Caspase nyhuv mechanism

Cov yam ntxwv ntawm cov hlwb apoptotic muaj xws li DNA fragmentation rau hauv cov seem ntawm 200 bp, chromatin concentration, cell membrane activation, cell shrinkage, thiab thaum kawg tsim cov apoptotic lub cev qhwv hauv cell membrane. Tom qab ntawd, lub cev apoptotic no tau nqos los ntawm lwm lub hlwb. Cov txheej txheem no siv sijhawm li 30-60 feeb. Tag nrho cov txheej txheem ntawm caspase induced kev hloov pauv cuam tshuam nrog apoptosis saum toj no tsis meej meej, tab sis tsawg kawg suav nrog peb lub tswv yim hauv qab no:

Inhibitor ntawm apoptosis

Cov hlwb nyob ib txwm tsis ua txhaum DNA vim hais tias nuclease tsis ua haujlwm. Qhov no yog vim hais tias nuclease thiab inhibitor yog ua ke. Yog tias tus inhibitor raug rhuav tshem, nuclease tuaj yeem qhib tau, ua rau DNA fragmentation. Nws paub tias caspase tuaj yeem tshem tawm qhov inhibitor los ua kom cov nuclease, yog li no enzyme hu ua caspase activated deoxyribonuclease CAD, thiab nws cov inhibitor hu ua ICAD. Yog li ntawd, nyob rau hauv ib txwm muaj xwm txheej, CAD tsis qhia kev ua si vim CAD-ICAD muaj nyob rau hauv daim ntawv ntawm ib tug inactive compound. Thaum ICAD yog hydrolyzed los ntawm Caspase, CAD yog endowed nrog nuclease kev ua, thiab DNA fragmentation yog generated. Nws yog ib qho tseem ceeb uas CAD tsuas tuaj yeem sib xyaw ua ke thiab qhia txog kev ua haujlwm thaum ICAD muaj, qhia tias CAD-ICAD muaj nyob rau hauv kev sib txuas lus, yog li nws yog qhov tsim nyog rau ICAD kom qhib thiab inhibit CAD.