KIFREIO

Keratin Intermediate Filaments as Regulators of Epithelial Intracellular Organization Keratin intermediate filaments are cytoskeletal proteins regulating the polarity and intracellular organization

Coordinatore	ABO AKADEMI    more  Organization address address: DOMKYRKOTORGET 3 city: ABO postcode: 20500 contact info Titolo: Prof. Nome: John Cognome: Eriksson Email: send email Telefono: 35822153313 Fax: 35823338000
Nazionalità Coordinatore	Finland [FI]
Totale costo	100˙000 €
EC contributo	100˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2007-4-3-IRG
Funding Scheme	MC-IRG
Anno di inizio	2008
Periodo (anno-mese-giorno)	2008-01-01   -   2011-12-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	ABO AKADEMI  Organization address address: DOMKYRKOTORGET 3 city: ABO postcode: 20500 contact info Titolo: Prof. Nome: John Cognome: Eriksson Email: send email Telefono: 35822153313 Fax: 35823338000	FI (ABO)	coordinator	0.00

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 Obiettivo del progetto (Objective)

'Keratin intermediate filaments are cytoskeletal proteins regulating the polarity and intracellular organization of epithelial cells, influencing interactions of epithelia with the surrounding environments. This is particularly relevant in the intestine, where a single cell layer of epithelial cells form a barrier between the luminal content and the underlying tissues. Keratin 8 (K8) null mice develop an ulcerative colitis-like inflammatory bowel disease (IBD) that responds to antibiotic therapy. K8 null colonocytes also mistarget ion transporters in association with abnormal chloride transport and diarrhea. The unexpected connection between K8 and colitis led to a proteomic approach, showing decreased expression of the ketogenic enzyme mHMG-CoAs in K8 null colonocytes. K8 null mice also develop autoantibodies against mHMG-CoAs. These findings raise the hypothesis that colonic keratins modulate ketone body metabolism, which is relevant to the IBD phenotype, since bacteria regulate mHMG-CoAs through butyrate, a major colonocyte energy source. The aims are to use microarray data to identify differences in K8 null ketone body metabolism and verify findings by inducing ketogenesis and measuring the ramifications of a blunted pathway. Mistargeting of butyrate transporters will also be investigated. K8 mutations predispose to liver disease but the role in IBD is unknown. Apart from contributing to the understanding of the biological roles of keratins, including ketone body metabolism, the study has broad ramifications for patients suffering from the common and incapacitating IBD-conditions, for patients with keratin mutations, and may aid in developing diagnostic/therapeutic modalities. I wish return to Europe and establish myself as a Finnish investigator after advanced training at Stanford University. The Turku-BioCity environment combined with my unique skills and collaborative networks with Stanford University provide excellent prospects for a fruitful synergy.'