. "GA303/04/0003" . . "Proteomic analysis of mouse model of hereditary hemochromatosis"@en . . "Following the new trends and developments in the research of iron metabolism we focused our attention to liver as the organ\u00A0critical for the pathogenesis of hereditary hemochromatosis type I.1)\u00A0 Proteomic analysis of molecular mechanism of hereditary hem"@en . . . . "1"^^ . . "Neuvedeno."@en . "V\u00A0souladu se sv\u011Btov\u00FDm v\u00FDvojem pohledu na d\u011Bdi\u010Dnou hemochromat\u00F3zu se vyv\u00EDjel i n\u00E1\u0161 v\u00FDzkum, p\u0159edev\u0161\u00EDm ve smyslu soust\u0159ed\u011Bn\u00ED v\u00FDzkumn\u00E9ho \u00FAsil\u00ED na c\u00EDlen\u00E9 studium jater.1) Proteomick\u00E9 studium molekul\u00E1rn\u00ED patogeneze d\u011Bdi\u010Dn\u00E9 heochromat\u00F3zyV\u00A0j\u00E1trech my\u0161\u00EDho modelu"@cs . . "0"^^ . . "D\u011Bdi\u010Dn\u00E1 hemochromat\u00F3za typu 1 je autozom\u00E1ln\u011B-recesivn\u00ED d\u011Bdi\u010Dn\u00E9 onemocn\u011Bn\u00ED metabioismu \u017Eeleza postihuj\u00EDc\u00ED z 200 - 300 jedinc\u016F. Nemocn\u00ED vst\u0159eb\u00E1vaj\u00ED z potravy velk\u00E9 mno\u017Estv\u00ED \u017Eeleza, kter\u00E9 se potom ukl\u00E1d\u00E1 v r\u016Fzn\u00FDch org\u00E1nech a tk\u00E1n\u00EDch. Depozice \u017Eeleza vede k oxidativn\u00EDmu po\u0161kozen\u00ED tk\u00E1n\u00ED a org\u00E1nov\u00E9mu selh\u00E1n\u00ED. Sou\u010Dasn\u00E1 znalost molekul\u00E1rn\u00EDho mechanismu tohoto onemocn\u011Bn\u00ED je bohu\u017Eel velmi omezen\u00E1 i navzdory znalosti mutovan\u00E9ho genu, kter\u00FD onemocn\u011Bn\u00ED zp\u016Fsobuje.V tomto projektu navrhujeme vyu\u017E\u00EDt modern\u00EDch proteomick\u00FDch metod - dvojrozm\u011Brn\u00E9 elektrofor\u00E9zy a hmotnostn\u00ED spektrometrie - k anal\u00FDze rozd\u00EDl\u016F v expresi b\u00EDlkovin mezi my\u0161\u00EDm modelem d\u011Bdi\u010Dn\u00E9 hemochromat\u00F3zy (HFE-knockout) a kontroln\u00EDm zv\u00ED\u0159etem. Projekt je zam\u011B\u0159en na tk\u00E1n\u011B kritick\u00E9 pro p\u0159et\u00ED\u017Een\u00ED \u017Eelezem - na enterocyty tenk\u00E9ho st\u0159eva a j\u00E1tra. Proteomick\u00E1 anal\u00FDza je schopn\u00E1 zachytit molekul\u00E1rn\u00ED zm\u011Bny vedouc\u00ED k celkov\u00E9mu p\u0159et\u00ED\u017Een\u00ED \u017Eelezem a identifikovat b\u00EDlkoviny pod\u00EDlej\u00EDc\u00ED se na patofyziologii d\u011Bdi\u010Dn\u00E9 hemochromat\u00F3zy." . . "http://www.isvav.cz/projectDetail.do?rowId=GA303/04/0003"^^ . "2007-10-16+02:00"^^ . . . "0"^^ . "Hereditary hemochromatosis Type 1 is an autosomal-recessive inherited disorder of iron metabolism affecting 1 in every 200-300 individuals. Hereditary hemochromatosis is the most common primary iron overload in populations of European ancestry. Individuals with this disease absorb excess iron, which accumulates in variety of organs. Iron accumulation leads to oxidative injury with consequent organ failure. Our knowledge of the molecular mechanism of the dysregulation of iron metabolism in hereditary hemochromatosis is very limited, despite the identification of mutations responsible for the disease. We propose to empoly proteomic techniques to analyze differences in protein expression between mouse model of HH (HFE-knockout mouse) and control mouse in two tissues critical for iron metabolism - intestinal absorptive enterocytes and liver. This analysis has the potential to capture molecular changes leading to - and connected with - systemic iron overload, and to find candidate proteins"@en . . . "Proteomick\u00E1 anal\u00FDza my\u0161\u00EDho modelu heredit\u00E1rn\u00ED hemochromat\u00F3zy" . "13"^^ . . . . "13"^^ . . . .