Peptide name : P3Bax

Source/Organism : Effectors (BAK, BAX)

Linear/Cyclic : Linear

Chirality : L

Peptide length: 32

C-terminal modification: Linear

N-terminal modification : Not found

Non-natural peptide information: None

Assay type : Cell survival assay

Assay time : Not found

Activity : Not found

Cell line : NRP-154

Cancer type : Prostate cancer

Other activity : Not found

Amino acid composition bar chart :

Molecular mass : 3272.6166 Dalton

Aliphatic index : 0.640

Instability index : 40.1438

Hydrophobicity (GRAVY) : -0.181

Isoelectric point : 4.1369

Charge (pH 7) : -2.4939

Aromaticity : 0.062

Molar extinction coefficient (cysteine, cystine): (0, 0)

Hydrophobic/hydrophilic ratio : 1.28571428

hydrophobic moment : 0.9315

Missing amino acid : C,R,W,H,Y,N,V

Most occurring amino acid : G

Most occurring amino acid frequency : 7

Least occurring amino acid : D

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (0.2, 0.4, 0.2)

SMILES Notation: CC[C@H](C)[C@H](NC(=O)[C@H](Cc1ccccc1)NC(=O)CNC(=O)[C@H](CCC(N)=O)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](Cc1ccccc1)NC(=O)[C@H](C)NC(=O)CNC(=O)[C@@H](NC(=O)[C@H](CCCCN)NC(=O)[C@H](CCSC)NC(=O)[C@@H](NC(=O)[C@H](CCC(N)=O)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](CO)NC(=O)[C@H](CO)NC(=O)[C@@H](NC(=O)[C@@H]1CCCN1C(=O)CNC(=O)CNC(=O)[C@H](CO)NC(=O)CNC(=O)[C@H](CC(C)C)NC(=O)[C@H](CCC(N)=O)NC(=O)[C@H](CCC(=O)O)NC(=O)CNC(=O)[C@H](CO)NC(=O)CNC(=O)[C@H](CC(=O)O)NC(=O)[C@@H](N)CCSC)[C@@H](C)O)[C@@H](C)CC)[C@@H](C)O)C(=O)N[C@@H](CCC(N)=O)C(=O)O

1 : Li N, et al. The amino-terminal peptide of Bax perturbs intracellular Ca2+ homeostasis to enhance apoptosis in prostate cancer cells. Am J Physiol Cell Physiol. 2009; 296:C267-72. doi: 10.1152/ajpcell.00390.2008

Paper title : The amino-terminal peptide of Bax perturbs intracellular Ca2+ homeostasis to enhance apoptosis in prostate cancer cells.

Doi : https://doi.org/10.1152/ajpcell.00390.2008

Abstract : During apoptosis, proteolytic cleavage of Bax at the amino terminus generates a truncated Bax of approximately 18 kDa (p18Bax) and an amino-terminal peptide of approximately 3 kDa (p3Bax). Whereas extensive studies have shown that p18Bax behaves like a BH3 protein with enhanced pro-apoptotic function over that of the full-length Bax (p21Bax), little is known about the function of p3Bax in apoptosis. We have previously shown that Bax and Ca2+ play a synergistic role in amplifying apoptosis signaling and that store-operated Ca2+ entry (SOCE) contributes to Bax-mediated apoptosis in prostate cancer cells. Here we test whether p3Bax can contribute to regulation of Ca2+ signaling during apoptosis through use of a membrane-penetrating peptide to facilitate delivery of recombinant p3Bax into NRP-154 cells, a prostate epithelial cell line with tumorigenic capacity. We find that human immunodefficiency virus transactivator of transcription protein (TAT)-p3Bax fusion peptide can enhance thapsigargin-induced apoptosis in NRP-154 cells, elevate SOCE activity, and increase inositol 1,4,5-trisphosphate-sensitive intracellular Ca2+ stores. Our data indicates that p3Bax can modulate the entry of extracellular Ca2+ and thus regulate the amplification of apoptosis in prostate cancer cells.