p(HGNC:BAD)

Entity

Name

BAD

Namespace

hgnc

Namespace Version

20180906

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

AKT interacts with BAD to regulate apoptosis and, interestingly, also has many interacting partners in the insulin signaling pathway. Abeta increased activity of BAD, lowered the activity of the antiapoptotic protein BCL2, in rat hippocampal neurons in primary culture (Koriyama et al., 2003) and has been shown to be toxic to human neuroblastoma cells by increasing BAX activity and decreasing BCl-2 activity (Clementi et al., 2006). PubMed:19293145

In lung cancer cells, nicotine also exerts an antiapoptotic effect through activating BCL2-antagonist of cell death (BAD), a process that is inhibited by blockers of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway or the PI3K/AKT pathway (Jin et al., 2004). PubMed:19293145

In lung cancer cells, nicotine also exerts an antiapoptotic effect through activating BCL2-antagonist of cell death (BAD), a process that is inhibited by blockers of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway or the PI3K/AKT pathway (Jin et al., 2004). PubMed:19293145

In lung cancer cells, nicotine also exerts an antiapoptotic effect through activating BCL2-antagonist of cell death (BAD), a process that is inhibited by blockers of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway or the PI3K/AKT pathway (Jin et al., 2004). PubMed:19293145