Увійти

Готові списки джерел за темами / Propeptide de la sortiline

Добірка наукової літератури з теми "Propeptide de la sortiline"

Автор: Grafiati

Опубліковано: 6 липня 2024

Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями

Оберіть тип джерела:

Ознайомтеся зі списками актуальних статей, книг, дисертацій, тез та інших наукових джерел на тему "Propeptide de la sortiline".

Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.

Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.

Зміст

Статті в журналах
Дисертації
Книги
Частини книг
Тези доповідей конференцій

Статті в журналах з теми "Propeptide de la sortiline":

1

Hivelin, C., J. Mazella, and T. Coppola. "CA-143: Le propeptide de la sortiline module l'entrée de glucose dans les adipocytes et les myocytes." Diabetes & Metabolism 42 (March 2016): A74. http://dx.doi.org/10.1016/s1262-3636(16)30275-0.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

2

Hivelin, Céline, Jean Mazella, and Thierry Coppola. "Sortilin derived propeptide regulation during adipocyte differentiation and inflammation." Biochemical and Biophysical Research Communications 482, no. 1 (January 2017): 87–92. http://dx.doi.org/10.1016/j.bbrc.2016.10.139.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

3

Petersen, C. M. "Propeptide cleavage conditions sortilin/neurotensin receptor-3 for ligand binding." EMBO Journal 18, no. 3 (February 1, 1999): 595–604. http://dx.doi.org/10.1093/emboj/18.3.595.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

4

Mazella, J., C. Devader, M. Roulot, M. Borsotto, and C. Heurteaux. "Regulation of serum spadin propeptide: An antidepressant response probe." European Psychiatry 33, S1 (March 2016): S417. http://dx.doi.org/10.1016/j.eurpsy.2016.01.1507.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

ObjectivesWe previously discovered that spadin, a short analogue of the propeptide (PE) released from the maturation of sortilin, displays potent antidepressant properties. Since the PE level can be measured in the blood, we aimed to investigate how the PE serum concentration is regulated in mice. We wondered whether the PE serum levels vary between healthy subjects and patients with major depressive disorder (MDD).MethodsWe developped a dosing method based on the AlphaScreen™ technology (Perkin) which allow to selectively detect both PE, spadin and metabolic products from these peptides with a detection range of 1 ng/mL.ResultsWe found that insulin significantly up-regulated serum PE concentration from 26.15 ± 2.63 to 41.43 ± 6.27 nM (P = 0.0318). Analysis during circadian cycle in mice revealed that the amount of PE and its derivatives significantly varied during the cycle being higher during the period of maximal activity (dark period). We also measured serum insulin concentration between 1 and 7 pm and observed a significant rise confirming the relationships between insulin and PE concentration. We showed that the serum level of PE is lower in depressive patients than in healthy non-psychiatric. We observed that the weaker level of PE in depressive patients can recover the level of healthy subjects after a chronic antidepressant treatment.ConclusionsDosing the serum level of PE could be a promising approach for the diagnosis of depression and to determine the remission of the disease.Disclosure of interestThe authors have not supplied their declaration of competing interest.

5

Roulot, Morgane, Alessandra Minelli, Marco Bortolomasi, Elisabetta Maffioletti, Massimo Gennarelli, Marc Borsotto, Catherine Heurteaux, and Jean Mazella. "Increased serum levels of sortilin-derived propeptide after electroconvulsive therapy in treatment-resistant depressed patients." Neuropsychiatric Disease and Treatment Volume 14 (September 2018): 2307–12. http://dx.doi.org/10.2147/ndt.s170165.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

6

Devader, Christelle, Morgane Roulot, Sébastien Moréno, Alessandra Minelli, Marco Bortolomasi, Chiara Congiu, Massimo Gennarelli, Marc Borsotto, Catherine Heurteaux, and Jean Mazella. "Serum sortilin-derived propeptides concentrations are decreased in major depressive disorder patients." Journal of Affective Disorders 208 (January 2017): 443–47. http://dx.doi.org/10.1016/j.jad.2016.10.049.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

7

Mazella, Jean, and Jean-Pierre Vincent. "La sortiline : une protéine associée à de multiples fonctions." médecine/sciences 20, no. 6-7 (June 2004): 629–31. http://dx.doi.org/10.1051/medsci/2004206-7629.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

8

Kaufman, Beth D., Nancy Videon, Xuemei Zhang, Matthew A. Harris, Robert E. Shaddy, and Elizabeth Goldmuntz. "Procollagen type III amino-terminal propeptide: a serum biomarker of left ventricular remodelling in paediatric dilated cardiomyopathy." Cardiology in the Young 25, no. 2 (November 6, 2013): 228–36. http://dx.doi.org/10.1017/s1047951113001820.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

AbstractBackgroundProcollagen type III amino-terminal propeptide is a collagen III cleavage product released in blood. The serum levels of this propeptide in adults with dilated cardiomyopathy are associated with cardiac remodelling and prognosis. The utility of procollagen type III amino-terminal propeptide as a biomarker in paediatric dilated cardiomyopathy is unknown.MethodsThis was a prospective, longitudinal study of children with dilated cardiomyopathy and changes in procollagen type III amino-terminal propeptide. The serum level of propeptide was measured serially, compared with paediatric normal values, and correlated with clinical status and left ventricular size and function on echocardiograms and cardiac magnetic resonance imaging.ResultsProcollagen type III amino-terminal propeptide was measured serially in 149 samples from 39 patients, age 9.0±6.4 years, followed up for 16.8±16.3 months. Procollagen type III amino-terminal propeptide in dilated cardiomyopathy was higher than in normal children. On multivariate analyses, procollagen type III amino-terminal propeptide had a positive correlation with left ventricular dilation, left ventricular end-diastolic diameter index (p<0.0001), and left ventricular end-diastolic diameter Z-score (p=0.0003), and a negative correlation with shortening fraction changes over time (p=0.001). Patients with myocarditis (n=12) had higher procollagen type III amino-terminal propeptide values than those with idiopathic dilated cardiomyopathy (n=20).ConclusionsProcollagen type III amino-terminal propeptide increases with left ventricular dilation and decreases with improvement in systolic function in paediatric dilated cardiomyopathy, indicating a role as a biomarker of cardiac remodelling in children. The diagnostic utility of procollagen type III amino-terminal propeptide to differentiate myocarditis from idiopathic dilated cardiomyopathy warrants further investigation.

9

Meiring, S. M., B. D. P. Setlai, C. Theron, and R. Bragg. "The Use of Phage Display and Yeast Based Expression System for the Development of a Von Willebrand Factor Propeptide Assay: Development of a Von Willebrand Factor Propeptide Assay." BioMed Research International 2018 (2018): 1–7. http://dx.doi.org/10.1155/2018/6232091.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Background. The diagnosis of von Willebrand disease is complex due to the heterogeneity of the disease. About eighty percent of von Willebrand disease patients are diagnosed with a quantitative defect of von Willebrand factor (VWF) where fifty percent is due to an increased clearance of von Willebrand factor. These patients do not respond well to the treatment of choice, Desmopressin (DDAVP) due to decreased efficacy. The ratio between the VWF propeptide and the mature VWF antigen is used to diagnose these patients. Commercial VWF propeptide assays are too expensive for use in developing countries. In this study, we developed a cost-effective ELISA assay. Methods. We first displayed VWF propeptide on yeast. Antibody fragments were selected against the displayed VWF propeptide by using phage display technology. The antibodies were used to develop a cost-effective VWF propeptide assay and compared to a commercial VWF propeptide assay. Results. Two of these antibody fragments bound specific to the VWF propeptide and not to the yeast used for the expression of the propeptides. These purified antibody fragments were able to detect VWF propeptide in normal plasma. Conclusion. Our assay performed well when compared to a commercial kit. It also showed a higher binding affinity for VWF propeptide in plasma at especially lower plasma concentrations.

10

Emeis, Jef, Henk Bilo, Coen Stehouwer, Claus Thomsen, Ole Rasmussen, Kjeld Hermansen, Claes Wollheim, Jørgen Ingerslev, and Ulrich Vischer. "von Willebrand Factor (vWf) as a Plasma Marker of Endothelial Activation in Diabetes: Improved Reliability with Parallel Determination of the vWf Propeptide (vWf:AgII)." Thrombosis and Haemostasis 80, no. 12 (1998): 1002–7. http://dx.doi.org/10.1055/s-0037-1615401.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

SummaryElevated plasma von Willebrand factor (vWf) levels are found in diabetes and other vasculopathies, and predict cardiovascular mortality. vWf is stored and released from endothelial cell secretory granules, along with equimolar amounts of its propeptide (vWf:AgII). In the present study, we examined plasma propeptide levels as a marker of endothelial secretion in vivo, using an ELISA based on monoclonal antibodies. vWf but not propeptide levels are influenced by blood groups, explaining in part the smaller variation in plasma propeptide levels among normal individuals. In both controls and insulin-dependent diabetic patients, we found a close correlation between propeptide and immunoreactive vWf levels (r2 = 0.54, p <0.0001). vWf and propeptide were elevated in patient subgroups with microalbuminuria or overt diabetic nephropathy, whereas only the propeptide was significantly elevated in the normoalbuminuric subgroup. This observation suggests that in conjunction with vWf, propeptide measurements may improve the identification of endothelial activation, which occurs frequently even without increased urinary albumin excretion. In 12 NIDDM patients, a 3-week diet enriched in monounsaturated fat (MUFA) resulted in parallel decreases in vWf (-22%, p <0.05) and propeptide (-17%, p <0.05) levels, indicating that the experimental diet affected endothelial secretion rather than vWf catabolism. A carbohydrate-enriched control diet did not significantly influence either marker.Our results suggest that concomittant determinations of plasma vWf and propeptide are useful tools to assess endothelial activation in vivo, and reinforce our previous conclusion that a diet rich in MUFA can improve endothelial function in NIDDM.

Більше джерел

Дисертації з теми "Propeptide de la sortiline":

1

Hivelin, Céline. "Étude des mécanismes de libération du propeptide de la sortiline et de ses effets sur l’homéostasie glucidique." Thesis, Université Côte d'Azur (ComUE), 2016. http://www.theses.fr/2016AZUR4109/document.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

En France, l’obésité touche 15% de la population et est en perpétuelle augmentation. Elle est une cause majeure du diabète de type 2. Elle se traduit par un accroissement du nombre de cellules de stockage du gras (adipocytes) et une résistance périphérique à l’insuline. Chez des individus obèses, l’augmentation du nombre d’adipocytes est associée à une diminution de l’expression de la sortiline, protéine transmembranaire dont le clivage entraine la formation du propeptide (PE) et sa libération dans la circulation sanguine. L’analogue synthétique du PE, la spadine, est connu pour moduler l’activité du canal potassique TREK-1. Ce canal étant exprimé dans la cellule bêta pancréatique qui sécrète l’insuline, une hormone participant à la régulation du taux de glucose dans le sang, il est possible que la spadine joue un rôle dans l’homéostasie du glucose. Mes résultats confirment cette hypothèse. En effet, la spadine améliore la tolérance au glucose des souris, en favorisant la libération d’insuline. La spadine est également connue pour interagir avec sortiline, indispensable au trafic du transporteur de glucose Glut4 vers la membrane des adipocytes. Cette interaction spadine-sortiline suggère que la spadine pourrait moduler l’entrée du glucose dans les adipocytes via la sortiline. Mes résultats montrent que la spadine ne modifie pas les capacités de stockage du glucose des adipocytes. En conclusion, la spadine joue un rôle dans la sécrétion de l’insuline et dans la régulation de la glycémie, ce qui peut présenter un intérêt pharmaceutique
In France, approximately 15% of the population is obese and this number keeps rising up every year. Obesity is a major cause of diabetes, inducing an increase of the number of fat-filled cells, called the adipocytes, and a peripheral insulin resistance. This increase of the number of adipocytes is associated with a decrease of sortilin expression, a transmembrane protein which is involved in the release of a propeptide (PE) in the blood circulation. Spadin, a synthetic PE analog, is known to modulate the potassium TREK-1 channel activity. Since, this channel is expressed in pancreatic beta cells which secrete insulin, a hormone involved in blood glucose regulation, spadin may play a role in glucose homeostasis. Consistent with this hypothesis, spadin improves glucose tolerance in mice, by stimulating insulin release. Spadin is a natural peptide derived from sortilin, which is known to control the glucose transporter Glut4 trafficking to the plasma membrane of adipocytes. This suggests that spadin may regulate glucose storage in adipocytes by affecting the sortilin function. However, my results show that spadin has no effect on glucose storage. In summary, spadin is involved in insulin secretion and glucose homeostasis and may be an alternative treatment against obesity and diabetes

2

Hivelin, Céline. "Étude des mécanismes de libération du propeptide de la sortiline et de ses effets sur l’homéostasie glucidique." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2016. http://www.theses.fr/2016AZUR4109.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

En France, l’obésité touche 15% de la population et est en perpétuelle augmentation. Elle est une cause majeure du diabète de type 2. Elle se traduit par un accroissement du nombre de cellules de stockage du gras (adipocytes) et une résistance périphérique à l’insuline. Chez des individus obèses, l’augmentation du nombre d’adipocytes est associée à une diminution de l’expression de la sortiline, protéine transmembranaire dont le clivage entraine la formation du propeptide (PE) et sa libération dans la circulation sanguine. L’analogue synthétique du PE, la spadine, est connu pour moduler l’activité du canal potassique TREK-1. Ce canal étant exprimé dans la cellule bêta pancréatique qui sécrète l’insuline, une hormone participant à la régulation du taux de glucose dans le sang, il est possible que la spadine joue un rôle dans l’homéostasie du glucose. Mes résultats confirment cette hypothèse. En effet, la spadine améliore la tolérance au glucose des souris, en favorisant la libération d’insuline. La spadine est également connue pour interagir avec sortiline, indispensable au trafic du transporteur de glucose Glut4 vers la membrane des adipocytes. Cette interaction spadine-sortiline suggère que la spadine pourrait moduler l’entrée du glucose dans les adipocytes via la sortiline. Mes résultats montrent que la spadine ne modifie pas les capacités de stockage du glucose des adipocytes. En conclusion, la spadine joue un rôle dans la sécrétion de l’insuline et dans la régulation de la glycémie, ce qui peut présenter un intérêt pharmaceutique
In France, approximately 15% of the population is obese and this number keeps rising up every year. Obesity is a major cause of diabetes, inducing an increase of the number of fat-filled cells, called the adipocytes, and a peripheral insulin resistance. This increase of the number of adipocytes is associated with a decrease of sortilin expression, a transmembrane protein which is involved in the release of a propeptide (PE) in the blood circulation. Spadin, a synthetic PE analog, is known to modulate the potassium TREK-1 channel activity. Since, this channel is expressed in pancreatic beta cells which secrete insulin, a hormone involved in blood glucose regulation, spadin may play a role in glucose homeostasis. Consistent with this hypothesis, spadin improves glucose tolerance in mice, by stimulating insulin release. Spadin is a natural peptide derived from sortilin, which is known to control the glucose transporter Glut4 trafficking to the plasma membrane of adipocytes. This suggests that spadin may regulate glucose storage in adipocytes by affecting the sortilin function. However, my results show that spadin has no effect on glucose storage. In summary, spadin is involved in insulin secretion and glucose homeostasis and may be an alternative treatment against obesity and diabetes

3

Daziano, Guillaume. "Rôle du propeptide de la sortiline et de ses dérivés dans les mécanismes de survie de la cellule bêta pancréatique." Electronic Thesis or Diss., Université Côte d'Azur, 2021. http://www.theses.fr/2021COAZ6025.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

En 2019, la Fédération Internationale du Diabète a révélé que près de 500 millions de personnes étaient atteintes de diabète dans le monde. On estime que cette incidence atteindra les 700 millions de personnes en 2045. Outre, l’aspect financier de la prise en charge, le diabète est un véritable enjeu de santé publique. En effet, l’environnement hyperglycémique délétère associé au diabète est à l’origine de graves complications pouvant altérer le fonctionnement de nombreux organes tels que le cœur, le cerveau ou encore le rein. La résistance à l’insuline associée à la détérioration de la sécrétion d’insuline et à la perte de la masse cellulaire bêta pancréatique constituent les principales caractéristiques du diabète de type 2. Ainsi, afin d’améliorer la prise en charge des patients diabétiques, l’identification d’une approche thérapeutique maîtrisée permettant de protéger la masse cellulaire bêta et de favoriser la sécrétion d’insuline uniquement en réponse au glucose et ce, sans effets secondaires, apparaît idéale.Les précédents travaux du laboratoire ont identifié le PE endogène et ses dérivés synthétiques la Spadine et la Mini-Spadine comme des inhibiteurs sélectifs des canaux potassiques TREK-1 au fort potentiel antidépresseur et impliqués dans la sécrétion de sérotonine, la prolifération et la survie neuronale. Au niveau périphérique, la Spadine a été décrite in vitro et in vivo comme un peptide à l’effet incrétine comparable à celui de l’exendine-4, un antidiabétique couramment utilisé en clinique. Ainsi, à la suite de cette étude et par analogie aux effets protecteurs observés sur le neurone, nous avons émis l’hypothèse que le PE et ses dérivés pouvaient avoir un rôle bénéfique dans les mécanismes de survie de la cellule bêta pancréatique.Dans ce manuscrit, nous démontrons que le PE endogène et ses dérivés protègent les cellules bêta de l’apoptose induite par la présence chronique de l’interleukine pro-inflammatoire et diabétogène IL-1β, ainsi que d’un choc toxique aigu induit par la staurosporine. De plus, l’analyse des mécanismes intracellulaires révèle que ces peptides provoquent une augmentation de la concentration en calcium intracellulaire, activent les voies prolifératives et de survie ERK et Akt, et maintiennent l’activité du facteur transcriptionnel CREB dans un environnement délétère via un mécanisme dépendant des calmodulines kinases.Ainsi, ces travaux de thèse montrent que le PE et ses dérivés synthétiques protègent la cellule bêta pancréatique et initient des processus cellulaires vertueux par une voie de signalisation originale indépendante de la PKA, où le potentiel de membrane et le calcium occupent un rôle crucial. Ces données suggèrent le PE endogène et ses dérivés synthétiques comme une nouvelle classe de peptides protecteurs des cellules bêta pancréatiques
In 2019, the International Diabetes Federation revealed that nearly 500 million people have diabetes worldwide. It is estimated that this incidence will reach 700 million people by 2045. In addition to the financial aspect of treatment, diabetes is a real public health issue. Indeed, the deleterious hyperglycemic environment associated with diabetes is could induce serious complications, leading to a functional alteration of many organs such as the heart, the brain or the kidney. Insulin resistance associated with the deterioration of insulin secretion and the loss of pancreatic beta cell mass are the main characteristics of type 2 diabetes. Thus, in order to improve the management of diabetic patients, the identification of a controlled therapeutic approach to protect beta cell mass and promote insulin secretion only in response to glucose and without side effects, appears ideal.The laboratory has identified the endogenous PE and its synthetic derivatives Spadin and Mini-Spadin as selective inhibitors of TREK-1 potassium channels. By this mechanism, the peptides showed also a strong antidepressant potential by modulating serotonin secretion, neuronal proliferation and survival. At the peripheral level, Spadin has been described in vitro and in vivo as a peptide with an incretin effect comparable to that of exendin-4, an antidiabetic commonly used in the clinic. Thus, following this study and by analogy to the protective effects observed on the neuron, we hypothesized that PE and its derivatives may have a beneficial role in the survival mechanisms in the pancreatic beta-cell.In this thesis, we demonstrate that endogenous PE and its derivatives protect beta cells from apoptosis induced by the chronic presence of the pro-inflammatory and diabetogenic interleukin IL-1β, as well as from an acute toxic shock induced by staurosporine. Furthermore, analysis of intracellular mechanisms reveals that these peptides cause an increase in intracellular calcium concentration, activate the ERK and Akt proliferative and survival pathways, and maintain CREB transcriptional factor activity in a deleterious environment via a calmodulin kinase-dependent pathway.Thus, this work shows that PE and its synthetic derivatives protect the pancreatic beta-cell and initiate virtuous cellular processes through an original PKA-independent signaling pathway, where membrane potential and calcium play a crucial role. This suggests the sortilin-derived peptides as a new class of pancreatic beta-cell protective molecules

4

Moreno, Sébastien. "Le récepteur 3 de la neurotensine/Sortiline dans la régulation de l’état dépressif." Thesis, Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4136/document.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Le trouble dépressif majeur est une pathologie qui atteint 20% de la population et qui représente le premier facteur de morbidité et d’incapacité au niveau mondial. Récemment, le canal potassique TREK-1 est une cible potentielle avérée dans le traitement de la dépression. La délétion de ce canal ou son blocage par un peptide dérivé résultant de la maturation de la sortiline, le propeptide (PE) ou son analogue synthétique la Spadine, résulte en un phénotype de résistance à la dépression. La sortiline est une protéine capable de s’associer à TREK-1 mais également au facteur neurotrophique BDNF important pour la viabilité neuronale et la régulation de l’état dépressif. La sortiline est donc impliquée dans la régulation de l’adressage intracellulaire de TREK-1 et du BDNF. Mes travaux se sont d’abords focalisés sur les conséquences de la délétion du gène codant pour la sortiline (Sort1-/-) sur l’adressage de TREK-1 et du BDNF, et également sur le système neurotensinergique. Les résultats révèlent au niveau cérébral une diminution de l’expression membranaire de TREK-1 et une augmentation de BDNF. L’ensemble de ces modifications conduisent les souris Sort1-/- à développer un phénotype de résistance à la dépression. De plus, ces souris présentent une augmentation de la concentration en neurotensine cérébrale ainsi que de son récepteur 2, ce qui entraine une résistance à la douleur. Par la suite, nous avons montré une diminution de la concentration sérique du PE chez les personnes dépressives, un niveau restauré après traitement avec des antidépresseurs. En conclusion, la sortiline joue un rôle prépondérant dans la régulation du trouble dépressif et aussi dans la nociception
Major depressive disorder is a condition that affects 20% of the population and is the leading cause of morbidity and disability worldwide. Recently, the TREK-1 potassium channel has been shown to be a potential target in the treatment of depression. The deletion of this channel or its blocking by a derived peptide resulting from the maturation of Sortilin, propeptide (PE), or its synthetic analogue Spadin, results in a phenotype of resistance to depression in mice. Sortilin is a protein able to bind with TREK-1 but also with the neurotrophic factor BDNF, an important factor for neuronal viability and depressive state regulation. Sortilin is therefore involved in regulating the intracellular addressing of TREK-1 and BDNF. Initially, my work focused on the consequences of the deletion of the Sortilin gene (sort1-/-) on the TREK-1 and BDNF addressing, and the neurotensinergic system. The results showed a decrease in TREK-1 membrane expression at the cerebral level and an increase in BDNF. All of these changes lead the Sort1-/- mice to develop a phenotype of resistance to depression. In addition, these mice show an increase in brain neurotensin concentration and its receptor 2, leading to increased resistance to pain perception. In a second phase, I was interested in whether PE, a potential antidepressant, showed serum variations in depressed patients and could be an indicator of depressive syndrome. We showed that the serum PE level is significantly reduced in depressed people, a level restored after treatment with antidepressants. In conclusion, Sortilin plays a major key in the regulation of depressive disorder and also in nociception

5

Moreno, Sébastien. "Le récepteur 3 de la neurotensine/Sortiline dans la régulation de l’état dépressif." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4136.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Le trouble dépressif majeur est une pathologie qui atteint 20% de la population et qui représente le premier facteur de morbidité et d’incapacité au niveau mondial. Récemment, le canal potassique TREK-1 est une cible potentielle avérée dans le traitement de la dépression. La délétion de ce canal ou son blocage par un peptide dérivé résultant de la maturation de la sortiline, le propeptide (PE) ou son analogue synthétique la Spadine, résulte en un phénotype de résistance à la dépression. La sortiline est une protéine capable de s’associer à TREK-1 mais également au facteur neurotrophique BDNF important pour la viabilité neuronale et la régulation de l’état dépressif. La sortiline est donc impliquée dans la régulation de l’adressage intracellulaire de TREK-1 et du BDNF. Mes travaux se sont d’abords focalisés sur les conséquences de la délétion du gène codant pour la sortiline (Sort1-/-) sur l’adressage de TREK-1 et du BDNF, et également sur le système neurotensinergique. Les résultats révèlent au niveau cérébral une diminution de l’expression membranaire de TREK-1 et une augmentation de BDNF. L’ensemble de ces modifications conduisent les souris Sort1-/- à développer un phénotype de résistance à la dépression. De plus, ces souris présentent une augmentation de la concentration en neurotensine cérébrale ainsi que de son récepteur 2, ce qui entraine une résistance à la douleur. Par la suite, nous avons montré une diminution de la concentration sérique du PE chez les personnes dépressives, un niveau restauré après traitement avec des antidépresseurs. En conclusion, la sortiline joue un rôle prépondérant dans la régulation du trouble dépressif et aussi dans la nociception
Major depressive disorder is a condition that affects 20% of the population and is the leading cause of morbidity and disability worldwide. Recently, the TREK-1 potassium channel has been shown to be a potential target in the treatment of depression. The deletion of this channel or its blocking by a derived peptide resulting from the maturation of Sortilin, propeptide (PE), or its synthetic analogue Spadin, results in a phenotype of resistance to depression in mice. Sortilin is a protein able to bind with TREK-1 but also with the neurotrophic factor BDNF, an important factor for neuronal viability and depressive state regulation. Sortilin is therefore involved in regulating the intracellular addressing of TREK-1 and BDNF. Initially, my work focused on the consequences of the deletion of the Sortilin gene (sort1-/-) on the TREK-1 and BDNF addressing, and the neurotensinergic system. The results showed a decrease in TREK-1 membrane expression at the cerebral level and an increase in BDNF. All of these changes lead the Sort1-/- mice to develop a phenotype of resistance to depression. In addition, these mice show an increase in brain neurotensin concentration and its receptor 2, leading to increased resistance to pain perception. In a second phase, I was interested in whether PE, a potential antidepressant, showed serum variations in depressed patients and could be an indicator of depressive syndrome. We showed that the serum PE level is significantly reduced in depressed people, a level restored after treatment with antidepressants. In conclusion, Sortilin plays a major key in the regulation of depressive disorder and also in nociception

6

Massa, Fabienne. "Rôle du système neurotensinergique dans la prolifération et l'adhésion des cellules cancéreuses de colon." Nice, 2011. http://www.theses.fr/2011NICE4055.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

La neurotensine (NT) est un peptide qui peut agir autant en périphérie qu’au niveau du système nerveux central. Deux de ses récepteurs appartiennent à la famille des récepteurs à sept domaines transmembranaires couplés aux protéines G (NTSR1 et NTSR2) tandis que le troisième est un récepteur à un seul segment transmembranaire appartenant à la famille des récepteurs de type I (NTSR3 ou sortiline). La NT et le NTSR1 sont très impliqués dans la progression tumorale et sont surexprimés dans un très grand nombre de cancer. Les effets prolifératifs de la NT résultent de l’activation du NTSR1 qui peut transactiver le récepteur de l’Epidermal Growth Factor (EGF). Nous avons démontré que, dans les cellules HT29, des adénocarcinomes de colon humain, la NT ne transactive pas l’EGFR pour induire la prolifération cellulaire. Quant au NTSR3, il est impliqué dans l’adressage des protéines, la prolifération, la différentiation. . . De plus, une fois à la membrane plasmique, le NTSR3 peut être hydrolysé et libéré sous forme soluble dans le milieu extracellulaire (sNTSR3). Lors de ma thèse, j’ai déterminé que le sNTSR3 était une molécule biologiquement active puisqu’elle induit une libération rapide du calcium intracellulaire. Le sNTSR3 active des voies de signalisation intracellulaires comme le complexe FAK-Src, la PKCα et la voie Pi3K aboutissant à une augmentation de l’adhésion des cellules cancéreuses. Par ailleurs, le sNTSR3 augmente l’expression de la E-Cadhérine, l’espacement entre les cellules et potentialise les effets le l’EGF sur la prolifération cellulaire. Ces données nous indiquent que le sNTSR3 serait une molécule impliquée dans la progression tumorale
Neurotensin (NT) can act in periphery and in the central nervous system. Two of this receptors are G protein coupled receptors (NTSR1 and NTSR2) and the third, is a type I receptor with one transmembrane domain (NTSR3 or sortilin). NT and NTSR1 are both implicated in tumoral progression and there are overexpressed in a lot of cancer. NT induces proliferation of cancerous cells which are mediated by NTSR1 which may transactivate the Epidermal Growth Factor Receptor (EGFR). We demonstrated that NT doesn’t transactivate the EGFR in HT29 cell line, a human adenocarcinoma of colon. NTSR3 is a multifunctional protein, is implicated in sorting of proteins, proliferation, differenciation… Moreover, once at the plasma membrane, NTSR3 can be hydrolysed and freed in a soluble form, in the extracellular medium (sNTSR3). During my PhD, I demonstrated that the sNTSR3 is an active molecule with a biological activity, as it induces the release of intracellular calcium. The sNTSR3 activates intracellular signaling like the complex FAK-Src, PKCα and Pi3K pathway, leading to an increase in cancerous cell adhesion. Furthermore, sNTSR3 increases E-Cadherin expression, space between cells and enhances the proliferation induced by EGF. Taken together, these results indicate that the soluble form of NTSR3 can be implicated in tumoral progression

7

Hassan, Noor. "Characterization and engineering of carbohydrate-active enzymes for biotechnological applications." Doctoral thesis, KTH, Industriell bioteknologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-165613.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Extremozymes are enzymes produced by microorganisms that live in extreme habitats. Due to their higher stability, extremozymes is attracting interest as biocatalysts in various industrial processes. In this context, carbohydrate-active extremozymes can be used in various processes relevant to the paper, food and feed industry. In this thesis, the crystal structure, biochemical characterization and the capacity to synthesize prebiotic galacto-oligosaccharides (GOS) were investigated for a β-glucosidase (HoBGLA) from the halothermophilic bacterium Halothermothrix orenii. The wild-type enzyme displays favorable characteristics for lactose hydrolysis and produces a range of prebiotic GOS, of which β-D-Galp-(1→6)-D-Lac and β-D-Galp-(1→3)-D-Lac are the major products (Paper I). To further improve GOS synthesis by HoBGLA, rational enzyme engineering was performed (Paper II). Six enzyme variants were generated by replacing strategically positioned active-site residues. Two HoBGLA variants were identified as potentially interesting, F417S and F417Y. The former appears to synthesize one particular GOS product in higher yield, whereas the latter produces a higher yield of total GOS. In Paper III, the high-resolution crystal structure and biochemical characterization of a hemicellulase (HoAraf43) from H. orenii is presented. HoAraf43 folds as a five-bladed β-propeller and displays α-Larabinofuranosidase activity. The melting temperature of HoAraf43 increases significantly in the presence of high salt and divalent cations, which is consistent with H. orenii being a halophile. Furthermore, the crystal structures of a thermostable tetrameric pyranose 2-oxidase from Phanerochaete chrysosporium (PcP2O) were determined to investigate the structural determinants of thermostability (Paper IV). PcP2O has an increased number of salt links between subunits, which may provide a mechanism for increased stability. The structures also imply that the N-terminal region acts as an intramolecular chaperone during homotetramer assembly.

QC 20150429

8

Niemelä, Onni. "Aminoterminal propeptide of type III procollagen and basement related antigens in alcoholic liver disease." Oulu : University of Oulu, 1985. http://catalog.hathitrust.org/api/volumes/oclc/14472875.html.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

9

Cacciatore, Angela [Verfasser], and Hans-Ruprecht [Akademischer Betreuer] Neuberger. "Prokollagen Propeptide : Marker für atriale Fibrose und Vorhofflimmern? / Angela Cacciatore. Betreuer: Hans-Ruprecht Neuberger." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2013. http://d-nb.info/1052907148/34.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

10

Iyappan, Saravanakumar. "The function of the beta6/Pre7 propeptide for 20S proteasome biogenesis in baker's yeast." [S.l. : s.n.], 2004. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB11612026.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Більше джерел

Книги з теми "Propeptide de la sortiline":

1

Davies, Darryl. Interactions between integrins and the c-propeptide domain of fibrillar collagens. Manchester: University of Manchester, 1996.

Знайти повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Частини книг з теми "Propeptide de la sortiline":

1

Shinde, Ujwal, and Masayori Inouye. "Propeptide-Mediated Folding in Subtilisin: The Intramolecular Chaperone Concept." In Advances in Experimental Medicine and Biology, 147–54. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0319-0_16.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

2

Harris, Robert B., Jun ling You, Saskia C. F. Milton, Raymond C. DeLisle Milton, N. S. Rangaraju, and Christopher P. Baker. "The Role of Propeptide Hormone Protein Conformation in Limited Endoproteolysis." In Natural and Engineered Pest Management Agents, 230–48. Washington, DC: American Chemical Society, 1993. http://dx.doi.org/10.1021/bk-1994-0551.ch016.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

3

McAlinden, Audrey, Naoshi Fukui, and Linda J. Sandell. "Type IIA procollagen NH2-propeptide functions as an antagonist of bone morphogenetic proteins." In The Many Faces of Osteoarthritis, 5–16. Basel: Birkhäuser Basel, 2002. http://dx.doi.org/10.1007/978-3-0348-8133-3_1.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

4

Wu, Deguang, Yefu Chen, Jun Lu, Yanan Qi, Cuiying Zhang, and Dongguang Xiao. "Effect of Proteinase A Propeptide Deletion on its Enzyme Activity in Saccharomyces cerevisiae." In Proceedings of the 2012 International Conference on Applied Biotechnology (ICAB 2012), 1459–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-37925-3_155.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

5

Hartmann, D. J., J. C. Trinchet, B. Galet, P. Callard, B. Nusgens, Ch M. Lapiere, M. Beaugrand, and G. Ville. "MEASUREMENT OF SERLM PROCOLLAGEN TYPE III N-TERMINAL PROPEPTIDE IN PATIENTS WITH ALCOHOLIC LIVER DISEASE." In Proceedings of the Third Symposium, Lyon, France, June 26–28, 1985, edited by Jacques Bienvenu, J. A. Grimaud, and Philippe Laurent, 443–48. Berlin, Boston: De Gruyter, 1986. http://dx.doi.org/10.1515/9783110860757-057.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

6

Bayer, Milan, and Vladimir Palicka. "Utilization and Reference Values of Bone Turnover Markers: Osteocalcin and Procollagen Type 1 N-Propeptide." In Biomarkers in Bone Disease, 239–52. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-007-7693-7_37.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

7

Bayer, Milan, and Vladimir Palicka. "Utilization and Reference Values of Bone Turnover Markers: Osteocalcin and Procollagen Type 1 N-Propeptide." In Biomarkers in Bone Disease, 1–15. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-7745-3_37-1.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

8

Hamilton, Maureen A., and Timothy S. Charlebois. "Extracellular Propeptide Processing of Recombinant Human Factor Ix by a Secreted Form of the Endoprotease, Pace." In Animal Cell Technology, 495–501. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5404-8_79.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

9

Dodojacek, R., G. Höfler, B. Leschnik, and W. Muntean. "A Novel Type of Mutation at the Propeptide Cleavage Site (Ala+1Thr) Causing Symptomatic Protein C Type II Deficiency." In 30th Hemophilia Symposium Hamburg 1999, 126–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-18240-2_16.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

10

Oldenburg, J., E. M. Quenzel, U. Harbrecht, A. Fregin, W. Kress, C. R. Müller, H. J. Hertfelder, R. Schwaab, H. H. Brackmann, and P. Hanfland. "Missense Mutations at ALA-10 in the Factor IX Propeptide: A Novel Mechanism for Severe Bleeding During Oral Anticoagulant Therapy." In 27. Hämophilie-Symposion Hamburg 1996, 285–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80403-8_43.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Тези доповідей конференцій з теми "Propeptide de la sortiline":

1

Busby, S., K. Berkner, L. Halfpap, J. Gambee, and A. Kumar. "ALTERATION OF PROPTIDE SEQUENCE IMPAIRS BIOLOGICAL ACTIVITY OF HUMAN FACTOR VII." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643784.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

We have investigated the effect of altering the leader sequence of human factor VII on its biological activity. Factor VII is a vitamin K-dependent blood coagulation protein whose activity depends on the presence of gamma-carboxyglutamic acid (gla) residues in its amino terminal region. Since factor VII and other vitamin K-dependent proteins exhibit structural homology in the propeptide, it has been suggested that the propeptide is involved in gamma-carboxylation. Recently, two factor IX patients were identified with point mutations which prevented the processing of the propeptide and generated a factor IX with greatly reduced biological activity (Diuguid et al., PNAS 83; 5803; Bentley et al., Cell 45: 343). To examine this question using recombinant DNA technology, we altered the sequence of the factor VII propeptide by in vitro mutagenesis of the factor VII cDNA and then expressed the altered genes in baby hamster kidney (BHK) cells. For the 60 and 38 aa leader forms of factor VII, the arg (R) at -1 was changed to ser (S), yielding the sequence HRRRS before the +1 ala. In addition, for the 60 aa leader form, a ser was inserted after the arg at -1, resulting in the sequence HRRRRS before the +1 ala. As determined by ELISA, the mutant proteins were synthesized and secreted by BHK cells at levels comparable to the wild-type forms of factor VII. Analysis by radioimmune precipitation and SDS-PAGE indicated that substitution of arg by ser at -1 prohibits processing of the factor VII propeptide, whereas, insertion of a ser after the four arg's does not. However, all three proteins have reduced biological activity by approximately 5-fold when compared to the wild-type forms with the one-stage clotting assay. All three proteins are also quantitatively precipitated by Ba citrate, indicating they are at least partially gamma-carboxylated. These results suggest that the correct sequence of the propeptide, not just cleavage of the propeptide, is necessary for generating a biologically active molecule. The effect of these sequence alterations on gamma-carboxylation will be evaluated further by analysis of the amino acid sequence and composition of the mutant proteins.

2

Jorgensen, M. J., MJ Rabiet, A. B. Cantor, B. Furie, C. L. Brown, C. B. Shoemaker та B. C. Furie. "VITAMIN K-DEPENDENT γ-CARBOXYLATION OF FACTOR IX REQUIRES A RECOGNITION SITE CONTAINED WITHIN THE PROPEPTIDE". У XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643564.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

The vitamin K-dependent proteins, including Factor IX (FIX), are calcium-binding proteins that undergo vitamin K-dependent post-translational modification to convert amino terminal glutamic aoid residues to Gla residues. Sequence homology among the propeptides of these proteins suggests a role for this region in designating the adjacent glutamic acid-rich domain for γ-carboxylation during intraoellular processing. Mutations vere made in the propeptide (residues -1 to -18) of FIX, and the effects on γ-carboxylation were assessed. The human FIX cDNA coding sequenoe was modified using oligonucleotide-directed site-specific mutagenesis and was expressed in Chinese hamster ovary cells. The extent of γ-carboxylation of secreted FIX was determined by (1) ability to interact with conformation-specific antibodies directed against the Gla-dependent, metal-stabilized, native structure of FIX, and (2) direct Gla analysis of the alkaline hydrolysate. Using the unmodified coding sequence, 64 ± 17 % of recombinant Factor IX bound to the conformation-specific antibodies, and 9.4 ± 0.7 Gla residues were found (compared with 12 Gla in plasma FIX). When the 18-residue propeptide was deleted, secreted FIX contained no detectable native FIX antigen and no detectable Gla. Similarly, point mutations leading to substitution of Ala for Phe at residue -16 or Glu for Ala at residue -10 led to secretion of FIX containing 2% and 6% native antigen, respectively, and approximately 1-2 Gla residues. The molecular weight of each of the reoombinant FIX species, as estimated by SDS-PAGE, was identical to that of plasma FIX. NH2-terminal sequence analysis of the mutant FIX speoies yielded the NH2-terminal sequence of plasma FIX. These data indicate that the mutations made in the propeptide did not interfere with intracellular proteolytic prooessing of FIX. We conolude that the FIX propeptide participates in defining a recognition site that designates an adjacent glutamic acid-rich domain for γ-carboxylation. The association of the propeptide with the γ-carboxylation recognition site provides the first demonstration of a specific function served by a propeptide in post-translational protein processing.

3

Zhu, Anqi, Pinyao He, Haiyan Wang, and Yunfei Chen. "Detection of the C-terminal Propeptide of Proaerolysin by Aerolysin Nanopore." In 2022 IEEE International Conference on Manipulation, Manufacturing and Measurement on the Nanoscale (3M-NANO). IEEE, 2022. http://dx.doi.org/10.1109/3m-nano56083.2022.9941648.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

4

Foster, D., B. Schach, M. Rudisky, K. Berkner, A. Kumar, A. Kumar, C. Sprecher, F. Hagen, and E. W. Davie. "The Effect of Changes in the Leader Sequence of Human Protein C on Biosynthetic Processing and Gamma-Carboxylation." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643993.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Protein C is the precursor to a serine protease in plasma which contains gamma-carboxy glutamic acid and functions as a potent anticoagulant. Protein C shows considerable structural homology with the other vitamin K-dependent coagulation factors including prothrombin, factor VII, factor IX and factor X. Sequence analysis ofthe cDNAs for these proteins has revealedthe presence of a prepro leader sequence that contains a pre sequence or hydrophobic signal sequence and a propeptide containing a number of highly conserved amino acids. The pre region is removed from thegrowing polypeptide chain by signal peptidase, while the pro region is subsequently removed from the protein prior to secretion. Deletion mutants have been constructed in the propeptide portion of the cDNAfor human protein C in order to test the possibility that the propeptide portion of the 42 amino acid leader sequence serves as a molecular signal for gamma-carboxylation.Accordingly, these mutants containthe pre-peptide (hydrophobic leader) plusportions of the pro-peptide at the amino terminus of the light chain. These deletions include the removal of 4, 9, 12, 15, 16 or 17 amino acids from the carboxyl end of the leader sequence of 42 amino acids. The mutant proteins were expressed in carboxylation-competent mammalian cells and were then examined by Western blotting, barium citrate adsorption and precipitation, amino acid sequence analysis, and biological activity and compared with the native protein present in normal plasma. These studies have shown that deletions inthe pro-peptide region interfere with gamma-carboxylation and removal of the pro-peptide. Deletion of residues -1 through -12 had little effect on the carboxylationor secretion. Deletion of -1 through -17 completely abolished gamma-carboxylation, but had no measurable effect on secretion.Amino terminal sequence analysis of thelatter mutant showed that the light chainbegan with Thr-Pro-Ala-Pro... This corresponds to a sequence in the prepro leader starting at -24. This indicates that the signal peptidase cleavage site for human protein C is between residues -25 and -24 and removal of the pro-peptide had been blocked by the deletion.Furthermore, during biosynthesis and secretion, the amino-terminal region of the propeptide (residues from about -12 through -17) are important for carboxylation of protein C, while the carboxyl-terminal portion of the peptide (residues -1 through -4) are important for the removal of the proleader sequence by proteolytic processing.

5

Wellhöfer, T., H. J. Kolde, O. Tiebel, B. Krammer-Steiner, M. Steiner, and J. Lüdemann. "A New Rapid, Specific, and Simple ELISA for von Willebrand Factor Propeptide." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680243.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

6

Bañares-Hidalgo, A., E. J. Cabré, F. Gil, A. Bolaños, S. Aller, B. Amor, G. Castañer, et al. "Production of recombinant forms of the propeptide COOH-terminal and the saposin B-type domain of the propeptide NH2-terminal of the precursor of pulmonary surfactant protein B." In Proceedings of the II International Conference on Environmental, Industrial and Applied Microbiology (BioMicroWorld2007). WORLD SCIENTIFIC, 2009. http://dx.doi.org/10.1142/9789812837554_0148.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

7

Furis, B. C., M. J. Jorgensem, M. J. Rabiet, A. B. Contor, C. L. Brown, C. B. Shoemaker, and B. Furie. "RECOGNITION SITE DIRECTING GAMMA-CARBOXYLATION RESIDES ON THE PROPEPTIDES OF FACTOR IX AND PROTRROMBIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643992.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Factor IX and prothrombin vitamin K-dependent proteins that participate in blood coagulation undergo post-translationalmodification in which glutamic acid residues in the amino terminus of the protein are converted to gamma-carboxyglutamic acid residues. This modification confers divalent metal ion binding ability upon the proteins.As a consequence of binding divalent metal ions these proteins undergoconformational changes necessary for biological function.The vitamin K-dependent proteins are synthesized with an NH2-terminal extension. The region distal to the NH2-terminus of the mature protein is a prototypic signal sequence while the proximal region is a propeptide with homology among the vitamin K-dependent proteins. The boundary between the pre and pro sequences has been established for factor IX by analysis of three naturally occurring factor IX mutants factor IX Cambridge factor IX Oxford-3 and factor IX San Dimas, in which processing is incomplete.For human factor IX the propeptide extends from residue -18 to -1. The homology among the propeptides of vitamin K-dependent proteins suggests that the propeptide may designate adjacent gamma-carboxyglutamic acids for carboxylation. To test this hypothesis alterations in sequence were introduced into the propeptide region of human factor IX cDNA by oligonucleotide directed site specific mutagenesis.Mutated genes were expressed in Chinese hamster ovary cells. Rapid and efficient isolationof the mutant proteins by immunoaffinity chromatography permitted detailed analysis of the mutants on quantities of protein easily obtainable at low expression levels. The extent of gamma-carboxylation was assessed by the ability of the mutant proteins to interact with conformation specific antibodies directed against the gamma-carboxyglutamic acid-dependent metal stabilized native structure of factor IX as well as by direct amino acid analysis. Unmodified recombinant factor IX contained, on average, 9 gamma-carboxyglutamic acid residues, as compared to 12 for plasma factor IX. About 70% of the recombinant wild type factor IX bound to the conformation specific antibodies. Deletion of the propiece or point mutations at residues -10 or -16 led to secretion of uncarboxylated factor IX unreaotive with antibodies specific for the native structure but with the NH2-terminus of mature factor IX. In order to assess the universality of these observations we have recently cloned human prothrombin cDNA and expressed the gene in the same Chinese hamster ovary cell system used for factor IX. In contrast to factor IX, at low levels ofexpressionof the prothrombin gene, the prothrombin is fully carboxylated relative to a plasma prothrombin standard.The recombinant prothrombin exhibits the same specific clotting activity as plasma derivedprothrombin and is fully native as evaluated by conformation specific antibodies. At high levels of expression the capacityof the cells to carboxylate prothrombin can be exceeded leading to secretion of under carboxylated prothrombin. However, the absolute amount of fully carboxylated prothrombin that can be produced in this system appears to be a least fivefold greater that the absolute amount of highly carboxylated factor IX that can be synthesized.The elimination of carboxylation observed upon mutation of the propiece of factor IX suggest that the propiece contains a recognition element required for carboxylation of the protein. Assignment of a functional role to the propiece of factor IX represents the first determination of function for any pro sequence. It is anticipated that extension of these studies to prothrombin will demonstrate that this recognition signal is used by all the members of this class of proteins. In order to determine if the propiece is sufficient to designate a protein for gamma-carboxylation we are currently constructing chimeric proteins incorporating the propieceof prothrombin into the cDNA of normally uncarboxylated proteins.

8

Salameh, Janelle W., Charles S. Umbaugh, and Marxa L. Figueiredo. "Abstract LB-260: Development and validation of propeptide therapeutics for treating bone metastatic prostate cancer." 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-lb-260.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

9

Simbrunner, B., I. Villesen, B. Scheiner, DJ Bauer, R. Paternostro, P. Schwabl, A. Stättermayer, et al. "Von Willebrand Factor (VWF) propeptide levels are similarly accurate for assessing portal hypertension as compared to VWF antigen." In 54. Jahrestagung & 31. Fortbildungskurs der Österreichischen Gesellschaft für Gastroenterologie & Hepatologie – ÖGGH (Hybrid Veranstaltung). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1734276.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

10

Syrkis, Joanna Patrycja, Katarzyna Aleksandra Kujawa, Patrycja Jakubowska, and Katarzyna Marta Lisowska. "#817 Overexpression of lysil oxidase propeptide (LOX-PP) results in decreased proliferation and improved chemosensitivity of ovarian cancer cells." In ESGO 2023 Congress. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/ijgc-2023-esgo.652.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.