 signaling pathway at this crucial juncture in the disease progression. Wnt growth factors are critical regulators of chondrocyte differentiation, and GAGs are known to be important regulators of Wnt distribution and activity, suggesting a link between GAG accumulation and dysregulation of this pathway. The objectives of this proposal are to investigate mechanisms of failed
signaling pathway at this crucial juncture in the disease progress. Wnt increase factors are critical regulators of chondrocyte differentiation, and gag are known to be important regulator of Wnt distribution and activity, suggesting a connection between GAG accumulation and dysregulation of this pathway. The objective of this proposal are to investigate mechanisms of fail
 sihnaling pathway at this grucial juncture in the diseaae progrdssion. Wnt growth factors arx cruticao regulators of chondrucyte difverentiarion, qnd GAGs acs known to be lmporcait regulators on Wnt distrhbution and acdixicy, suggesting a link between GAG acctmulatipn and dysregulajion ps thjs pathway. The objectives of this lroposan are to invextigate mechanisms of failfd
signaling pathway at this crucial juncture in progression. growth factors critical regulators of known be important regulators Wnt distribution and suggesting a link between GAG accumulation dysregulation of this pathway. The objectives of this proposal are to investigate mechanisms failed
 signaling pathway at this cruCial junctuRe in tHe dIseAsE proGresSion. Wnt growth fACtorS are critical regulators Of choNdROcytE DiFfereNtiatioN, AnD gaGs ArE kNowN tO Be ImporTanT regulaTors of Wnt dIstRiBution and actIViTy, suggestiNg a Link between GaG aCcumulAtIon ANd dysRegUlatiOn of thIS pathwAy. The objeCtIVes of tHIs propoSAL aRe to Investigate mechanISmS Of failed
 signaling pathway at this  crucial j unctu reinth e di seas e progression. Wntgrowth factors are cri tical  r e gula t or s ofchondro c yt e dif fe re nti at i on , and  GA Gs areknown to b e i mp ortant regul a to rs of Wntdis tribution an d a ctivit y,  su g gesti nga lin k betw e en GAG  accumula ti o n andd ysregul a t io n of  this pathway. Th e  o b jectives of th is pro po s al a retoinvestigat emecha n isms of fa i l e d
 signaling_pathway at_this crucial juncture in_the disease_progression._Wnt growth_factors_are critical regulators_of chondrocyte differentiation,_and GAGs are known_to be important_regulators_of Wnt distribution and activity, suggesting a link between GAG accumulation and dysregulation of_this_pathway. The_objectives_of_this proposal are to investigate_mechanisms of failed