"Study using knock-in mouse model elucidated the role of the p38alpha-TAB1 interaction during myocardial ischemia in vivo suggested that persistent p38alpha activation may be the result of the disinhibition of MAP2K3 access in the absence of TAB1 docking on p38alpha and proposed that TAB1 phosphorylation downstream of p38alpha is associated with cardiac damage during ischemia."xsd:string