Isolated by screening for Bcl-2 interacting proteins, Bad shows significant homology to Bcl-2 within the Bcl-2 homology domains 1 and 2 (BH1 and BH2). In addition, several other proteins involved in cell death such as Bax, Bcl-X[L], Mcl-1, and A1 share similar homology with Bcl-2. Bcl-2 is known to oppose several apoptotic signals and is considered to be a central downstream cell death repressor. Bcl-X[L] represses apoptosis, but its short form, Bcl-X[S], promotes cell death. Bax is known to homodimerize as well as heterodimerize with Bcl-2. An excess concentration of Bax opposes the ability of Bcl-2 to repress cell death. Bad can selectively dimerize with Bcl-X[L] and Bcl-2, but not with Bax, Bcl-X[S], Mcl-1, A1, or itself. In mammalian cells, Bad binds more strongly to Bcl-X[L] than Bcl-2. This may explain why Bad reverses the death repressor activity of Bcl-X[L], but not that of Bcl-2. The formation of the Bad-Bcl-X[L] heterodimer displaces Bax and restores favorable conditions for apoptosis.
原厂资料：
注意事项：
1.Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2.Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing. .
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