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You searched for subject:(ADP secretion). Showing records 1 – 3 of 3 total matches.

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1. Elaib, Ziane. Rôle des pompes à calcium SERCA3 dans les fonctions plaquettaires : Role of Calcium ATPase SERCA3 in Platelet Functions.

Degree: Docteur es, Sciences de la vie et de la santé, 2017, Université Paris-Saclay (ComUE)

L'élévation de la concentration du calcium (Ca2+) cytosolique est responsable de l’activation plaquettaire. Cette élévation est due à l'entrée du Ca2+ à partir du milieu extérieur (influx) ou sa translocation (mobilisation) dans le cytosol depuis ses réserves internes. Les SERCAs (Sarco/Endoplasmic Reticulum Ca2+ ATPases) pompent le Ca2+ depuis le cytosol vers les réserves internes, maintenant le Ca2+ cytosolique bas (100 nM) et les plaquettes au repos. D'autre part elles assurent une concentration calcique élevée (≥1 mM) dans les réserves calciques permettant sa mobilisation, et enfin modulent l'intensité et la forme du signal calcique lors de l'activation. Mais les rôles respectifs des SERCAs plaquettaires, SERCA2b et SERCA3, sont encore mal définis. D’où l’intérêt de mon projet qui a été de déterminer si SERCA3 avait un rôle fonctionnel précis et spécifique. Nous avons observé sur des souris SERCA3-/- un défaut de l'hémostase et s’accompagne d’une résistance à la thrombose dû à un déficit de sécrétion d'ADP, entrainant un défaut d'agrégation et d'adhérence. SERCA3 semble contrôler une voie de sécrétion initiale d'ADP capable d’agir en synergie avec une faible activation plaquettaire, aboutissant à un renforcement de la sécrétion et de l'agrégation. De plus, l’utilisation des inhibiteurs pharmacologiques spécifiques de SERCA2b (thapsigargine) ou SERCA3 (tBHQ), a montré que la sécrétion initiale d'ADP n'était pas dépendante de la mobilisation des réserves SERCA2b mais dépendait spécifiquement des réserves SERCA3. Nous avons retrouvé la même voie de sécrétion d'ADP dépendante de SERCA3 dans les plaquettes humaines. Nous avons en particulier montré par le suivi d'une cohorte de patientes atteintes d'obésité morbide, un déficit d'agrégation, une faible mobilisation calcique et un taux faible de SERCA3 plaquettaire, revenus à la normale après retour à un poids normal après chirurgie bariatrique. Surtout nous avons retrouvé, dans les plaquettes de ces patientes obèses, un défaut de sécrétion d'ADP associé au défaut de SERCA3. Il s'agit du premier défaut de SERCA3 plaquettaire lié à une pathologie humaine. Nous avons ensuite montré que la sécrétion initiale d'ADP était rapide (5 sec) et entièrement dépendante de SERCA3. A l'aide d'une sonde calcique fluorescente membranaire (FURA2-NearMem-AM), nous avons démontré l’existence d’une mobilisation calcique juxta-membranaire spécifique de SERCA3, indépendante de l'ADP, correspondant donc à une sécrétion primaire. Cette mobilisation SERCA3 s'est avérée indépendante d'IP3, mais dépendante du NAADP, qui mobilise spécifiquement les réserves SERCA3 et non SERCA2b. En conclusion, nous avons mis en évidence une nouvelle voie d'activation plaquettaire, indépendante de l'IP3 mais dépendante du NAADP qui libère le Ca2+ des stocks internes dépendants de SERCA3 et spécifiquement engagés dans la libération précoce d'ADP lors de l'activation plaquettaire. Ces données identifient de nouvelles cibles avec un intérêt thérapeutiques anti-thrombotiques potentiel.

The elevation of cytosolic…

Advisors/Committee Members: Rosa, Jean-Philippe (thesis director).

Subjects/Keywords: Formation du thrombus; Agrégation; Secretion de l'ADP; Signal inside-Out; Plaquette SERCA3 -/- de souris; Signalisation calcique; Thrombus formation; Aggregation; ADP secretion; Inside-Out signaling; Mouse SERCA3-/- platelets; Calcium signaling

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Elaib, Z. (2017). Rôle des pompes à calcium SERCA3 dans les fonctions plaquettaires : Role of Calcium ATPase SERCA3 in Platelet Functions. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2017SACLS310

Chicago Manual of Style (16th Edition):

Elaib, Ziane. “Rôle des pompes à calcium SERCA3 dans les fonctions plaquettaires : Role of Calcium ATPase SERCA3 in Platelet Functions.” 2017. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed November 29, 2020. http://www.theses.fr/2017SACLS310.

MLA Handbook (7th Edition):

Elaib, Ziane. “Rôle des pompes à calcium SERCA3 dans les fonctions plaquettaires : Role of Calcium ATPase SERCA3 in Platelet Functions.” 2017. Web. 29 Nov 2020.

Vancouver:

Elaib Z. Rôle des pompes à calcium SERCA3 dans les fonctions plaquettaires : Role of Calcium ATPase SERCA3 in Platelet Functions. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2017. [cited 2020 Nov 29]. Available from: http://www.theses.fr/2017SACLS310.

Council of Science Editors:

Elaib Z. Rôle des pompes à calcium SERCA3 dans les fonctions plaquettaires : Role of Calcium ATPase SERCA3 in Platelet Functions. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2017. Available from: http://www.theses.fr/2017SACLS310

2. Ewell, Sharday. Adap1 And Arf6 Mediate Regulated Secretory Trafficing In Neurosecretory Cells And Neurons.

Degree: 2013, University of Alabama – Birmingham

ADP ribosylation factor 6 (Arf6) is a member of the Arf family of small GTPases known to function in vesicular membrane trafficking and cytoskeletal organization. Arf6 cycles between its GTP and GDP bound states, facilitated by GTP exchange factors (GEFs) and GTPase activating proteins (GAPs), respectively. In my dissertation studies I have investigated the neuronal functions of Arf6 and ADAP1, an Arf6 GAP and candidate PI 3-kinase target required for dendritic differentiation in developing neurons. I demonstrated that in neurosecretory PC12 cells and neurons, ADAP1 and Arf6 colocalize with regulated secretory granules (SGs) that traffic chromogranin B and brain-derived neurotrophic factor (BDNF), a secreted factor important for neuronal development and synaptic plasticity. Using a pulse-chase assay in PC12 cells to monitor trafficking of chromogranin B, I demonstrated that siRNA-mediated knockdown (or expression of inactive mutants) of ADAP1 or Arf6, resulted in an inhibition of the trafficking and maturation of regulated SGs. In neurons, knock down of ADAP1 or Arf6 leads to an increase in the colocalization of BDNF-GFP with furin, a peptidase localized to immature SGs, suggesting that ADAP1 and Arf6 participate in the maturation of BDNF containing SGs. Knock down of ADAP1 or Arf6 in neurons also impairs dendritic differentiation. Intriguingly, this impairment is rescued by the overexpression of BDNF. Together my studies indicate a role for ADAP1 and Arf6 in the trafficking of chromogranin B and BDNF-containing regulated SGs in neurons, which may underlie their roles in regulating dendritic differentiation.

PhD

1 online resource (xvi, 167 pages) :illustrations

Ph.D.University of Alabama at Birmingham2013.

Neurobiology

Medicine

ADAP1, Arf6, BDNF, Dendritic differentiation, Regulated secretory trafficking

UNRESTRICTED

Advisors/Committee Members: Anne Theibert, McMahon,Lori Pozzo-Miller,Lucas Sztul,Elizabeth Wilson,Scott.

Subjects/Keywords: ADP-Ribosylation Factors – metabolism<; /br>; Brain-Derived Neurotrophic Factor – metabolism.<; /br>; Brain-Derived Neurotrophic Factor – secretion.<; /br>; Dendritic Cells<; /br>; GTP Phosphohydrolases – metabolism.<; /br>; Nervous System Diseases – genetics<; /br>; Nervous System Diseases – metabolism

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Ewell, S. (2013). Adap1 And Arf6 Mediate Regulated Secretory Trafficing In Neurosecretory Cells And Neurons. (Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1657

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Ewell, Sharday. “Adap1 And Arf6 Mediate Regulated Secretory Trafficing In Neurosecretory Cells And Neurons.” 2013. Thesis, University of Alabama – Birmingham. Accessed November 29, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1657.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Ewell, Sharday. “Adap1 And Arf6 Mediate Regulated Secretory Trafficing In Neurosecretory Cells And Neurons.” 2013. Web. 29 Nov 2020.

Vancouver:

Ewell S. Adap1 And Arf6 Mediate Regulated Secretory Trafficing In Neurosecretory Cells And Neurons. [Internet] [Thesis]. University of Alabama – Birmingham; 2013. [cited 2020 Nov 29]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1657.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ewell S. Adap1 And Arf6 Mediate Regulated Secretory Trafficing In Neurosecretory Cells And Neurons. [Thesis]. University of Alabama – Birmingham; 2013. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1657

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

3. Johanna Carolina Sierra. Mechanism of action of AexU, a new type III secretion system effector from an emerging human pathogen Aeromonas hydrophila.

Degree: PhD, Microbiology and Immunology, 2010, The University of Texas Medical Branch

Our laboratory first reported the complete sequence of the type III secretion system (T3SS) from a diarrheal isolate SSU of A. hydrophila. We identified an effector protein (designated as AexU) of the T3SS, which exhibited ADP-ribosyltransferase (ADPRT) and GTPase-activating protein (GAP) activity. AexU was successfully expressed in the HeLa cell Tet-Off system and I provided evidence that cells expressing and producing the full length AexU showed actin reorganization followed by apoptosis. Earlier, we showed that the ÄaexU null mutant was attenuated in a mouse model, and I now demonstrated that while the parental A. hydrophila strain could be detected in the lung, liver, and spleen of infected mice, the ÄaexU mutant was rapidly cleared from these organs resulting in increased survivability of animals. The GAP activity of AexU was mainly responsible for host cell apoptosis and disruption of actin filaments. Further, AexU prevented phosphorylation of c-Jun, JNK and IêBá and inhibited IL-6 and IL-8 secretion from HeLa cells. Our data indicated that AexU operated by inhibiting NF-êB and inactivating Rho GTPases. Importantly, however, when the ÄaexU null mutant was complemented with the mutated aexU gene devoid of ADPRT and GAP activities, a higher mortality rate in mice with concomitant increase in the production of proinflammatory cytokines/chemokines was noted. These data indicated that either such a mutated AexU is a potent inducer of them or that AexU possesses yet another unknown activity that is modulated by ADPRT and GAP activities and results in this aberrant cytokine/chemokine production responsible for increased animal death. Advisors/Committee Members: Ashok Chopra (advisor), Vladimir Motin (committee member), Judith Johnson (committee member), Johnny Peterson (committee member), Eric Smith (committee member).

Subjects/Keywords: type III secretion system; septicemic mouse model of infection; GAP activity; AexU; Aeromonas hydrophila; ADP-ribosyltransferase activity

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Sierra, J. C. (2010). Mechanism of action of AexU, a new type III secretion system effector from an emerging human pathogen Aeromonas hydrophila. (Doctoral Dissertation). The University of Texas Medical Branch. Retrieved from http://hdl.handle.net/2152.3/176

Chicago Manual of Style (16th Edition):

Sierra, Johanna Carolina. “Mechanism of action of AexU, a new type III secretion system effector from an emerging human pathogen Aeromonas hydrophila.” 2010. Doctoral Dissertation, The University of Texas Medical Branch. Accessed November 29, 2020. http://hdl.handle.net/2152.3/176.

MLA Handbook (7th Edition):

Sierra, Johanna Carolina. “Mechanism of action of AexU, a new type III secretion system effector from an emerging human pathogen Aeromonas hydrophila.” 2010. Web. 29 Nov 2020.

Vancouver:

Sierra JC. Mechanism of action of AexU, a new type III secretion system effector from an emerging human pathogen Aeromonas hydrophila. [Internet] [Doctoral dissertation]. The University of Texas Medical Branch; 2010. [cited 2020 Nov 29]. Available from: http://hdl.handle.net/2152.3/176.

Council of Science Editors:

Sierra JC. Mechanism of action of AexU, a new type III secretion system effector from an emerging human pathogen Aeromonas hydrophila. [Doctoral Dissertation]. The University of Texas Medical Branch; 2010. Available from: http://hdl.handle.net/2152.3/176

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