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SiCMetabol SIGNED

Signaling Cascades in Metabolic Diseases

Total Cost €

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EC-Contrib. €

0

Partnership

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 SiCMetabol project word cloud

Explore the words cloud of the SiCMetabol project. It provides you a very rough idea of what is the project "SiCMetabol" about.

modules    ubiquitin    course    canonical    pharmacological    regulating    diabetes    implicated    cross    pkds    laboratory    liver    dysfunction    talk    lipolysis    resistance    phosphorylation    adipokines    shown    levels    hyperlipidemia    phosphatases    adipose    attenuate    mechanisms    normalization    hyperglycemia    glucose    majority    family    poorly    insulin    hypothesize    molecular    people    lipids    metabolism    function    components    hepatic    screening    regulators    predisposing    relative    peripheral    disease    abundance    decreased    homeostasis    cascades    tissue    suffer    plan    leads    localization    defective    t2d    pkd    deficiency    rates    million    determines    caused    lipogenesis    classes    obesity    utilize    worldwide    suggest    kinases    perturbations    attributed    strategies    380    regulation    signaling    over    gluconeogenesis    secretion    organs    pkd2    molecules    metabolic    roles    characterizing    pkd3    risk    combination    networks    pkd1    central    treatment    controls    parallel   

Project "SiCMetabol" data sheet

The following table provides information about the project.

Coordinator
JULIUS-MAXIMILIANS-UNIVERSITAT WURZBURG 

Organization address
address: SANDERRING 2
city: WUERZBURG
postcode: 97070
website: http://www.uni-wuerzburg.de

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Germany [DE]
 Project website https://www.uni-wuerzburg.de/en/rvz/research/research-groups/sumara-group/
 Total cost 1˙499˙128 €
 EC max contribution 1˙499˙128 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2015-STG
 Funding Scheme ERC-STG
 Starting year 2016
 Duration (year-month-day) from 2016-06-01   to  2021-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    JULIUS-MAXIMILIANS-UNIVERSITAT WURZBURG DE (WUERZBURG) coordinator 1˙499˙128.00

Map

 Project objective

Over 380 million people suffer from diabetes worldwide, with majority of cases being attributed to type 2 diabetes (T2D). Obesity is a major risk factor predisposing to the development of this disease. T2D is characterized by peripheral insulin resistance in combination with relative insulin deficiency that results in hyperglycemia and hyperlipidemia. Liver and adipose tissue are central for regulation of glucose and lipids levels. However, during T2D the hepatic glucose uptake is reduced while rates of gluconeogenesis and lipogenesis are increased. In the adipose tissue, T2D leads to decreased glucose uptake, perturbations in secretion of adipokines and increased lipolysis. Importantly, dysfunction of the liver and the adipose tissue during T2D is caused by defective phosphorylation signaling cascades and normalization of these pathways was shown to attenuate the course of T2D. However, the specific roles of different classes of signaling molecules in these organs remain poorly characterized. We hypothesize that the cross-talk of different classes of signaling molecules determines regulation of metabolism. Thus, we aim to identify the signaling networks regulating metabolism. The results generated in my own laboratory suggest that the Pkd family kinases are the crucial regulators of metabolic homeostasis. Specifically, Pkd1 and Pkd2 promote obesity and diabetes while Pkd3 controls liver function. Thus, we plan to characterize the molecular mechanisms controlling Pkds signaling. In parallel, we will utilize screening approaches to identify novel, non-canonical signaling modules (phosphatases and components of the ubiquitin system) regulating abundance, localization and phosphorylation of targets of Pkds and, in the long term, also other kinases implicated in T2D. By identifying and characterizing the essential signaling networks in liver and adipose tissue the project will contribute to more targeted pharmacological strategies for the treatment of T2D.

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