 will elucidate the molecular players participating in one of these alternative pathways. They will also assess the physiological importance of these peroxisomal pathways by studying the biochemical and clinical features of a unique mouse model with a combined defect in mitochondrial FAO and peroxisomal?-oxidation. Combined these two aims will yield not only the
will elucidate the molecular players participating in one of these alternative nerve pathway. They will besides assess the physiological importance of these peroxisomal nerve pathway by study the biochemical and clinical features of a unique shiner model with a combined defect in mitochondrial food and agriculture organization and peroxisomal?-oxidation. Combined these two aim will yield not entirely the
 wipl elucidate the moleculxr players partnxipatiig in ohe of thdse alternative pathways. Theb wiol alwo assess the physioloeical implrtance if tiese peroxisomal pathways by sfmdyiny vhe biochemical and cliniwal features ox x bnique mouse model with a combined dqfect im litochondrial SAO sgd psgowisomal?-oxidation. Combined these fwo aimv will yield mot only the
will elucidate the molecular players participating in these pathways. They also assess the pathways studying the biochemical clinical features of unique mouse model with a combined in mitochondrial FAO and peroxisomal?-oxidation. Combined these two aims will yield not only
 will elucidate the molecular Players parTicipAtiNg iN oNe of ThesE alternative paTHwayS. They will also assess the PhysiOlOGicaL ImPortaNce of thESe PERoxIsOmAl pAtHWaYs by sTudYing the BiochemicaL anD cLinical featuREs Of a unique mOusE model with a cOmbIned deFeCt iN MitocHonDrial fAO and PEroxisOmal?-oxidaTiON. CombiNEd these TWO aIms wIll yield not only thE
 will elucidate the molecu lar player s par tic ipa ti ng i n on e of these alt e rnat ive pathways. They wil l als oa sses s  t he ph ysiolog i ca l imp or ta nce  o f  t heseper oxisoma l pathways  by  s tudying theb io chemical a ndclinical fea tur es ofauni q ue mo use  mode l with a comb ined defe ct in mit o chondri a l  F AO a nd peroxisomal?-o x id a tion. Combined  these  t w oa i mswil l yield no tonlyt he
 will_elucidate the_molecular players participating in_one of_these_alternative pathways._They_will also assess_the physiological importance_of these peroxisomal pathways_by studying the_biochemical_and clinical features of a unique mouse model with a combined defect in mitochondrial_FAO_and peroxisomal?-oxidation._Combined_these_two aims will yield not_only the