las mic ▁calci um ▁activ ates ▁Ca 2 + / cal mod ul in - dependent ▁protein ▁kin ase ▁( Ca M K II ). ▁Activ ated ▁Ca M K II ▁dest abil izes ▁ β - c aten in ▁via ▁a ▁poor ly ▁character ized ▁mechanism , ▁but ▁which ▁likely ▁involves ▁ β - c aten in ▁ph osph ory lation ▁by ▁Ca M K II . ▁The ▁ β - c aten in ▁trans cription al ▁program ▁( which ▁is ▁required ▁for ▁normal ▁neural ▁cr est ▁cell ▁development ) ▁is ▁thereby ▁suppress ed , ▁resulting ▁in ▁prem ature ▁neural ▁cr est ▁cell ▁apo pt osis ▁( cell ▁death ). ▁ ▁Inter actions ▁ ▁B eta - c aten in ▁has ▁been ▁shown ▁to ▁interact ▁with : ▁▁ ▁A PC , ▁▁ ▁A X IN 1 , ▁▁ ▁And ro gen ▁re ceptor , ▁▁ ▁C BY 1 , ▁▁ ▁CD H 1 , ▁▁ ▁CD H 2 , ▁▁ ▁CD H 3 , ▁▁ ▁CD K 5 R 1 , ▁▁ ▁CH UK , ▁▁ ▁CT N ND 1 , ▁▁ ▁CT N NA 1 , ▁▁ ▁E G FR , ▁▁ ▁Emer in ▁▁ ▁E SR 1 ▁▁▁ ▁F HL 2 , ▁▁ ▁G SK 3 B , ▁▁ ▁H ER 2 / ne u , ▁▁ ▁H NF 4 A , ▁▁ ▁I K K 2 , ▁▁ ▁LE F 1 , ▁▁ ▁M AG I 1 , ▁▁ ▁M UC 1 , ▁▁ ▁NR 5 A 1 ,