Peptide name : L-amino-acid oxidase ACTX-8

Source/Organism : Venom base

Linear/Cyclic : Linear

Chirality : L

Peptide length: 19

C-terminal modification: Linear

N-terminal modification : Not found

Non-natural peptide information: None

Assay type : MTT assay

Assay time : 24h

Activity : MIC : 20 μg/ml

Cell line : HeLa

Cancer type : Cervical cancer

Other activity : Not found

Amino acid composition bar chart :

Molecular mass : 2400.4684 Dalton

Aliphatic index : 0.463

Instability index : 36.3632

Hydrophobicity (GRAVY) : -1.678

Isoelectric point : 4.05

Charge (pH 7) : -5.1889

Aromaticity : 0.157

Molar extinction coefficient (cysteine, cystine): (1490, 1490)

Hydrophobic/hydrophilic ratio : 0.46153846

hydrophobic moment : -0.125

Missing amino acid : C,W,H,Q,T,M,I,K,S,V,G

Most occurring amino acid : E

Most occurring amino acid frequency : 5

Least occurring amino acid : A

Least occurring amino acid frequency : 1

Secondary structure fraction (Helix, Turn, Sheet): (0.4, 0.3, 0.2)

SMILES Notation: CC(C)C[C@H](NC(=O)[C@H](Cc1ccccc1)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](Cc1ccc(O)cc1)NC(=O)[C@H](CC(N)=O)NC(=O)[C@H](CC(N)=O)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](Cc1ccccc1)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](CC(C)C)NC(=O)[C@@H]1CCCN1C(=O)[C@H](CC(N)=O)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CC(=O)O)NC(=O)[C@H](CC(=O)O)NC(=O)[C@H](C)N)C(=O)O

1 : Zhang L and Wei LJ. ACTX-8, a cytotoxic L-amino acid oxidase isolated from Agkistrodon acutus snake venom, induces apoptosis in Hela cervical cancer cells. Life Sci. 2007; 80:1189-97. doi: 10.1016/j.lfs.2006.12.024

Paper title : ACTX-8, a cytotoxic L-amino acid oxidase isolated from Agkistrodon acutus snake venom, induces apoptosis in Hela cervical cancer cells.

Doi : https://doi.org/10.1016/j.lfs.2006.12.024

Abstract : ACTX-8 is a protein isolated from Agkistrodon acutus snake venom in our laboratory. It demonstrates cytotoxic activity on various carcinoma cell lines in vitro. However, the mechanism by which ACTX-8 inhibits cell proliferation remains poorly understood. In this study the influence of ACTX-8 on the activation of apoptotic pathway in Hela cells was investigated. We demonstrated that cell death induced by ACTX-8 was concentration- and time-dependent. Apoptotic changes such as phosphatidyl serine externalization and DNA fragmentation were detected in ACTX-8-treated cells. Caspase activation and reactive oxygen species (ROS) production were involved in ACTX-8-induced apoptosis, but pan caspase inhibitor, z-VAD-fmk, could not inhibit cell death induced by ACTX-8 completely, which proved the existence of another pathway for ACTX-8-induced cell death. We found cytochrome c release into cytosol and mitochondrial membrane potential (MMP) dissipation in ACTX-8-treated cells, which indicated that mitochondrial pathway played a role in ACTX-8-induced cell apoptosis. The ratio of expression levels of pro- and anti-apoptotic Bcl-2 family members was not changed by ACTX-8 treatment. However Bad and Bax were translocated from cytosol into mitochondria, and the coimmunoprecipitation result indicated that in mitochondria Bak and Bcl-xL dissociation was followed by the binding of Bad and Bcl-xL. Taken together, the study indicated mitochondrial pathway played an important role in the ACTX-8-induced apoptosis, which was regulated by Bcl-2 family members.