- First try to dissolve a small amount of peptide in either water or buffer. The more charged residues on a peptide, the more soluble it is in aqueous solutions. - If the peptide doesn’t dissolve try an organic solvent e.g. DMSO, then dilute using water or buffer. - Consider that any solvent used must be compatible with your assay. If a peptide does not dissolve and you need to recover it, lyophilise to remove the solvent. - Gentle warming and sonication can effectively aid peptide solubilisation. If the solution is cloudy or has gelled the peptide may be in suspension rather than solubilised. - Peptides containing cysteine are easily oxidised, so should be prepared in solution just prior to use.
Preparation and Storage
Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
Bcl 2 Antagonist of Cell Death
Bcl 2 Binding Component 6
BCL X / BCL 2 Binding Protein
BCL X Binding Protein
Bcl XL/Bcl 2 Associated Death Promoter
Bcl-2-binding component 6
Bcl-2-like protein 8
Bcl-XL/Bcl-2-associated death promoter
Bcl2 antagonist of cell death
BCL2 antagonist of cell death protein
BCL2 associated agonist of cell death
Bcl2 Associated Death Promoter
BCL2 binding component 6
BCL2 binding protein
Bcl2 Like 8 Protein
Proapoptotic BH3 Only Protein
Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2 (By similarity). Appears to act as a link between growth factor receptor signaling and the apoptotic pathways.
Expressed in a wide variety of tissues.
Belongs to the Bcl-2 family.
Intact BH3 motif is required by BIK, BID, BAK, BAD and BAX for their pro-apoptotic activity and for their interaction with anti-apoptotic members of the Bcl-2 family.
Phosphorylated on one or more of Ser-75, Ser-99, Ser-118 and Ser-134 in response to survival stimuli, which blocks its pro-apoptotic activity. Phosphorylation on Ser-99 or Ser-75 promotes heterodimerization with 14-3-3 proteins. This interaction then facilitates the phosphorylation at Ser-118, a site within the BH3 motif, leading to the release of Bcl-X(L) and the promotion of cell survival. Ser-99 is the major site of AKT/PKB phosphorylation, Ser-118 the major site of protein kinase A (CAPK) phosphorylation. Ser-75 is phosphorylated by AKT/PKB, protein kinase A and PIM2.
Mitochondrion outer membrane. Cytoplasm. Upon phosphorylation, locates to the cytoplasm.