Relevant bibliographies by topics / PCSK7 / Dissertations / Theses
To see the other types of publications on this topic, follow the link: PCSK7.

Dissertations / Theses on the topic 'PCSK7'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 dissertations / theses for your research on the topic 'PCSK7.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.

1

GRENI, FEDERICO. "Variabilità fenotipica nell'emocromatosi: studio di due potenziali modificatori genetici in PCSK7 e GNPAT." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/140994.

Full text
Abstract:
Introduction and aim: Hereditary hemochromatosis (HH) is a genetic disease characterized by a progressive iron overload in different tissues. Homozygosity for the p.C282Y mutation is the most frequent genotype associated with the disease and it is directly responsible for an inappropriate production of hepcidin, the main regulator of iron homeostasis. Several evidences indicated that p.C282Y homozygous genotype has an incomplete penetrance due to the combined action of genetic and acquired modifier factors. Recently, the attention was focused on GNPAT rs11558492 and PCSK7 rs236918 single nucle
APA, Harvard, Vancouver, ISO, and other styles
2

Bhat, Mamatha. "Expression of PCSK9 in Hepatocellular Carcinoma." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=106271.

Full text
Abstract:
Hepatocellular carcinoma (HCC) is an often fatal condition due to late diagnosis, resistance to existing anticancer agents, as well as underlying liver disease that can limit the use of hepatotoxic chemotherapy. Proprotein convertases (PCs) are serine proteases that convert a variety of growth factors, cell surface glycoproteins, receptors and metalloproteinases into their active forms, thus regulating the biological activity of these proteins. PCs have been found to be upregulated in various malignancies. Growth factors implicated in HCC, such as IGF-1, HGF, VEGF and PDGF, have all been shown
APA, Harvard, Vancouver, ISO, and other styles
3

DA, DALT LORENZO. "IMPACT OF PCSK9 ON EXTRAHEPATIC TISSUES." Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/813080.

Full text
Abstract:
Introduzione e scopo: la proproteina convertasi subtilisina kexin tipo 9 (PCSK9) è una glicoproteina di 692 amminoacidi che appartiene alla famiglia delle proproteine convertasi. È prodotta principalmente dal fegato dal quale viene secreta nel torrente circolatorio. PCSK9 interagisce con diversi recettori della famiglia dell’LDLr, inclusi VLDLr, LRP1 ma anche con CD36, e guida la loro degradazione lisosomiale. La mancanza di PCSK9 determina quindi una maggiore espressione dei recettori della famiglia LDLr e favorisce l'accumulo di lipidi nei tessuti extraepatici. L’eccesso di lipidi cellulari
APA, Harvard, Vancouver, ISO, and other styles
4

Stefan, Elias. "Familjär hyperkolesterolemi (FH) – analys av prevalens i Stockholm och hälsoekonomiska konsekvenser av tidigdiagnostik och behandling." Thesis, Uppsala universitet, Institutionen för farmaci, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-434844.

Full text
Abstract:
Background: Familial hypercholesterolemia (FH) is a genetic disorder estimated to affect 0,4 % of the world's population (1 in 250). Patients with FH have abnormally high LDL-cholesterol.  Aim: The aim of this study was to estimate the prevalence of FH in Stockholm County and to evaluate the health economic impact of diagnosing people with FH early in life. Methods: Two algorithms were used to estimate the number of people with high LDLcholesterol. The first method applied data on cholesterol measurements from patients in Stockholm County between 2006-2008 and a modified version of Dutch Lipid
APA, Harvard, Vancouver, ISO, and other styles
5

Giunzioni, I. "MACROPHAGE EXPRESSION OF PCSK9 INFLUENCES ATHEROSCLEROSIS DEVELOPMENT." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/229332.

Full text
Abstract:
Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) regulates low‐density lipoprotein (LDL) cholesterol levels by binding and degrading hepatic LDL receptor (LDLR), thus promoting atherosclerosis. Little is known of PCSK9 effect in macrophages and whether this contributes to the development of the atheroma. To test the effect of human (h) PCSK9 expression on atherosclerosis we developed transgenic mice expressing hPCSK9 on wild type (WT), LDLR‐/‐ or apoE‐/‐ background. We first demonstrated that both mPCSK9 and hPCSk9 are expressed at the mRNA level and secreted in the culture medium by MPM.
APA, Harvard, Vancouver, ISO, and other styles
6

Kourimate, Sanae. "Pcsk9 : régulation et implication dans le syndrome métabolique." Nantes, 2008. https://archive.bu.univ-nantes.fr/pollux/show/show?id=4ac185ba-f999-45ff-9241-4278a9699b5c.

Full text
Abstract:
Proprotein convertase subtilisin/kexin type 9 (PCSK9) est une serine protéase, jouant un rôle important dans la régulation des niveaux de cholestérol circulant. Les mutations gains de fonctions de PCSK9 sont associées à une hypercholestérolémie autosomale dominante due à une élévation des concentrations en Low Density Lipoprotein associées au cholestérol (LDLc). A l'inverse, des mutations perte de fonction de PCSK9, sont associées à une diminution de ces concentrations et à une réduction de 88% du risque d'apparition de maladies coronariennes. Dans le réticulum endoplasmique, Pro-PCSK9 subit u
APA, Harvard, Vancouver, ISO, and other styles
7

CANCLINI, LAURA. "PROPROTEIN CONVERTASE SUBTILISIN/KEXIN TYPE 9 PREFERENTIALLY ASSOCIATES WITH A SPECIFIC LDL SUBFRACTION: A DETAILED CHARACTERIZATION AND STUDY OF THE EFFECTS OF ANTI-PCSK9 MABS TREATMENT." Doctoral thesis, Università degli Studi di Milano, 2022. https://hdl.handle.net/2434/947250.

Full text
Abstract:
BACKGROUND AND AIM: Proprotein Convertase Subtilysin/Kexin Type 9 is a key regulator of LDL-C levels. Nevertheless, its physiological modulation is not fully understood. It is unclear whether PCSK9 has biological effects other than degrading the LDLR; consensus is lacking also on how PCSK9 is transported in the bloodstream, and whether this influences PCSK9 function. There are several conflicting data about PCSK9’s possible association with different lipoprotein subtypes. The biological function of the lipoprotein-bound PCSK9, also, is still a matter of debate. Due to its role in modulating pl
APA, Harvard, Vancouver, ISO, and other styles
8

Dewpura, Thilina. "Importance of phosphorylation in PCSK9 processing, stability and function." Thesis, University of Ottawa (Canada), 2010. http://hdl.handle.net/10393/28604.

Full text
Abstract:
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a secreted glycoprotein regulating the degradation of low density lipoprotein receptor. Single nucleotide polymorphisms in PCSK9 associate with both hyper- and hypo-cholesterolemia; studies show significant reduction in risk of coronary heart disease for 'loss of function' PCSK9 carriers. We used a combination of mass spectrometry and radiolabeling to report that PCSK9 is phosphorylated at two sites, Ser47 in its propeptide, and Ser688 in its C-terminus. Site directed mutagenesis (SDM) demonstrated that a Golgi casein kinase-like kinase
APA, Harvard, Vancouver, ISO, and other styles
9

Roubtsova, Anna. "Partial hepatectomy and liver regeneration in PCSK9 knockout mice." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112356.

Full text
Abstract:
The proprotein convertase subtilisin/kexin type 9, PCSK9, belongs to the proprotein convertase (PC) family. Human mutations in the gene encoding PCSK9 lead to either familial hyper- or hypocholesterolemia, resulting from a gain or loss of function, respectively. Mice lacking PCSK9 are viable and show a 42% decrease in plasma cholesterol levels. The enzyme triggers the degradation of the low density lipoprotein receptor (LDLR) through a partially unknown mechanism.<br>PCSK9 is very abundant in the liver and intestine during development and adulthood. Hepatocytes have a capacity to reproduce the
APA, Harvard, Vancouver, ISO, and other styles
10

Torrinha, José Maria de Queiroz e. Lencastre Fleming. "Inibidores PCSK9: nova estratégia para o tratamento da hipercolesterolemia." Master's thesis, [s.n.], 2015. http://hdl.handle.net/10284/5293.

Full text
Abstract:
Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências Farmacêuticas<br>As doenças cardiovasculares são uma das principais causas de morbilidade e mortalidade a nível mundial. Neste enquadramento, um dos principais fatores de risco associado às doenças cardiovasculares é a hipercolesterolemia. As opções farmacológicas existentes para o tratamento e prevenção desta dislipidemia centram-se, sobretudo, no uso de fármacos como as estatinas, a ezetimiba, os fibratos, o ácido nicotínico e as resinas seques
APA, Harvard, Vancouver, ISO, and other styles
11

Vila, Belmonte Àlex. "Estimación de la prevalencia de la Hipercolesterolemia Familiar y de las características clínicas asociadas en Cataluña." Doctoral thesis, Universitat de Girona, 2019. http://hdl.handle.net/10803/670206.

Full text
Abstract:
Familial hypercholesterolemia (FH) is the most frequent hereditary cause of premature coronary heart disease. The aim of this doctoral thesis is to determine the prevalence of subjects with FH phenotype (FH-P); to describe their clinical characteristics and the lipid-lowering therapy that they follow; as well as to estimate the number and type of patients eligible for treatment with proprotein convertase subtilisin/kexin type 9 inhibitors (iPCSK9) according to the different indication criteria of the scientific societies and the National Health System (NHS). This research was done based on da
APA, Harvard, Vancouver, ISO, and other styles
12

Ramin-Mangata, Stéphane. "Le rôle du récepteur aux LDL et de PCSK9 dans le diabète de type 2." Thesis, La Réunion, 2020. http://www.theses.fr/2020LARE0005.

Full text
Abstract:
Les statines sont des médicaments hypolipémiants largement prescrits dans le cadre des maladies cardiovasculaires. Elles inhibent la synthèse endogène de cholestérol et induisent l’activation de l’expression du LDLR par le facteur de transcription SREBP-2. Ce sont des médicaments dont le bénéfice est indiscutable d’un point de vue cardiovasculaire. Néanmoins, l’action des statines est limitée par la proprotéine convertase subtilisin kexin type 9 (PCSK9), l’inhibiteur naturel du récepteur aux LDL (LDLR), qui est également sous la dépendance de SREBP-2. Ainsi, de nouvelles stratégies hypolipémia
APA, Harvard, Vancouver, ISO, and other styles
13

Choquet, Hélène. "Contribution du gène PCSK1 aux formes monogéniques et polygéniques d'obésité." Phd thesis, Université du Droit et de la Santé - Lille II, 2010. http://tel.archives-ouvertes.fr/tel-00576415.

Full text
Abstract:
Quatre études de liaison génome entier ont mis en évidence une région commune de5,6 Mb dans la région du chromosome 5q15 liée à des traits associés à l'obésité, cette région incluant le gène de la prohormone convertase 1 (PCSK1). Une mutation Pc1 chez la souris a été associée à l'obésité, l'hyperphagie et à une augmentation de l'efficacité du métabolisme. La déficience complète en PCSK1 a été associée à une forme récessive rare d'obésité chezl'homme, et depuis 1997 seuls trois patients présentant cette déficience ont été décrits dans la littérature. Les porteurs de mutations délétères PCSK1 pr
APA, Harvard, Vancouver, ISO, and other styles
14

Shore, Robert. "A functional characterisation of the PCSK6 locus associated with handedness." Thesis, University of St Andrews, 2016. http://hdl.handle.net/10023/15719.

Full text
Abstract:
Humans display a 90% population level bias towards right-handedness, implying the vast majority of people have a left-hemisphere dominant for motor control. Although handedness presents a weak, but very consistent heritability across the literature (estimated to be approximately 25%), to date few genetic loci associated with this complex trait have been identified and replicated in subsequent studies. One such gene which has been found to be associated with handedness and subsequently replicated is PCSK6, most recently through a quantitative GWAS (P < 0.5*10−8, Brandler et al. (2013)). Interes
APA, Harvard, Vancouver, ISO, and other styles
15

Sarkar, Samantha Khadija. "The Regulation of PCSK9 Structure and Function Through Lipoprotein Interactions." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39099.

Full text
Abstract:
Proprotein convertase subtilisin / kexin type 9 (PCSK9) is a negative regulator of the low-density lipoprotein receptor, and PCSK9 inhibition has become an important cholesterol-lowering therapeutic strategy. PCSK9 also associates with LDL particles, and evidence suggests that the activity of PCSK9 may be regulated by LDL binding. We have investigated the biochemistry of the interaction between PCSK9 and lipoproteins. Through mutagenesis and in-vitro binding assays, we found conserved motifs in the PCSK9 N-terminus that play a role in LDL binding. Through secondary structure studies using circ
APA, Harvard, Vancouver, ISO, and other styles
16

Choquet, Hélène. "Contribution du gène PCSK1 aux formes monogéniques et polygéniques d’obésité." Thesis, Lille 2, 2010. http://www.theses.fr/2010LIL2S012/document.

Full text
Abstract:
Quatre études de liaison génome entier ont mis en évidence une région commune de5,6 Mb dans la région du chromosome 5q15 liée à des traits associés à l’obésité, cette région incluant le gène de la prohormone convertase 1 (PCSK1). Une mutation Pc1 chez la souris a été associée à l’obésité, l’hyperphagie et à une augmentation de l’efficacité du métabolisme. La déficience complète en PCSK1 a été associée à une forme récessive rare d’obésité chezl’homme, et depuis 1997 seuls trois patients présentant cette déficience ont été décrits dans la littérature. Les porteurs de mutations délétères PCSK1 pr
APA, Harvard, Vancouver, ISO, and other styles
17

Haas, Mary Elizabeth. "Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) in Secondary Hyperlipidemias." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493577.

Full text
Abstract:
Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) has emerged over the past decade as an important regulator of plasma cholesterol and cardiovascular disease risk. PCSK9 promotes degradation of low density lipoprotein (LDL) receptors, thereby decreasing LDL clearance. Accordingly, patients with gain-of-function mutations in PCSK9 have increased LDL cholesterol and increased risk of cardiovascular disease. Conversely, PCSK9 inhibitors recently approved by the FDA are effective in reducing LDL cholesterol. While the contribution of PCSK9 to familial hypercholesterolemia is well-established,
APA, Harvard, Vancouver, ISO, and other styles
18

Ricci, C. "PCSK9 AND INFLAMMATION: IN VITRO STUDY ON HEPATOCYTES AND MACROPHAGES." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/541464.

Full text
Abstract:
TNF-alpha induces proprotein convertase subtilisin kexin type 9 (PCSK9) expression in hepatic HepG2 cell line, through the activation of suppressor of cytokine signaling 3 (SOCS3): Background. The suppressor of cytokine signaling (SOCS) proteins are negative regulators of the JAK/STAT pathway activated by pro-inflammatory cytokines, including the tumor necrosis factor- (TNF-). SOCS3 is also implicated in hypertriglyceridemia associated to insulin-resistance (IR). Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) levels are frequently found to be positively correlated to IR and plasma ve
APA, Harvard, Vancouver, ISO, and other styles
19

BOTTA, MARGHERITA. "DECIPHERING THE ROLE OF ADIPOKINES ON PCSK9 REGULATION: EXPERIMENTAL EVIDENCE." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/695060.

Full text
Abstract:
Background: Adipose tissue is an endocrine organ secreting active molecules, namely, adipokines. In a condition of dysfunctional visceral fat depots, adipokines may be detrimental for the cardiovascular system. The present study was aimed at evaluating some of the molecular mechanisms linking adipokines and the expression of proprotein convertase subtilisin/kexin 9 (PCSK9), the key regulator of low-density lipoprotein receptor and also involved in triglycerides (TG) metabolism. This latter evidence come from genetic studies reporting high levels of TG in patients with gain of function (GOF) mu
APA, Harvard, Vancouver, ISO, and other styles
20

Nguyen, My-Anh. "Characterization of PCSK9-mediated LDLR Degradation in Hepatic and Fibroblast Cells." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/26114.

Full text
Abstract:
The discovery that proprotein convertase subtilisin/kexin type 9 (PCSK9) mediates degradation of low-density lipoprotein receptors (LDLR) indicates a critical role in LDL metabolism. PCSK9 is a secreted protein that binds to the epidermal growth factor-like (EGF)-A domain of LDLR and directs the receptor for degradation in lysosomes by an unknown mechanism. A gain-of-function mutation, D374Y, increases binding to LDLR EGF-A >10-fold and is associated with a severe form of hypercholesterolemia in humans. Similar to previous studies, data obtained in my project has established that PCSK9 was ca
APA, Harvard, Vancouver, ISO, and other styles
21

Sarkar, Samantha Khadija. "Asociation of PCSK9 with Low Density Lipoproteins (LDL) in the Regulation of LDL-Cholesterol Levels." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32825.

Full text
Abstract:
Proprotein Convertase Subtilisin / Kexin Type-9 (PCSK9) has emerged as a major regulator of plasma cholesterol levels. PCSK9 is secreted mainly from the liver and circulates as a plasma protein. PCSK9 binds cell surface low-density lipoprotein (LDL) receptors and mediates their degradation upon endocytosis in the liver. This decreases the liver’s ability to clear LDL-cholesterol from the blood. PCSK9 is also capable of binding LDL particles themselves; this interaction inhibits the ability of PCSK9 to bind and mediate LDLR degradation in cultured hepatic cells, but its effect on PCSK9 function
APA, Harvard, Vancouver, ISO, and other styles
22

Molin, Tor. "Evolokumabs effekt och kostnadseffektivitet hos patienter utan familjär kolesterolemi." Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-85420.

Full text
Abstract:
Atherosclerosis is the underlying cause for many serious cardiovascular diseases which causes over 50 % of all deaths in Sweden. Atherosclerotic plaque builds up in the vessel walls over decades that will eventually lead to a complete block of an artery or cause thrombosis when the plaque ruptures, this leads to myocardial infarction and stroke. A major contributing factor to the buildup of plaque is cholesterol, especially low density lipoprotein, LDL. LDL can oxidize and start an inflammation process and together with cells from the immune system form the basis for a plaque. Proprotein conve
APA, Harvard, Vancouver, ISO, and other styles
23

Bigolin, Paola. "Ipercolesterolemia familiare: dal genotipo al fenotipo ed implicazione terapeutiche dei nuovi farmaci biologici ipocolesterolemizzanti." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3426245.

Full text
Abstract:
AIMS: Familial Hypercholesterolemia (FH) is a frequent genetic cause of early coronary artery disease, and is still under-diagnosed and under-treated. With the advent of PCSK9 inhibitors as adjunctive therapy to maximal lipid-lowering therapy, a significant reduction in cholesterol levels of low-density lipoprotein (LDL-C) and cardiovascular events was observed, while maintaining a good safety and tolerance profile. Ultrasonography (US) detects Achilles tendon (AT) xanthomas in patients (pts) with FH. Given the recent introduction of new therapies, there are no studies in the literature that e
APA, Harvard, Vancouver, ISO, and other styles
24

Mishra, Priyambada. "Study of Inhibitory Effect of Epididymal Cres on Pc4/Pcsk4 Activity." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19954.

Full text
Abstract:
PC4/PCSK4 is the major Proprotein Convertase (PC) enzyme that plays a key role in mammalian fertilisation. It is detected in the acrosomal granules of round spermatids, acrosomal ridges of elongated spermatids and sperm plasma membrane overlying the acrosome with K-X-K/X-R as its preferred cleavage motif. Such motifs are present in male germ cell proteins ADAMs, proPACAP and proIGF-1/2 and these precursor proteins are processed most likely by PC4 during spermatogenesis, sperm maturation and sperm-egg interaction. For fertilization to occur, the mature sperm must penetrate the Zona Pelucida (ZP
APA, Harvard, Vancouver, ISO, and other styles
25

Denis, Nicholas. "Quantitative Subcellular Analysis of the Effects of the Enigmatic Protein PCSK9." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20133.

Full text
Abstract:
PCSK9 is the third gene implicated in autosomal dominant hypercholesterolemia, due to its role in promoting the degradation of the low density lipoprotein receptor (LDLR). Little is known regarding the mechanism by which it promotes the degradation of LDLR, nor the effects PCSK9 has on other cellular proteins. I report here the first quantitative subcellular proteomic study of proteins affected by the expression of a variant of PCSK9. I show that the expression levels of 293 proteins were affected by the expression of the PCSK9-ACE2-V5 construct. Of particular interest, is a protein involve
APA, Harvard, Vancouver, ISO, and other styles
26

Vilaplana, Saiz Marta. "Design and synthesis of new potentially inhibitors of PCSK9 and KRAS proteins." Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/673609.

Full text
Abstract:
This thesis shows the research carried out on two specific diseases: familial hypercholesterolemia, which is included within the cardiovascular diseases group, and cancer. These diseases are the major cause of deaths in Spain and worldwide. The study of familial hypercholesterolemia is of great interest, as it is mainly caused by a protein called PCSK9 whose atypical functioning leads to an increase of LDL-C in blood. Thus, the study of new diseases results in the study of new therapeutic targets. Therefore, a thorough investigation on the PCSK9 protein has been conducted by means of molecular
APA, Harvard, Vancouver, ISO, and other styles
27

Ngqaneka, Thobile. "The impact of Niacin on PCSK9 levels in vervet monkeys (Chlorocebus aethiops)." University of Western Cape, 2020. http://hdl.handle.net/11394/7931.

Full text
Abstract:
Magister Pharmaceuticae - MPharm<br>Cardiovascular diseases (CVDs) such as ischaemic heart diseases, heart failure and stroke remain a major cause of death globally. Various deep-rooted factors influence CVD development; these include but are not limited to elevated blood lipids, high blood pressure, obesity and diabetes. A considerable number of proteins are involved directly and indirectly in the transport, maintenance and elimination of plasma lipids, including high and low-density lipoprotein cholesterol (HDL-C and LDL-C). There are several mechanisms involved in the removal of LDL p
APA, Harvard, Vancouver, ISO, and other styles
28

Balzarotti, G. "PCSK9 (PROPROTEIN CONVERTASE SUBTILISIN/KEXIN TYPE 9)AND GLUCOSE METABOLISM: WHICH CONNECTION?" Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/543205.

Full text
Abstract:
PCSK9 (proprotein convertase subtilisin/kexin type 9) and glucose metabolism: which connection? Background: PCSK9 (proprotein convertase subtilisin/kexin type 9), is a protein, mainly synthesized and secreted by the liver, which binds to specific target proteins and escorts them towards lysosomes for degradation. The best defined activity of PCSK9 is its ability to modulate the hepatic uptake of LDL cholesterol (LDL-C), by enhancing the intracellular degradation of the LDL receptor (LDLR). In humans, several mutations in PCSK9 gene were described, both “gain-of-function” mutations associate
APA, Harvard, Vancouver, ISO, and other styles
29

Moreau, François. "Rôle de PCSK9 et conséquences des chirurgies bariatriques sur le métabolisme intestinal du cholestérol." Thesis, Nantes, 2017. http://www.theses.fr/2017NANT4069/document.

Full text
Abstract:
L’intestin est un acteur majeur du métabolisme du cholestérol de part son rôle dans dans l’absorption, la sécrétion des lipoprotéines et l’efflux transintestinal de cholestérol (TICE). De plus, c’est le second organe majeur, après le foie, à exprimer la Proproteine Convertase Subtilisine Kexine de type 9 (PCSK9), un inhibiteur naturel du récepteur aux LDL. Notre analyse des mécanismes moléculaires impliqués dans l’ hypocholestérolémie induite par les chirurgies bariatriques montre que la sleeve gastrectomie induit une hypocholestérolémie transitoire et modérée lié aux modifications de prise al
APA, Harvard, Vancouver, ISO, and other styles
30

Lasica, Rick, and Ashley Loy. "Cost-Effectiveness Analysis of PCSK9 Inhibitors for the Treatment of Heterozygous Familial Hypercholesterolemia." The University of Arizona, 2017. http://hdl.handle.net/10150/624203.

Full text
Abstract:
Class of 2017 Abstract<br>Objectives: To determine the cost-effectiveness of proprotein convertase subtilisin kexin 9 (PCSK9) inhibitors with high-intensity statins compared to high-intensity statins alone for the treatment of heterozygous familial hypercholesterolemia (HeFH). Methods: A Markov model was built through TreeAge Pro to model two groups: patients taking PCSK9 inhibitors with high-intensity statins or high-intensity statins alone. For each group, there were five health states that patients could be in: well, unstable angina, myocardial infarction, ischemic stroke, or death. The da
APA, Harvard, Vancouver, ISO, and other styles
31

Alghamdi, Rasha Hassen. "Development of Inhibitors of Human PCSK9 as Potential Regulators of LDL-Receptor and Cholesterol." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/30492.

Full text
Abstract:
Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) is the ninth member of the Ca+2-dependent mammalian proprotein convertase super family of serine endoproteases that is structurally related to the bacterial subtilisin and yeast kexin enzymes. It plays a critical role in the regulation of lipid metabolism and cholesterol homeostasis by binding to and degrading low-density lipoprotein-receptor (LDL-R) which is responsible for the clearance of circulatory LDL-cholesterol from the blood. Owing to this functional property, there is plenty of research interest in the development of functional inhibit
APA, Harvard, Vancouver, ISO, and other styles
32

Thain, Katherine Roberta. "Identifying functional single nucleotide polymorphisms in two candidate genes (PROC and PCSK9) in sepsis." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44755.

Full text
Abstract:
Genetic variation contributes to outcome from sepsis. A large number of associations have been observed between genetic variants and sepsis outcome, however, identification of causal single nucleotide polymorphisms (SNPs), or their mechanisms of action, have not been successfully elucidated. The aims of this project are to identify causal variants in two candidate genes and determine whether these variants are involved in the mechanisms leading to altered outcomes in sepsis. The known pathophysiology of sepsis is complex and involves dysregulation of several systemic processes, including t
APA, Harvard, Vancouver, ISO, and other styles
33

Honorato, Aldrina Laura da Silva Costa. "Investigação de mutações no gene PCSK9 em famílias com diagnóstico clínico de Hipercolesterolemia Familiar." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17138/tde-07122018-091850/.

Full text
Abstract:
A hipercolesterolemia familiar (HF) é uma alteração de origem genética comum que pode se manifestar clinicamente desde o nascimento e provoca um aumento nos níveis plasmáticos de LDL-colesterol (LDL-c), xantomas e doença coronária prematura. Sua detecção e tratamento precoce reduzem a morbidade e mortalidade coronária. A identificação e rastreamento em cascata familiar usando níveis de LDL-c e detecção genética é a estratégia mais aconselhável e rentável para descoberta de novos casos. O tratamento crônico com estatinas reduz o risco cardiovascular da população em geral, contudo, estudos clíni
APA, Harvard, Vancouver, ISO, and other styles
34

Duff, Christopher. "Post-translational regulation of the low-density lipoprotein receptor : PCSK9 as a therapeutic target." Thesis, University of Leeds, 2010. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.749285.

Full text
APA, Harvard, Vancouver, ISO, and other styles
35

Matyas, Angela. "The Functional Characterization of PCSK9's Binding Interactions with LDL and the LDL Receptor." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40592.

Full text
Abstract:
Elevated plasma cholesterol is a risk factor for cardiovascular disease. Proprotein convertase subtilisin/kexin type 9 (PCSK9) hinders the uptake of low-density lipoprotein cholesterol (LDL-c) by mediating degradation of LDL receptors (LDLRs) in the liver. Gain-of-function (GOF) mutations in PCSK9 cause familial hypercholesterolemia (FH). In normolipidemic human plasma, 30-40% of PCSK9 is bound to LDL particles, and this association with LDL inhibits PCSK9’s ability to mediate LDLR degradation in cultured cells. To further investigate the physiological relevance of this interaction, we analyze
APA, Harvard, Vancouver, ISO, and other styles
36

Guerardel, Audrey. "Analyse de deux gènes candidats physiologiques et positionnels de l'obésité humaine CART et PCSK1." Lille 2, 2005. http://www.theses.fr/2005LIL2S012.

Full text
Abstract:
L'obésité commune est une maladie multifactorielle, dont l'émergence récente comme maladie de masse, est liée à l'occidentalisation du mode de vie. Elle est la conséquence d'une diminution de l'activité physique et d'un accès illimité à une alimentation calorique. Néanmoins, les facteurs génétiques influencent la prédisposition individuelle, comme l'attestent des études familiales et l'identification de formes monogéniques d'obésité. Les déterminants des formes polygéniques fréquentes (95%) sont encore peu caractérisés, même si des études récentes ont montré notamment le rôle de certains gènes
APA, Harvard, Vancouver, ISO, and other styles
37

Martin, San Sebastian Ander. "Study of PCSK9 convertase in liver sinusoidal endothelial cells during colorectal carcinoma liver metastasis." Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0434.

Full text
Abstract:
Le cancer colorectal (CRC) est l'une des principales causes de décès liés au cancer, principalement en raison de son potentiel élevé de métastases, en particulier vers le foie. L'irrigation sanguine directe du foie à partir du côlon en fait une cible fréquente des métastases du CRC, aggravant ainsi le pronostic des patients. Comprendre les mécanismes moléculaires de ce processus est essentiel pour développer de nouvelles thérapies.La métastase est un processus complexe impliquant l'invasion locale, l'entrée dans la circulation sanguine, la survie en circulation et la colonisation éventuelle da
APA, Harvard, Vancouver, ISO, and other styles
38

Cho, Elizabeth. "Using Pharmacogenetics to Find Treatment for Familial Hypercholesterolemia Patients with Both apoB and PCSK9 Mutations." Scholarship @ Claremont, 2019. https://scholarship.claremont.edu/scripps_theses/1229.

Full text
Abstract:
Familial hypercholesterolemias (FH) are inherited mutations that cause elevated total cholesterol and low-density lipoprotein cholesterol levels (LDL-C) which lead to premature coronary heart diseases. Pharmacogenetics is the study of inherited genetic differences in drug metabolic pathways which can affect the patient’s response to the drug. Single Nucleotide Morphism (SNP) mutations in the LDLR, apoB, LDRAP1, and PCSK9 genes are linked to familial hypercholesterolemia. The mutations in the LDLR gene are the most common while mutations in the apoB and PCSK9 genes are the least common in hyper
APA, Harvard, Vancouver, ISO, and other styles
39

COGGI, DANIELA. "RELATIONSHIP BETWEEN PLASMA LEVELS OF PCSK9, VASCULAR EVENTS AND MARKERS OF SUBCLINICAL ATHEROSCLEROSIS AND INFLAMMATION." Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/811217.

Full text
Abstract:
Contesto e scopo: La proproteina convertasi subtilisina/kexina di tipo 9 (PCSK9), uno dei principali regolatori del metabolismo del recettore delle LDL, è stata associata allo sviluppo di aterosclerosi. Diversi studi hanno confermato tale associazione attraverso vie lipidiche e non lipidiche. Tuttavia, le relazioni dirette tra PCSK9 circolante e marcatori di aterosclerosi subclinica e clinica sono ancora da chiarire. Pertanto, abbiamo valutato le relazioni tra i livelli plasmatici di PCSK9 ed alcuni indici di aterosclerosi subclinica (marcatori di imaging) e clinica (eventi vascolari; EV). Un
APA, Harvard, Vancouver, ISO, and other styles
40

Ly, Kévin. "Élucidation et identification des différents interacteurs impliqués dans le mécanisme de régulation du LDLR par la protéine PCSK9." Thèse, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/9786.

Full text
Abstract:
Résumé : Les maladies cardiovasculaires représentent la principale cause de mortalité mondiale, soit le tiers des décès annuels selon l’Organisation mondiale de la Santé. L’hypercholestérolémie, caractérisée par une élévation des niveaux plasmatiques de lipoprotéines de faible densité (LDL), est l’un des facteurs de risque majeur pour les maladies cardiovasculaires. La proprotéine convertase subtilisine/kexine type 9 (PCSK9) joue un rôle essentiel dans l’homéostasie du cholestérol sanguin par la régulation des niveaux protéiques du récepteur LDL (LDLR). PCSK9 est capable de se lier au LDLR et
APA, Harvard, Vancouver, ISO, and other styles
41

Roalkvam, Ness Tonje. "PCSK9-hemmere som kolesterolsenkere- koster det mer enn det smaker? : Hvilken evidens finnes det for kostnadseffektivitet?" Thesis, Umeå universitet, Farmakologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-121836.

Full text
APA, Harvard, Vancouver, ISO, and other styles
42

Concepción, Carrillo Luis Edgar, and Esquivel Brandon Iturbe. "Descripción de la expresión de PCSK9 en pacientes del CMLALM con alta sospecha de hipercolesterolemia familiar." Tesis de Licenciatura, Universidad Autónoma del Estado de México, 2021. http://hdl.handle.net/20.500.11799/111123.

Full text
Abstract:
La Hipercolesterolemia Familiar (HF) se define como una enfermedad hereditaria autosómica dominante del metabolismo de las lipoproteínas, caracterizada por concentraciones plasmáticas de colesterol LDL (cLDL) entre 350 y 550 mg/dL, en la forma heterocigota, y mayores de 550 mg/dL en la homocigota, Este trastorno se debe a un grupo de errores genéticos que resultan en niveles anormalmente elevados de colesterol LDL (c-LDL), que causan deposición de placas ateroscleróticas en las arterias incrementando el riesgo de infarto agudo de miocardio en población joven. Se sabe que existen tres mutacion
APA, Harvard, Vancouver, ISO, and other styles
43

Boyer, Marjorie. "Impact d'interventions non pharmacologiques sur les biomarqueurs émergents du risque cardiovasculaire : fonctionnalité des HDL et PCSK9." Doctoral thesis, Université Laval, 2018. http://hdl.handle.net/20.500.11794/32490.

Full text
Abstract:
Les maladies cardiovasculaires (MCV) représentent la première cause de mortalité au monde, malgré des progrès significatifs dans la prise en charge des facteurs de risque traditionnels. De nouveaux biomarqueurs émergent, par exemple la capacité d’efflux du cholestérol (CEC) des HDL qui serait associée aux MCV indépendamment des concentrations de cholestérol HDL. Un autre biomarqueur est la proprotéine convertase subtilisine/kexine de type 9 (PCSK9), qui augmente les niveaux de cholestérol LDL en dégradant le récepteur aux LDL. Les facteurs qui influencent la CEC des HDL et la quantité de PCSK9
APA, Harvard, Vancouver, ISO, and other styles
44

Chu, Ge. "PCSK9 and Its Variants: An Unbiased Global Proteomic Study to Identify Interactors and Effects on Protein Trafficking." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32988.

Full text
Abstract:
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a secreted glycoprotein that promotes degradation of low-density lipoprotein receptors. Gain- and loss-of-function variants of PCSK9 cause hypercholesterolemia and hypocholesterolemia, respectively. Although it has been a decade since the discovery of PCSK9, its effect in terms of global protein changes and interactions still require further understanding. This study provided a global outlook at the protein changes caused by PCSK9 and its variants in human hepatic HUH7 cell line. First, a proteomics-based method for protein subcellular d
APA, Harvard, Vancouver, ISO, and other styles
45

Garçon, Damien. "Effet intestinal de PCSK9 au delà du métabolisme du cholestérol : focus sur la lipémie postprandiale et l'allergie alimentaire." Thesis, Nantes, 2020. http://www.theses.fr/2020NANT1011.

Full text
Abstract:
PCSK9 (ProProtein Convertase Subtilisin Kexin Type 9) est le 3e gène responsable de l’hypercholestérolémie familiale. En effet, PCSK9 est un inhibiteur naturel du récepteur au LDL. Les patients présentant des mutations gain de fonction pour PCSK9 sont à très haut risque concernant les maladies cardiovasculaires. En plus de son impact sur le métabolisme du cholestérol, PCSK9 joue un rôle dans un autre facteur de risque cardiovasculaire : la lipémie postprandiale. Ce phénomène caractérisé par une élévation des triglycérides plasmatiques après un repas est facteur de risque des maladies cardiovas
APA, Harvard, Vancouver, ISO, and other styles
46

Langhi, Cédric. "Implication de PCSK9 dans les maladies métaboliques : régulation par les acides biliaires et rôle fonctionnel dans le pancréas." Nantes, 2009. https://archive.bu.univ-nantes.fr/pollux/show/show?id=8ce2a36e-ee33-47ea-b8e8-fc89d736a8f4.

Full text
Abstract:
PCSK9 (proprotein convertase subtilisin kexin type 9) est le 3ème gène impliqué dans l'hypercholestérolémie familiale dominante, après les mutations des gènes codant pour le récepteur aux LDL (LDLR) et pour son ligand l’apo-B. PCSK9 agit comme un inhibiteur de l'expression hépatique du LDLR par un mécanisme post-traductionnel. En se liant au domaine extracellulaire du LDLR à la surface des membranes plasmiques, PCSK9 induit l'internalisation du LDLR et sa dégradation dans les lysosomes. Ainsi les mutations de PCSK9 associées à l'hypercholestérolémie sont des mutations gain de fonction. A l'inv
APA, Harvard, Vancouver, ISO, and other styles
47

Bélanger, Jasmin Stéphanie. "A putative role for PCSK9 in synaptic remodelling and plasticity in response to brain injury: implications for Alzheimer's disease." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96705.

Full text
Abstract:
Since the association of the ε4 allele of the apolipoprotein E (apoE) withAlzheimer's disease (AD) risk, growing evidences support a role for cholesterolmetabolism in the pathophysiology of this disease. Many genes involved in lipidmetabolism have now been studied and associate with the risk of AD. PCSK9 is aproprotein convertase recently identified as the third gene linked to familialhypercholesterolemia. It is a key regulator of plasma cholesterol concentrations byenhancing the degradation of cell surface low-density-lipoprotein receptor (LDLR). Thepresent project derives from the global hyp
APA, Harvard, Vancouver, ISO, and other styles
48

Bourbiaux, Kévin. "Développement de peptides structurés pour l’inhibition de l’interaction PCSK9/LDLR et le rétablissement de l’absorption cellulaire du LDL-c." Thesis, Montpellier, 2020. http://www.theses.fr/2020MONTS009.

Full text
Abstract:
La proprotéine convertase subtilisine/kexine de type 9 (PCSK9) régule la concentration des récepteurs des lipoprotéines de basse densité (LDLR) au niveau de la membrane cellulaire et par conséquent le taux de LDL-cholestérol dans le système vasculaire. PCSK9 est donc une cible essentielle dans le traitement des maladies cardiovasculaires (MCV). A ce jour, les anticorps monoclonaux anti-PCSK9 associés aux statines est la seule thérapie disponible ciblant PCSK9 en dépit des risques d’immunogénicité, une administration sous-cutanée contraignante et un coût élevé. Néanmoins, de petits peptides pos
APA, Harvard, Vancouver, ISO, and other styles
49

Öijerholm, Mikael. "Aspects of the choice of sampling frequency in the control system of a gas turbine." Thesis, Linköping University, Linköping University, Automatic Control, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-17678.

Full text
Abstract:
<p>At Siemens, plcs are used to control the gas turbines, and to execute the code in the plcs cyclic interrupts are used. If the execution time for the interrupt becomes close to the cyclic time of the interrupt the load of the plc increases. High load levels can lead to situations were segments of code are not executed on time or even not executed at all. In this thesis an analysis of the regulators used to govern a gas turbine has been performed. The purpose of the analysis is to study the performance of the regulators for different cycle times with the aim to be able to reduce the load by s
APA, Harvard, Vancouver, ISO, and other styles
50

SCRIMALI, Chiara. "A novel therapeutic strategy to cure the Homozygous Familial Hypercholesterolemia with residual LDL receptor activity." Doctoral thesis, Università degli Studi di Palermo, 2020. http://hdl.handle.net/10447/395446.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'PCSK7' for other source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography