Bid BH3 peptide acetate is a pro- apoptotic peptide derived from the Bid protein. Through its α-helical conformation, Bid BH3 peptide inserts into the hydrophobic grooves of anti-apoptotic Bcl-2 family proteins ( Bcl-xl, Bcl-2, Bcl-w and Bax ), competitively displaces and releases the pro-apoptotic proteins Bax/Bak, thereby initiating mitochondrial outer membrane permeabilization (MOMP) and the caspase cascade for apoptosis. Bid BH3 peptide acetate can be used in cancer-related research [1] [2].
In Vitro, Bid BH3 peptide acetate (10 μM; 6 h) acetate does not induce apoptosis in Jurkat E6.1 cells, while bivalent and pentavalent dextran-conjugated Bid BH3 peptide acetate increase caspase-3 activity by 12-fold and 21-fold, respectively, following nucleofection[1]. Monomeric Bid BH3 peptide (10 μM) acetate conjugated to nonaarginine does not induce apoptosis in Jurkat E6.1 cells, while bivalent and pentavalent dextran-conjugated Bid BH3 peptide acetate with nonaarginine increase caspase-3 activity by 7-fold and 17-fold, respectively[1]. Pentavalent dextran-conjugated Bid BH3 peptide (10 μM; 8 h) acetate induces early apoptosis in Jurkat E6.1 cells, as evidenced by Annexin-V staining and intact cell membrane integrity[1]. Bid BH3 peptide (0.05-0.07 mM) acetate is released as an unfolded species from its complex with truncated human BCL-w when BCL-w binds to 5-6 mM DPC micelles, and the released peptide binds to DPC micelles at concentrations up to 50 mM[2].
References:
[1]. Richter M, et al. Multivalent design of apoptosis-inducing bid-BH3 peptide-oligosaccharides boosts the intracellular activity at identical overall peptide concentrations. Chemistry (Weinheim an der Bergstrasse, Germany). 2012 Dec 21;18(52):16708-15.
[2]. Denisov AY, et al. Structural model of the BCL-w-BID peptide complex and its interactions with phospholipid micelles. Biochemistry. 2006 Feb 21;45(7):2250-6.
In Vitro, Bid BH3 peptide acetate (10 μM; 6 h) acetate does not induce apoptosis in Jurkat E6.1 cells, while bivalent and pentavalent dextran-conjugated Bid BH3 peptide acetate increase caspase-3 activity by 12-fold and 21-fold, respectively, following nucleofection[1]. Monomeric Bid BH3 peptide (10 μM) acetate conjugated to nonaarginine does not induce apoptosis in Jurkat E6.1 cells, while bivalent and pentavalent dextran-conjugated Bid BH3 peptide acetate with nonaarginine increase caspase-3 activity by 7-fold and 17-fold, respectively[1]. Pentavalent dextran-conjugated Bid BH3 peptide (10 μM; 8 h) acetate induces early apoptosis in Jurkat E6.1 cells, as evidenced by Annexin-V staining and intact cell membrane integrity[1]. Bid BH3 peptide (0.05-0.07 mM) acetate is released as an unfolded species from its complex with truncated human BCL-w when BCL-w binds to 5-6 mM DPC micelles, and the released peptide binds to DPC micelles at concentrations up to 50 mM[2].
References:
[1]. Richter M, et al. Multivalent design of apoptosis-inducing bid-BH3 peptide-oligosaccharides boosts the intracellular activity at identical overall peptide concentrations. Chemistry (Weinheim an der Bergstrasse, Germany). 2012 Dec 21;18(52):16708-15.
[2]. Denisov AY, et al. Structural model of the BCL-w-BID peptide complex and its interactions with phospholipid micelles. Biochemistry. 2006 Feb 21;45(7):2250-6.