Alaabta

Dayactirka myelin-ka ee lagu guuleysto ee CNS ee qaangaarka ah wuxuu u baahan yahay soo saarid adag oo waqtigeeda leh ee borotiinnada myelin-ka si ay u abuuraan galmo cusub oo myelin ah.Hababka sharciyeynta ee hoose iyo saldhigga molecular ee kakan ee dib-u-soo-nooleynta myelin, si kastaba ha ahaatee, ayaa ah mid si liidata loo fahmay.Halkan, waxaan ku baarnaa doorka ERK MAP kinase calaamadinta habkan.Tirtirka shuruuda ah ee Erk2 ee unugyada lineage oligodendrocyte waxay keentay remyelination dib u dhac ka dib dhaawaca demyelinating ee jiirka qaangaarka ah ee corpus callosum.Dayactirka daahista ayaa ku yimid natiijo la'aan gaar ah oo ku timid tarjumaada borotiinka myelin-ka weyn, MBP.Maqnaanshaha ERK2, firfircoonida borotiinka ribosomal S6 kinase (p70S6K) iyo bartilmaameedkeeda hoose, borotiinka ribosomal S6 (S6RP), ayaa wiiqay waqti xasaasi ah markii oligodendrocytes premyelinating ay u gudubtay unug qaangaar ah oo awood u leh inay soo saaraan galka cusub ee myelin.Markaa, waxaanu ku sharaxnay xidhiidh muhiim ah oo ka dhexeeya ERK MAP kinase signaling cascade iyo mishiinada tra nslational gaar ahaan remyelinating oligodendrocytes in vivo.Natiijooyinkani waxay soo jeedinayaan doorka muhiimka ah ee ERK2 ee xakamaynta tarjumaadda ee MBP, borotiinka myelinka oo u muuqda mid muhiim u ah hubinta jiilka waqtiga ee galka cusub ee myelin ka dib dhaawaca demyelinating ee CNS ee qaangaarka ah.