts) 2, no. 1 (March 24, 2018): 77–78. http://dx.doi.org/10.29256/v.02.01.2018.escbm34.

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LIU, TIMON CHENG-YI, LING ZHU, and XIANG-BO YANG. "PHOTOBIOMODULATION-MEDIATED PATHWAY DIAGNOSTICS." Journal of Innovative Optical Health Sciences 06, no. 01 (January 2013): 1330001. http://dx.doi.org/10.1142/s1793545813300012.

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Cellular pathways are ordinarily diagnosed with pathway inhibitors, related gene regulation, or fluorescent protein markers. They are also suggested to be diagnosed with pathway activation modulation of photobiomodulation (PBM) in this paper. A PBM on a biosystem function depends on whether the biosystem is in its function-specific homeostasis (FSH). An FSH, a negative feedback response for the function to be performed perfectly, is maintained by its FSH-essential subfunctions and its FSH-non-essential subfunctions (FNSs). A function in its FSH or far from its FSH is called a normal or dysfunctional function. A direct PBM may self-adaptatively modulate a dysfunctional function until it is normal so that it can be used to discover the optimum pathways for an FSH to be established. An indirect PBM may self-adaptatively modulate a dysfunctional FNS of a normal function until the FNS is normal, and the normal function is then upgraded so that it can be used to discover the redundant pathways for a normal function to be upgraded.
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Tang, Xiao, Daqiao Guo, Changpo Lin, Zhenyu Shi, Ruizhe Qian, Weiguo Fu, Jianjun Liu, Xu Li, and Longhua Fan. "hCLOCK Causes Rho-Kinase-Mediated Endothelial Dysfunction and NF-κB-Mediated Inflammatory Responses." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/671839.

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Background. The human Circadian Locomotor Output Cycle protein Kaput (CLOCK) gene was originally discovered as a regulator of essential human daily rhythms. This seemingly innocuous gene was then found to be associated with a multitude of human malignancies, via several biochemical pathways. We aimed to further investigate the role of hCLOCK in the hypoxia-oxidative stress response system at the biochemical level.Methods. Expression levels of Rho GTPases were measured in normoxic and hypoxic states. The effect of hCLOCK on the hypoxic response was evaluated with the use of a retroviral shRNA vector system, a Rho inhibitor, and a ROS scavenger by analyzing expression levels of hCLOCK, Rho GTPases, and NF-κB pathway effectors. Finally, in vitro ROS production and tube formation in HUVECs were assessed.Results. Hypoxia induces ROS production via hCLOCK. hCLOCK activates the RhoA and NF-κB signaling pathways. Conversely, inhibition of hCLOCK deactivates these pathways. Furthermore, inhibition of RhoA or decreased levels of ROS attenuate these pathways, but inhibition of RhoA does not lead to decreased levels of ROS. Overall findings show that hypoxia increases the expression of hCLOCK, which leads to ROS production, which then activates the RhoA and NF-κB pathways.Conclusion. Our findings suggest that hypoxic states induce vascular oxidative damage and inflammation via hCLOCK-mediated production of ROS, with subsequent activation of the RhoA and NF-κB pathways.
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Dusaban, Stephanie S., and Joan Heller Brown. "PLCε mediated sustained signaling pathways." Advances in Biological Regulation 57 (January 2015): 17–23. http://dx.doi.org/10.1016/j.jbior.2014.09.014.

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Zhang, Qing, Jia Liu, Mengmeng Zhang, Shujun Wei, Ruolan Li, Yongxiang Gao, Wei Peng, and Chunjie Wu. "Apoptosis Induction of Fibroblast-Like Synoviocytes Is an Important Molecular-Mechanism for Herbal Medicine along with its Active Components in Treating Rheumatoid Arthritis." Biomolecules 9, no. 12 (November 28, 2019): 795. http://dx.doi.org/10.3390/biom9120795.

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Rheumatoid arthritis (RA) is a known chronic autoimmune disease can cause joint deformity and even loss of joint function. Fibroblast-like synoviocytes (FLS), one of the main cell types in synovial tissues of RA patients, are key effector cells in the development of RA and are considered as promising therapeutic targets for treating RA. Herbal medicines are precious resources for finding novel agents for treating various diseases including RA. It is reported that induction of apoptosis in FLS is an important mechanism for the herbal medicines to treat RA. Consequently, this paper reviewed the current available references on pro-apoptotic effects of herbal medicines on FLS and summarized the related possible signal pathways. Taken together, the main related signal pathways are concluded as death receptors mediated apoptotic pathway, mitochondrial dependent apoptotic pathway, NF-κB mediated apoptotic pathways, mitogen-activated protein kinase (MAPK) mediated apoptotic pathway, endoplasmic reticulum stress (ERS) mediated apoptotic pathway, PI3K-Akt mediated apoptotic pathway, and other reported pathways such as janus kinase/signal transducers and activators of transcription (JAK-STAT) signal pathway. Understanding the apoptosis induction pathways in FLS of these herbal medicines will not only help clear molecular mechanisms of herbal medicines for treating RA but also be beneficial for finding novel candidate therapeutic drugs from natural herbal medicines. Thus, we expect the present review will highlight the importance of herbal medicines and its components for treating RA via induction of apoptosis in FLS, and provide some directions for the future development of these mentioned herbal medicines as anti-RA drugs in clinical.
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Dissertations / Theses on the topic "Mediated pathways"

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Raval, Raju R. "Hypoxia-mediated pathways in cancer." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433331.

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Prado, Sánchez Judith. "Regulation of neuroinflammation by cGMP-mediated pathways." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/96910.

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En el trabajo aquí presentado se investigó la participación de los niveles intracelulares de GMP-cíclico (CMPC) en la regulación de diferentes aspectos de la neuroinflamación. En el primer capítulo hemos observado que los cultivos de astrocitos y de celulas microgliales aisladas de rata expresan la maquinaria necesaria para sintetizar GMPc en repuesta a Péptidos Natriuréticos (PN) y también los enzimas necesarios para degradar el nucleótido. También se investigaron los efectos de la estimulación por PN en la expresión de la proteína pro-inflamatoria iNOS. Hemos observado que el pretratamiento con ANP hace disminuir los niveles de la proteína iNOS inducida por el agente pro-inflamatorio LPS a través de un mecanismo dependiente de NPR-A-PKG en células microgliales cultivadas de rata. Además hemos observado que esta regulación a la baja parece estar hecha a nivel de traducción, sin afectar a la transcripción o la tasa de degradación de la proteína. Sobre la base de datos obtenidos en nuestro laboratorio en cultivos de células gliales, se ha demostrado que las vías mediadas por GMPc regulan la dinámica del citoesqueleto, la expresión de GFAP en los astrocitos y la motilidad, así como la expresión de genes inflamatorios en la microglía que se demuestra en el primer capítulo, lo que sugiere un papel en la regulación del fenotipo reactivo glial. En el segundo capítulo, hemos querido verificar si el GMPc regula la respuesta inflamatoria glial in vivo después de un daño producido en el SNC causado por una criolesión focal en la corteza cerebral en ratas y ratones. Se investigó el efecto de 3 dosis de tratamiento con dos inhibidores de diferentes fosfodiesterasas de GMPc (PDE), zaprinast y sildenafilo. Hemos observado que el inhibidor no selectivo de PDE-GMPc zaprinast potencia la astrogliosis alrededor de la lesión, mientras que produce una disminución de la activación de macrófagos/microglía, el estrés oxidativo y muerte neuronal en la rata. Se observó también que el tratamiento con el inhibidor selectivo de la PDE5 sildenafilo reproduce en los ratones los cambios en la reactividad glial y los efectos antioxidantes y antiapoptóticos observados anteriormente con el zaprinast en ratas, indicando que la inhibición de la PDE5 es responsable de estas acciones neuroprotectoras. Sin embargo, los efectos de sildenafilo no se observaron en los ratones deficientes en MT-I/II. Asimismo, se muestra que el sildenafilo aumenta significativamente los niveles de las proteínas MT-I/II en homogenados corticales de ratones lesionados así como la inmunotinción de MT-I/II en las células gliales alrededor de la lesión, y disminuye la activación del factor transcriptor de STAT3, apoyando la participación de estas proteínas en los efectos neuroprotectores del sildenafilo en la lesión cerebral focal. Como resultado de los efectos antiinflamatorios y neuroprotectores observados por los inhibidores de la PDE5 en el modelo criolesión, en el tercer capítulo se investigó si el tratamiento con sildenafilo podría tener efectos beneficiosos en un modelo de EAE inducido por MOG35-55, un modelo animal de esclerosis múltiple, una enfermedad en la que existe una respuesta inflamatoria alterada. Se demuestra que el tratamiento con sildenafilo después del inicio de la enfermedad reduce notablemente los síntomas clínicos de la EAE mediante la prevención de la pérdida axonal y la promoción de la remielinización. Por otra parte, el sildenafilo disminuye la infiltración de leucocitos CD3+ así como la activación de microglia/macrófagos en la médula espinal, al tiempo que aumenta la presencia de Foxp3-Tregs. Además, el tratamiento con sildenafilo disminuye la expresión de ICAM-1 en las células infiltradas de la médula espinal. La presencia de astrocitos reactivos que forman estructuras similares a cicatrices alrededor de los infiltrados se potenció por el tratamiento con sildenafilo, sugiriendo un posible mecanismo para restringir la propagación de leucocitos en el parénquima sano. Se demuestra también que el tratamiento con sildenafilo al inicio de los síntomas clínicos, cuando el proceso inflamatorio es más fuerte, impide el avance de la enfermedad y regula la respuesta adaptativa inmune periférica y los niveles de la PDE5. Teniendo en cuenta todos los resultados obtenidos se demuestra que la modulación de los niveles intracelulares de GMPc tiene efectos beneficiosos en los procesos neuroinflamatorios y que estos beneficios están relacionados con la regulación de la gliosis reactiva, el estrés oxidativo, factores antioxidantes, la respuesta inmune adaptativa y la infiltración de células inmunes en el SNC que conducen a una disminuición en el daño neuronal.
In the present work we investigated the involvement of intracellular cGMP levels in regulating different aspects of neuroinflammation. In the first chapter we observed that cultured rat astrocytes and microglial cells express the necessary machinery to synthesize cGMP in response NPs and to degrade the nucleotide. We also investigated the effects of NP stimulation in the expression of the pro-inflammatory protein iNOS. We observed that pretreatment with ANP down-regulates iNOS protein levels induced by the pro-inflammatory agent LPS by an NPR-A-PKG dependent mechanism in rat cultured microglial cells. In addition we found that this down-regulation seems to be done at translational level, without affecting transcription or protein degradation rate. Based on evidence obtained in our laboratory in cultured glial cells indicates that cGMP-mediated pathways regulate cytoskeleton dynamics, GFAP expression and motility in astrocytes, as well as inflammatory gene expression in microglia found in the first chapter, suggesting a role in the regulation of the glial reactive phenotype. In the second chapter we wanted to examine if cGMP regulates the glial inflammatory response in vivo following CNS damage caused by a focal cryolesion onto the cortex in rats and mice. We investigated the effect of 3 doses of treatment with two different cGMP-phosphodiesterase (PDE) inhibitors, zaprinast and sildenafil. We observed that the non-selective GMP-PDE inhibitor zaprinast enhances astrogliosis around the lesion while decreasing macrophage/microglial activation, oxidative stress and neuronal death in rat. We observed also that treatment with the selective PDE5 inhibitor sildenafil reproduces in mice the changes in glial reactivity and the antioxidant and antiapoptotic effects previously observed with zaprinast in rats indicating that inhibition of PDE5 is responsible for these neuroprotective actions. However, sildenafil effects were not observed in mice deficient in MT-I/II. We further show that sildenafil significantly increases MT-I/II protein levels in lesioned cortical homogenates and MT-I/II immunostaining in glial cells around the lesion, and decreases activation of the transcriptor factor STAT3, supporting the involvement of these proteins in the neuroprotective effects of sildenafil in focal brain lesion. As a result of the anti- inflammatory and neuroprotective effects observed by PDE5 inhibitors in the cryolesion model, in the third chapter we investigate if treatment with sildenafil could have beneficial effects in a MOG35-55-induced EAE model, an animal model of MS, a disease where an altered inflammatory response occurs. We show that treatment with sildenafil after disease onset markedly reduces the clinical signs of EAE by preventing axonal loss and promoting remyelination. Furthermore, sildenafil decreases CD3+-leukocyte infiltration and microglial/macrophage activation in the spinal cord, while increasing Foxp3-Tregs. In addition, sildenafil treatment decreased ICAM-1 in spinal cord infiltrated cells. The presence of reactive astrocytes forming scar-like structures around infiltrates was enhanced by sildenafil suggesting a possible mechanism for restriction of leukocyte spread into healthy parenchyma. We show also that treatment with sildenafil at the onset of clinical symptoms, when the inflammatory process is stronger, prevent disease advance and regulates peripheral adaptative immune response and PDE5 levels. Taking in account all the results obtained we evidenced that modulation of intracellular cGMP levels have beneficial effects in neuroinflammatory processes and that this benefits are related to regulation of reactive gliosis, oxidative stress, antioxidant factors, adaptative immune response and infiltration of immune cells into CNS leading to decrease neuronal damage.
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Vosten, Alexander. "Mathematical modelling of scaffold-mediated signalling pathways." Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/213225/1/Alexander_Vosten_Thesis.pdf.

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This thesis concerns the role of specialized molecules called scaffold proteins in the processing of signals in cellular protein networks. In particular, comprehensive mathematical models are developed of the mitogen-activated protein kinase cascade (MAPK) – an evolutionarily conserved signalling motif. Due to the complexity of the biological systems being modelled, an original method of algebraic analysis was used to ease computation time. These novel models and analysis provide new evidence that scaffold proteins have significant and unexpected potential to increase the possibility of switch-like responses known as bistability and ultrasensitivity.
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Wong, Tsz-yeung, and 王子揚. "IBDV-mediated antiviral responses by TLR3 signaling pathways." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41897201.

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Charlesworth, Amanda. "Signalling pathways mediated by the bombesin/GRP receptor." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244267.

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Zhu, Liang. "RAP1-TRIGGERED PATHWAYS FOR TALIN-MEDIATED INTEGRIN ACTIVATION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1512580363343006.

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Wong, Tsz-yeung. "IBDV-mediated antiviral responses by TLR3 signaling pathways." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B41897201.

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Boyer, Robert D. (Robert Damian) 1978. "Stress-mediated reaction pathways for dislocation nucleation in copper." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/39550.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Materials Science and Engineering, 2007.
Includes bibliographical references (p. 111-119).
The ductile behavior of metals requires dislocation nucleation, from either homogeneous or heterogeneous sources, in order to produce the large number of dislocations necessary for extensive plastic deformation. As with the majority of the defect processes that comprise deformation and failure of materials, dislocation nucleation is well described in the framework of transition state theory as a stress-mediated, thermally activated process. We have used reaction pathway sampling methods and well-fit empirical potentials to determine the stress-dependent behavior of and atomistic mechanisms for dislocation nucleation at stresses much lower than typically accessible to atomistic techniques. We have shown that a significant range of stresses exist for which homogeneous dislocation loop nucleation is feasible because the critical nucleate transitions to an in-plane shear perturbation where the shear displacement of most particles is significantly less than the Burger's vector. We have also revealed that the common structural conception of activation volume for dislocation nucleation does not apply for all stresses and in general over-predicts the stress-dependence of activation by considering only the shear displacement of the critical defect.
(cont.) Furthermore, by considering the full reaction pathway for dislocation nucleation in perfect crystals and at a vacancy, we have provided a fully atomistic description of shear localization via an expanded one-dimensional chain analysis of the wave-steepening behavior. Lastly, both breaking the local atomic symmetry and increasing the extent of heterogeneous nucleation sites are shown to lower the activation energy for dislocation nucleation. In general we have applied reaction pathway sampling to the problem of dislocation nucleation in Cu not only for a perfect crystal, but also in the presence of point defects, vacancy clusters and nanowire surfaces. As a result the strength of a variety of nucleation sites in mediating activation as well as specific atomistic mechanisms for dislocation nucleation have been discussed from both structural and energetic perspectives.
by Robert D. Boyer.
Ph.D.
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Sickle, Eugene Stanford. "Cycloaddition-fragmentation mediated pathways to ring D modified 19-norsteroids." Doctoral thesis, University of Cape Town, 1997. http://hdl.handle.net/11427/17967.

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An efficient strategy for the synthesis of 14β-3'-oxobutyl 19-norsteroids has been developed and the intramolecular reactivity of the derived compounds has been investigated. The approach is based on cycloaddition of methyl vinyl ketone to 3-methoxyestra-1,3,5(10),14,16-pentaen-17-yl acetate which proceeded with a high degree of regio- and stereoselectivity to give 16α-acetyl-3-methoxy-14, 17α-ethenoestra-1 ,3,5(1 O)-trien-17β-yl acetate. The cycloadduct underwent base mediated fragmentation, affording an efficient and stereocontrolled synthesis of 3-methoxy-14β-3'-oxobutylestra-1,3,5(10),15-tetraen-17-one which in turn gave 3-methoxy-5',6'-dihydro-15αH-benzo[14,15]-14β-estra-1,3,5(1O)-trien-4'(3'H), 17-dione via an intramolecular Michael reaction. Regioselective deoxygenation of the dione at C-4', followed by standard functional group modifications provided the parent 14β-perhydrobenzo[14,15]-estradiol analogues. An alternative, more expedient, route to this novel steroidal ring system was developed which relied on an anionic oxy-Cope rearrangement as the key step. Thus methylenation of the cycloadducts derived from reaction of the dienyl acetate and selected dienophiles (acrolein and methyl vinyl ketone) gave after hydrolysis of the bridgehead ester, substrates which underwent [3,3]sigmatropic rearrangement to generate a series of 14β-perhydrobenzo[14,15]-17-ketones.
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Perens, Gregory S. "NMDA Receptor-mediated Synaptic Plasticity in Developing Mammalian Visual Pathways." VCU Scholars Compass, 1995. https://scholarscompass.vcu.edu/etd/5246.

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Precise connections in many mammalian nervous systems require a great deal of remodeling during development. In the visual system, many excess synapses are originally formed in the lateral geniculate nucleus and striate cortex. Only the correct set of axon terminals are retained during normal development, while imprecise ones withdraw. The mechanism by which only correct axons are retained requires neural activity, and may be regulated by specific receptors at synapses. The transmission of neural signals at these synapses is carried out in part by the glutamate-activated NMDA receptor. It is hypothesized that NMDA receptor activation plays a crucial role in enhancing only those connections in the immature system which will form a retinotopically correct map in the LGN and cortex. NMDA receptor activation requires depolarization of the neuron membrane. Possibly, only neurons transmitting information from nearby areas in the retina summate to produce NMDA receptor- mediated currents. The result is an influx of Ca++ ions that has been shown to cause trophic effects within the cell that could enhance the synaptic connection. Thus, NMDA receptors may act to detect coincident neural activity in immature animals, thereby allowing only visuo-topically related axon terminals to undergo enhancement of synaptic transmission and structure. As development proceeds, NMDA receptor function decreases, possibly reducing these intracellular effects. Blocking NMDA receptor activation experimentally does alter the normal set of connections in the visual system. Yet, is there a direct cause- and-effect relation between NMDA receptor activity and anatomical changes? Many cellular events probably result from NMDA-mediated currents. Intracellular changes in phosphorylation states and protein levels could eventually alter a synapse at the anatomical level. Study of the changing NMDA receptor subunit types making up the receptor within visual system structures could reveal, in part, the means by which plasticity is down-regulated. The experimental regulation of these subunits in vivo could reveal important information concerning their specific function if plasticity and development were to be altered as a result. A summary of previous studies, and proposals for further research concerning the role of the NMDA receptor and its various types in developing visual pathways are presented in this manuscript.
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Books on the topic "Mediated pathways"

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Muise, Brandon. Examining caspase mediated apoptotic pathways through RNAi as a means of procaspase downregulation. Sudbury, Ont: Laurentian University, 2006.

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Porges, Stephen W. Vagal Pathways. Edited by Emma M. Seppälä, Emiliana Simon-Thomas, Stephanie L. Brown, Monica C. Worline, C. Daryl Cameron, and James R. Doty. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190464684.013.15.

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In this chapter, contemplative practices are conceptualized as methods that function as neural exercises enhancing vagal regulation of the autonomic nervous system. The model presented proposes that specific voluntary behaviors (e.g., breath, vocalizations, and posture), which characterize ancient rituals and form the core of contemplative practices, can trigger a physiological state mediated by vagal pathways that fosters health and optimizes subjective experiences. The model emphasizes that, in order for the positive benefits of contemplative practices to be experienced, the rituals associated with contemplative practices (e.g., chants, prayers, meditation, and dance) must be performed in a context defined by physical features that are calming and soothing and promote feelings of safety.
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Sukhai, Mahadeo A. Cytokine-mediated pathways of mdr1 gene regulation in cultured rat hepatocytes. 2001.

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Cozza, Cynthia L. A model for the prediction of biologically mediated reductive dechlorination pathways. 1990.

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Price, Chane, Zahid Huq, Eellan Sivanesan, and Constantine Sarantopoulos. Pain Pathways and Pain Physiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457006.003.0001.

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Pain is a multidimensional sensory experience that is mediated by complex peripheral and central neuroanatomical pathways and mechanisms. Typically, noxious stimuli activate specific peripheral nerve terminals onto Aδ‎ and C nerve fibers that convey pain and generate signals that are relayed and processed in the spinal cord and then conveyed via the spinothalamic tracts to the contralateral thalamus and from there to the brain. Acute pain is self-limited and resolves with the healing process, but conditions of extensive injury or inflammation sensitize the pain pathways and generate aberrant, augmented responses. Peripheral and central sensitization of neurons (as a result of spatially and temporally excessive inflammation or intense afferent signal traffic) may result in hyperexcitability and chronicity of pain, with spontaneous pain and abnormal evoked responses to stimuli (allodynia, hyperalgesia). Finally, neuropathic pain follows injury or disease to nerves as a result of hyperexcitability augmented by various sensitizing mechanisms.
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Lee, David WK. Dopamine-induced Gbetagamma-mediated inhibitory pathways in vesicle release in an identified respiratory Lymnaea neuron. 2007.

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Herman, James P. Limbic Pathways to Stress Control. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0008.

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Appropriate control of the HPA (hypothalamo-pituitary-adrenocortical axis) is required for adaptation to physiological and environmental challenges. Inadequate control is linked to numerous stress-related pathologies, including PTSD, highlighting its importance in linking physiological stress responses with behavioral coping strategies. This chapter highlights neurocircuit mechanisms underlying HPA axis adaptation and pathology. Control of the HPA stress response is mediated by the coordinated activity of numerous limbic brain regions, including the prefrontal cortex, hippocampus, and amygdala. In general, hippocampal output inhibits anticipatory HPA axis responses, whereas amygdala subnuclei participate in stress activation. The prefrontal cortex plays an important role in inhibition of context-dependent stress responses. These regions converge on subcortical structures that relay information to paraventricular nucleus corticotropin-releasing hormone neurons, controlling the magnitude and duration of HPA axis stress responses. The output of these neural networks determines the net effect on glucocorticoid secretion, both within the normal adaptive range and in pathological circumstances.
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Blunt, MO, A. Stannard, E. Pauliac-Vaujour, CP Martin, Ioan Vancea, Milovan Suvakov, Uwe Thiele, Bosiljka Tadic, and P. Moriarty. Patterns and pathways in nanoparticle self-organization. Edited by A. V. Narlikar and Y. Y. Fu. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780199533046.013.8.

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This article reviews relatively recent forms of self-assembly and self-organization that have demonstrated particular potential for the assembly of nanostructured matter, namely biorecognition and solvent-mediated dynamics. It first considers the key features of self-assembled and self-organized nanoparticle arrays, focusing on the self-assembly of nanoparticle superlattices, the use of biorecognition for nanoparticle assembly, and self-organizing nanoparticles. It then describes the mechanisms and pathways for charge transport in nanoparticle assemblies, with particular emphasis on the relationship between the current–voltage characteristics and the topology of the lattice. It also discusses single-electron conduction in nanoparticle films as well as pattern formation and self-organization in dewetting nanofluids.
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Huang, Ruili, and Menghang Xia, eds. Tox21 Challenge to Build Predictive Models of Nuclear Receptor and Stress Response Pathways as Mediated by Exposure to Environmental Toxicants and Drugs. Frontiers Media SA, 2017. http://dx.doi.org/10.3389/978-2-88945-197-5.

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Dupuy, Béatrice, and Muriel Grosbois, eds. Language learning and professionalization in higher education: pathways to preparing learners and teachers in/for the 21st century. Research-publishing.net, 2020. http://dx.doi.org/10.14705/rpnet.2020.44.9782490057757.

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In this volume, language learning and professionalization are explored by addressing the existing gap between pressing needs for enhanced soft skills in work environments wherein technology-mediated, multilingual communication is increasingly the norm, and current foreign language teaching and learning offerings in higher education. Considering theoretical, methodological, and pedagogical perspectives for preparing language learners and teachers in/for the 21st century, this volume’s eight chapters underscore that research findings should inform the design of learning experiences so that people’s communication needs in fast-changing work environments are met and the link between language education and professionalization, within a lifelong learning perspective, is sustained.
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Book chapters on the topic "Mediated pathways"

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Golstein, P. "Fas-Based T Cell-Mediated Cytotoxicity." In Pathways for Cytolysis, 25–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79414-8_2.

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Offermanns, S. "G Protein-Mediated Signalling Pathways." In Transgenic Models in Pharmacology, 165–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18934-0_6.

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Pandey, Amita, and Girdhar K. Pandey. "Signaling Pathways Downstream of the Guidance Cues and Receptors." In The UNC-53-mediated Interactome, 47–71. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-07827-4_4.

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Pugia, Michael. "Impact of Inflammation and Innate Immunity Response in Obesity Mediated Diabetes." In Inflammatory Pathways in Diabetes, 3–25. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-21927-1_1.

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Yamamoto, Masahiro, and Shizuo Akira. "Lipid A Receptor TLR4-Mediated Signaling Pathways." In Lipid A in Cancer Therapy, 59–68. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1603-7_6.

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Picciotto, Marina R. "Nicotine-Mediated Activation of Signal Transduction Pathways." In Novartis Foundation Symposia, 83–95. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470029237.ch7.

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Rabbany, Sina Y., Bi-Sen Ding, Clemence Larroche, and Shahin Rafii. "Mechanosensory Pathways in Angiocrine Mediated Tissue Regeneration." In Mechanical and Chemical Signaling in Angiogenesis, 19–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-30856-7_2.

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Irniger, Stefan, Özlem Sarikaya-Bayram, and Özgür Bayram. "6 Fungal MAP-Kinase-Mediated Regulatory Pathways." In Biochemistry and Molecular Biology, 97–117. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27790-5_6.

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Lowin, B., M. C. Peitsch, and J. Tschopp. "Perforin and Granzymes: Crucial Effector Molecules in Cytolytic T Lymphocyte and Natural Killer Cell-Mediated Cytotoxicity." In Pathways for Cytolysis, 1–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79414-8_1.

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Rodvold, Jeffrey J., Navin R. Mahadevan, and Maurizio Zanetti. "Cell-Nonautonomous ER Stress-Mediated Dysregulation of Immunity by Cancer Cells." In Stress Response Pathways in Cancer, 397–429. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9421-3_18.

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Conference papers on the topic "Mediated pathways"

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Codescu, Marius-Andrei, Moritz Weiß, Martin Brehm, Oleg Kornilov, Daniel Sebastiani, and Erik T. J. Nibbering. "Ultrafast Proton Transfer Pathways Mediated by Imidazole." In International Conference on Ultrafast Phenomena. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/up.2022.tu1a.4.

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We explore with ultrafast infrared spectroscopy and molecular dynamics simulations how imidazole, an amphoteric molecule that can act both as acid and as base, provides alternate proton transfer pathways in the tautomerization reaction of 7-hydroxyquinoline.
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Allen, Fred D., Clara F. Asnes, Alan Wells, Elliot L. Elson, and Douglas A. Lauffenburger. "Alternative Pathways of Epidermal Growth Factor Receptor Mediated Contractile Force in NR6 Fibroblasts." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0403.

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Abstract We investigated the contractile force response to epidermal growth factor (EGF) stimulation in 3T3-derived NR6 fibroblast cells in order to determine significant pathways of biochemical signaling that mediate the response. We examined the force generating specificity of the EGF receptor (EGFR) signaling mechanism by using mutant NR6 fibroblasts expressing variations of the EGFR construct. The wild-type (WT) cell presented the complete internalizing EGFR signaling construct while the c’973 cell presented an internalization-defective EGFR construct, and the M721 cell presented a kinase-defective EGFR construct making it signaling inert. Additionally we examined the roles of the phospholipasc C-γ (PLCγ) pathway by using the PLC inhibitor U73122 (1 μM) and the mitogen activated protein kinase (MAPK) pathway using the inhibitor PD98059 (10 μM) in the observed contractile force responses. We found that the WT cells showed a rapid but transient force increase within the first hour post-stimulation and the c’973 showed a more gradual increase in force which it sustained for several hours post-stimulation. Blocking the PLCγ activation in the WT cells reduced the peak force increase by 50% while blocking MAPK did not affect the force development in either WT or c’973 cells.
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Bode, A., J. Li, Y. Cho, R. Lubet, and C. Grubbs. "Lapatinib Suppresses RTK-Mediated Signaling through Multiple Signaling Pathways." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-1130.

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Jeong, Jieun, Eunhee G. Kim, Jae Y. Cho, Eugene C. Yi, and Kristine M. Kim. "Role of basigin in adaptor protein mediated signaling pathways." In Bioscience and Medical Research 2013. Science & Engineering Research Support soCiety, 2013. http://dx.doi.org/10.14257/astl.2013.33.05.

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Borri, A., P. Palumbo, and A. Singh. "Noise propagation in metabolic pathways: the role of growth-mediated feedback." In 2020 59th IEEE Conference on Decision and Control (CDC). IEEE, 2020. http://dx.doi.org/10.1109/cdc42340.2020.9303911.

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Vogel, Alfred, Xiao-Xuan Liang, Sebastian Freidank, and Norbert Linz. "Free-electron and thermally mediated pathways of photodamage in nonlinear microscopy." In Multiphoton Microscopy in the Biomedical Sciences XXI, edited by Ammasi Periasamy, Peter T. So, and Karsten König. SPIE, 2021. http://dx.doi.org/10.1117/12.2583102.

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DENZLER, D. N., CH HESS, S. FUNK, G. ERTL, M. BONN, CH FRISCHKORN, and M. WOLF. "SURFACE FEMTOCHEMISTRY: ULTRAFAST REACTION DYNAMICS DRIVEN BY HOT ELECTRON MEDIATED REACTION PATHWAYS." In With Foreword by Prof A H Zewail, Nobel Laureate in Chemistry, 1999. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812777980_0063.

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Heiser, Laura M., Chad A. Shaw, Nicholas J. Wang, Catie Grasso, Pavana Anur, Sam Ng, Theodore Goldstein, et al. "Abstract 5238: Acquired therapeutic resistance is mediated by deregulation of multiple pathways." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5238.

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Ferreira, Caroline M., Jesse W. Williams, Jiankun Tong, Bryan Clay, Kelly Blaine, Rebecca A. Shilling, and Anne Sperling. "The Contribution Of Intrinsic And Extrinsic Apoptotic Pathways In Th2-mediated Inflammation." 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.a4053.

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Xiao, Guan-Yu, and Sandra Schmid. "Abstract 966: Oncogenic signaling pathways differentially regulate clathrin-mediated endocytosis in cancer cells." 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.am2018-966.

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Reports on the topic "Mediated pathways"

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Cardo-Vila, Marina. Isolation of Signaling Molecules Involved in Angiogenic Pathways Mediated Alpha v Integrins. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada435432.

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Yi, Ping. The Regulation of Nuclear Receptor Coactivator SRC-3 Activity Through Membrane Receptor Mediated Signaling Pathways. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada460836.

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Zagozdzon, Radoslaw, and Hava Avraham. Effects of Csk Homologous Kinase Overexpression on HER2/Neu-Mediated Signal Transduction Pathways in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada436916.

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Zagozdzon, Radoslaw, and Hava Avraham. Effects of CSK Homologous Kinase Overexpression on HER2/Neu-Mediated Signal Transduction Pathways in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada416967.

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Zagozdzon, Radoslaw, and Hava Avraham. Effects of CSK Homologous Kinase Overexpression on HER2/Neu-Mediated Signal Transduction Pathways in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada425671.

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Friedman, Haya, Julia Vrebalov, and James Giovannoni. Elucidating the ripening signaling pathway in banana for improved fruit quality, shelf-life and food security. United States Department of Agriculture, October 2014. http://dx.doi.org/10.32747/2014.7594401.bard.

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Background : Banana being a monocot and having distinct peel and pulp tissues is unique among the fleshy fruits and hence can provide a more comprehensive understanding of fruit ripening. Our previous research which translated ripening discoveries from tomato, led to the identification of six banana fruit-associated MADS-box genes, and we confirmed the positive role of MaMADS1/2 in banana ripening. The overall goal was to further elucidate the banana ripening signaling pathway as mediated by MADS-boxtranscriptional regulators. Specific objectives were: 1) characterize transcriptional profiles and quality of MaMADS1/2 repressed fruit; 2) reveal the role of additional MaMADSgenes in ripening; 3) develop a model of fruit MaMADS-box mode of action; and 4) isolate new components of the banana ripening signaling pathway. Major conclusion: The functions of the banana MaMADS1-5 have been examined by complimenting the rinor the TAGL1-suppressed lines of tomato. Only MaMADS5 exhibited partial complementation of TAGL1-suppressed and rinlines, suggesting that while similar genes play corresponding roles in ripening, evolutionary divergence makes heterologous complementation studies challenging. Nevertheless, the partial complementation of tomato TAGL1-surpessed and rinlines with MaMADS5 suggests this gene is likely an important ripening regulator in banana, worthy of further study. RNA-seqtranscriptome analysis during ripening was performed on WT and MaMADS2-suppressed lines revealing additional candidate genes contributing to ripening control mechanisms. In summary, we discovered 39 MaMADS-box genes in addition to homologues of CNR, NOR and HB-1 expressed in banana fruits, and which were shown in tomato to play necessary roles in ripening. For most of these genes the expression in peel and pulp was similar. However, a number of key genes were differentially expressed between these tissues indicating that the regulatory components which are active in peel and pulp include both common and tissue-specific regulatory systems, a distinction as compared to the more uniform tomato fruit pericarp. Because plant hormones are well documented to affect fruit ripening, the expressions of genes within the auxin, gibberellin, abscisic acid, jasmonic acid, salicylic and ethylene signal transduction and synthesis pathways were targeted in our transcriptome analysis. Genes’ expression associated with these pathways generally declined during normal ripening in both peel and pulp, excluding cytokinin and ethylene, and this decline was delayed in MaMADS2-suppressed banana lines. Hence, we suggest that normal MaMADS2 activity promotes the observed downward expression within these non-ethylene pathways (especially in the pulp), thus enabling ripening progression. In contrast, the expressions of ACSand ACOof the ethylene biosynthesis pathway increase in peel and pulp during ripening and are delayed/inhibited in the transgenic bananas, explaining the reduced ethylene production of MaMADS2-suppressed lines. Inferred by the different genes’ expression in peel and pulp of the gibberellins, salicylic acid and cytokinins pathways, it is suggested that hormonal regulation in these tissues is diverse. These results provide important insights into possible avenues of ripening control in the diverse fruit tissues of banana which was not previously revealed in other ripening systems. As such, our transcriptome analysis of WT and ripening delayed banana mutants provides a starting point for further characterization of ripening. In this study we also developed novel evidence that the cytoskeleton may have a positive role in ripening as components of this pathway were down-regulated by MaMADS2 suppression. The mode of cytoskeleton involvement in fruit ripening remains unclear but presents a novel new frontier in ripening investigations. In summary, this project yielded functional understanding of the role and mode of action of MaMADS2 during ripening, pointing to both induction of ethylene and suppression of non-ethylene hormonal singling pathways. Furthermore, our data suggest important roles for cytoskeleton components and MaMADS5 in the overall banana ripening control network. Implications: The project revealed new molecular components/genes involved in banana ripening and refines our understanding of ripening responses in the peel and pulp tissues of this important species. This information is novel as compared to that derived from the more uniform carpel tissues of other highly studied ripening systems including tomato and grape. The work provides specific target genes for potential modification through genetic engineering or for exploration of useful genetic diversity in traditional breeding. The results from the project might point toward improved methods or new treatments to improve banana fruit storage and quality.
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Heidenreich, Kim, and Dan A. Linseman. Signaling Pathways that Mediate Neurotoxin-Induced Death of Dopamine Neurons. Fort Belvoir, VA: Defense Technical Information Center, November 2005. http://dx.doi.org/10.21236/ada447899.

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Heidenreich, Kim A. Signaling Pathways that Mediate Neurotoxin-Induced Death of Dopamine Neurons. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada429190.

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Coplin, David, Isaac Barash, and Shulamit Manulis. Role of Proteins Secreted by the Hrp-Pathways of Erwinia stewartii and E. herbicola pv. gypsophilae in Eliciting Water-Soaking Symptoms and Initiating Galls. United States Department of Agriculture, June 2001. http://dx.doi.org/10.32747/2001.7580675.bard.

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Many bacterial pathogens of plants can inject pathogenicity proteins into host cells using a specialized type III secretion system encoded by hrpgenes. This system deliver effector proteins, into plant cells that function in both susceptible and resistant interactions. We have found that the virulence of Erwinia stewartii(Es; syn. Pantoea stewartii) and Erwinia herbicola pv. gypsophilae (Ehg, syn. Pantoea agglomerans), which cause Stewart's wilt of corn and galls on Gypsophila, respectively, depends on hrpgenes. The major objectives of this project were: To increase expression of hrpgenes in order to identify secreted proteins; to identify genes for proteins secreted by the type-III systems and determine if they are required for pathogenicity; and to determine if the secreted proteins can function within eukaryotic cells. We found that transcription of the hrp and effector genes in Es and Ehg is controlled by at least four genes that constitute a regulatory cascade. Environmental and/or physiological signaling appears to be mediated by the HrpX/HrpY two component system, with HrpX functioning as a sensor-kinase and HrpY as a response regulator. HrpYupregulateshrpS, which encodes a transcriptional enhancer. HrpS then activates hrpL, which encodes an alternate sigma factor that recognizes "hrp boxes". All of the regulatory genes are essential for pathogenicity, except HrpX, which appears only to be required for induction of the HR in tobacco by Es. In elucidating this regulatory pathway in both species, we made a number of significant new discoveries. HrpX is unusual for a sensor-kinase because it is cytoplasmic and contains PAS domains, which may sense the redox state of the bacterium. In Es, a novel methyl-accepting protein may function upstream of hrpY and repress hrp gene expression in planta. The esaIR quorum sensing system in Es represses hrp gene expression in Es in response to cell-density. We have discovered six new type III effector proteins in these species, one of which (DspE in Ehg and WtsE in Es) is common to both pathogens. In addition, Es wtsG, which is a homolog of an avrPpiB from P. syringae pv. pisi, and an Ehg ORF, which is a homolog of P. syringae pv. phaseolicola AvrPphD, were both demonstrated to encode virulence proteins. Two plasmidborne, Ehg Hop proteins, HsvG and PthG, are required for infection of gypsophilia, but interestingly, PthG also acts as an Avr elicitor in beets. Using a calmodulin-dependent adenylate cyclase (cyaA) reporter gene, we were successful in demonstrating that an HsvG-CyaA fusion protein can be transferred into human HeLa cells by the type-III system of enteropathogenic E. coli. This is a highly significant accomplishment because it is the first direct demonstration that an effector protein from a plant pathogenic bacterium is capable of being translocated into a eukaryotic cell by a type-III secretion system. Ehg is considered a limiting factor in Gypsophila production in Israel and Stewart’s Wilt is a serious disease in the Eastern and North Central USA, especially on sweet corn in epidemic years. We believe that our basic research on the characterization of type III virulence effectors should enable future identification of their receptors in plant cells. This may lead to novel approaches for genetically engineering resistant plants by modifying their receptors or inactivating effectors and thus blocking the induction of the susceptible response. Alternatively, hrp gene regulation might also provide a target for plant produced compounds that interfere with recognition of the host by the pathogen. Such strategies would be broadly applicable to a wide range of serious bacterial diseases on many crops throughout the USA and Israel.
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Wilson, Thomas E., Avraham A. Levy, and Tzvi Tzfira. Controlling Early Stages of DNA Repair for Gene-targeting Enhancement in Plants. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7697124.bard.

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Gene targeting (GT) is a much needed technology as a tool for plant research and for the precise engineering of crop species. Recent advances in this field have shown that the presence of a DNA double-strand break (DSB) in a genomic locus is critical for the integration of an exogenous DNA molecule introduced into this locus. This integration can occur via either non-homologous end joining (NHEJ) into the break or homologous recombination (HR) between the broken genomic DNA and the introduced vector. A bottleneck for DNA integration via HR is the machinery responsible for homology search and strand invasion. Important proteins in this pathway are Rad51, Rad52 and Rad54. We proposed to combine our respective expertise: on the US side, in the design of zincfinger nucleases (ZFNs) for the induction of DNA DSBs at any desired genomic locus and in the integration of DNA molecules via NHEJ; and on the Israeli side in the HR events, downstream of the DSB, that lead to homology search and strand invasion. We sought to test three major pathways of targeted DNA integration: (i) integration by NHEJ into DSBs induced at desired sites by specially designed ZFNs; (ii) integration into DSBs induced at desired sites combined with the use of Rad51, Rad52 and Rad54 proteins to maximize the chances for efficient and precise HR-mediated vector insertion; (iii) stimulation of HR by Rad51, Rad52 and Rad54 in the absence of DSB induction. We also proposed to study the formation of dsT-DNA molecules during the transformation of plant cells. dsT-DNA molecules are an important substrate for HR and NHEJ-mediatedGT, yet the mode of their formation from single stranded T-DNA molecules is still obscure. In addition we sought to develop a system for assembly of multi-transgene binary vectors by using ZFNs. The latter may facilitate the production of binary vectors that may be ready for genome editing in transgenic plants. ZFNs were proposed for the induction of DSBs in genomic targets, namely, the FtsH2 gene whose loss of function can easily be identified in somatic tissues as white sectors, and the Cruciferin locus whose targeting by a GFP or RFP reporter vectors can give rise to fluorescent seeds. ZFNs were also proposed for the induction of DSBs in artificial targets and for assembly of multi-gene vectors. We finally sought to address two important cell types in terms of relevance to plant transformation, namely GT of germinal (egg) cells by floral dipping, and GT in somatic cells by root and leave transformation. To be successful, we made use of novel optimized expression cassettes that enable coexpression of all of the genes of interest (ZFNs and Rad genes) in the right tissues (egg or root cells) at the right time, namely when the GT vector is delivered into the cells. Methods were proposed for investigating the complementation of T-strands to dsDNA molecules in living plant cells. During the course of this research, we (i) designed, assembled and tested, in vitro, a pair of new ZFNs capable of targeting the Cruciferin gene, (ii) produced transgenic plants which expresses for ZFN monomers for targeting of the FtsH2 gene. Expression of these enzymes is controlled by constitutive or heat shock induced promoters, (iii) produced a large population of transgenic Arabidopsis lines in which mutated mGUS gene was incorporated into different genomic locations, (iv) designed a system for egg-cell-specific expression of ZFNs and RAD genes and initiate GT experiments, (v) demonstrated that we can achieve NHEJ-mediated gene replacement in plant cells (vi) developed a system for ZFN and homing endonuclease-mediated assembly of multigene plant transformation vectors and (vii) explored the mechanism of dsTDNA formation in plant cells. This work has substantially advanced our understanding of the mechanisms of DNA integration into plants and furthered the development of important new tools for GT in plants.
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