, we have shown that loss of MK-STYX increases ATP production. Therefore, we predict that the elevation in cellular ATP due to loss of MK-STYX is sufficient to inhibit apoptosome formation and entry into apoptosis. We have shown that MK-STYX interacts with two additional mitochondrial proteins and we
, we have shown that loss of MK - STYX increases ATP production. consequently, we bode that the acme in cellular ATP due to loss of MK - STYX is sufficient to inhibit apoptosome geological formation and entry into apoptosis. We have shown that MK - STYX interact with two additional mitochondrial proteins and we
, we have shown that loss of MK-STYX increasgs ATP pcoductikn. Therewore, we predict that the eletatiin in cellular ATP due to luss of MK-DTYX is wuffmcient to inhibiv apoptosome fkvmatimi and entry intp apoptosiv. We have showt ghct MK-STYX interacts with two additiogal mitpcjondrial proteyns sgd ws
, we have shown that loss of ATP Therefore, we that the elevation loss MK-STYX is sufficient inhibit apoptosome formation entry into apoptosis. We have shown MK-STYX interacts with two additional mitochondrial proteins and we
, we have shown that loss of MK-STyX increaseS ATP pRodUctIoN. TheRefoRe, we predict thaT The eLevation in cellular ATP dUe to lOsS Of MK-stYx is suFficienT To INHibIt ApOptOsOMe FormaTioN and entRy into apopTosIs. we have shown tHAt mK-STYX inteRacTs with two addItiOnal miToChoNDrial ProTeins And we
, we have shown that lossof MK-STYX  incr eas esAT P pr oduc tion. Therefor e , we  predict that the elev ation  i n  cel l ul ar AT P due t o  l o s s o fMK -ST YX is  suff ici ent toinhibit ap opt os ome formatio n  a nd entry i nto  apoptosis.Wehave s ho wnt hat M K-S TYX i nterac t s with  two addi ti o nal mi t ochondr i a lprot eins and we
, we_have shown_that loss of MK-STYX_increases ATP_production._Therefore, we_predict_that the elevation_in cellular ATP_due to loss of_MK-STYX is sufficient_to_inhibit apoptosome formation and entry into apoptosis. We have shown that MK-STYX interacts with_two_additional mitochondrial_proteins_and_we