cobra-cardiotoxin-proteins and Leukemia

cobra-cardiotoxin-proteins has been researched along with Leukemia* in 1 studies

Other Studies

1 other study(ies) available for cobra-cardiotoxin-proteins and Leukemia

Article	Year
A cyclic peptide, L1AD3, induces early signs of apoptosis in human leukemic T-cell lines. Journal of biochemical and molecular toxicology, 2004, Volume: 18, Issue:4 L1AD3 is a small cyclic synthetic peptide designed to resemble the first loop of a cobra venom cytotoxin. Instead of inducing membrane disruption similar to that caused by the parent toxin, L1AD3 promotes extensive and unusually rapid apoptosis in leukemic T-cells without making the plasma membrane permeable to small fluorescent dyes. Within 4 h, micromolar concentrations of L1AD3 almost totally inhibit thymidine incorporation, and ATP levels decrease significantly. By contrast, normal human white blood cells are not affected by L1AD3, nor is heart cell function affected by it. If L1AD3 kills by interacting with targets that are different from those of currently applied agents, this peptide, or a derivative of it, could become a useful adjunct for cancer chemotherapy. Topics: Amino Acid Sequence; Animals; Antineoplastic Agents; Apoptosis; Caspases; Cell Line; Cell Line, Tumor; Cell Survival; Circular Dichroism; Cobra Cardiotoxin Proteins; Humans; Leukemia; Leukocytes; Models, Molecular; Protein Conformation; Protein Structure, Tertiary; Rats; Structure-Activity Relationship; T-Lymphocytes	2004

Article

Year

A cyclic peptide, L1AD3, induces early signs of apoptosis in human leukemic T-cell lines.

Journal of biochemical and molecular toxicology, 2004, Volume: 18, Issue:4

L1AD3 is a small cyclic synthetic peptide designed to resemble the first loop of a cobra venom cytotoxin. Instead of inducing membrane disruption similar to that caused by the parent toxin, L1AD3 promotes extensive and unusually rapid apoptosis in leukemic T-cells without making the plasma membrane permeable to small fluorescent dyes. Within 4 h, micromolar concentrations of L1AD3 almost totally inhibit thymidine incorporation, and ATP levels decrease significantly. By contrast, normal human white blood cells are not affected by L1AD3, nor is heart cell function affected by it. If L1AD3 kills by interacting with targets that are different from those of currently applied agents, this peptide, or a derivative of it, could become a useful adjunct for cancer chemotherapy.

Topics: Amino Acid Sequence; Animals; Antineoplastic Agents; Apoptosis; Caspases; Cell Line; Cell Line, Tumor; Cell Survival; Circular Dichroism; Cobra Cardiotoxin Proteins; Humans; Leukemia; Leukocytes; Models, Molecular; Protein Conformation; Protein Structure, Tertiary; Rats; Structure-Activity Relationship; T-Lymphocytes

2004