Leinco Technologies

BID (Intermediate Domain) Blocking Peptide

Product Code:
 
LEI-B487
Product Group:
 
Peptides
Regulatory Status:
 
RUO
Shipping:
 
Ambient
Storage:
 
Store this peptide in working aliquots at -20°C in a manual defrost freezer. Avoid Repeated Freeze Thaw Cycles.
 

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LEI-B487-50ug50 ug£216.00
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This product comes from: US.
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  • Further Information
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Further Information

Concentration:
0.2 mg/ml
Format:
This peptide is formulated in PBS pH 7.2 (0.01 M Sodium Phosphate, 0.13 M NaCl) containing 0.1% bovine serum albumin and 0.02% sodium azide.
Formulation:
This peptide is formulated in PBS pH 7.2 (0.01 M Sodium Phosphate, 0.13 M NaCl) containing 0.1% bovine serum albumin and 0.02% sodium azide.
Long Description:
Bid is a member of the Bcl-2 family of proteins that regulates outer mitochondrial membrane permeability. Bid is a pro-apoptotic member that causes cytochrome c to be released from the mitochondria intermembrane space into the cytosol. In healthy cells Bid is cytosolic. In response to Fas ligand or TNF Bid is cleaved by caspase-8 and it then relocates to the mitochondria outer membrane. Cleavage of Bid by caspase-8 generates a new N-terminal that contains a terminal glycine. It appears that the glycine is myristoylated and myristoylation serves to target Bid to the mitochondria. Bid may then interact with another pro-apoptotic Bcl-2 family member Bak. Interaction of Bid with Bak causes altered mitochondrial membrane permeability. A 9 - 13 amino acid stretch called the BH3 region (Bcl-2 homology region) appears to mediate the Bid interaction with other Bcl-2 family members. Bid is neutralized by binding to the anti-apoptotic member Bcl-x.
Target:
BID

References

1. Jaffer ZM and Chernoff J. p21-activated kinases: three more join the Pak. Int. J. Biochem. Cell Biol. 2002; 34:713-7. 2. Rudel T and Bokoch GM. Membrane and morphological changes in apoptotic cells regulated by caspase-mediated activation of PAK2. Science 1997; 276:1571-4. 3. Vilas GL, Corvi MM, Plummer GJ, et al. Posttranslational myristoylation of caspase-activated p21-activated protein kinase 2 (PAK2) potentiates late apoptotic events. Proc. Natl. Acad. Sci. USA 2006; 103:6542-7.