Involvement of c-jun N-terminal kinase in G2/M arrest and caspase-mediated apoptosis induced by cardiotoxin III (Naja naja atra) in K562 leukemia cells

Cardiotoxin III‐induced apoptosis is mediated by Ca2+‐dependent caspase‐12 activation in K562 cells

“…In our previous study, immunoblotting analyses were applied to measure the expression of phosphorylation of three members of the MAPK family (ERK, JNK, and p38 MAPK). Our data show that only JNK was involved in CTX III-induced cytotoxicity, because inhibition of JNK, but not ERK and JNK, partly prevented CTX III-induced cell death and apoptosis [14]. Another important issue was that because both caspase-12 activation and JNK phosphorylation were involved in CTX III-induced apoptosis, it would be interesting to know which of these two phenomena occurred first.…”

“…It has also been shown that JNK played an important role in CTX III-mediated G2/M arrest and apoptosis in K562 cells [14]. However, the JNK inhibitor or the caspase-3 and the caspase-9 inhibitor partly reversed the CTX III-induced apoptosis.…”

“…In our previous studies, Cardiotoxin III (CTX III) had been demonstrated to induce dose-and time-dependent apoptosis in K562 cells via the intrinsic pathway of apoptosis involving mitochondrial membrane permeability, the release of cytochrome c, and resulting caspase activation [12,13]. It has also been showed that cJun N-terminal kinase (JNK) played an important role in CTX III-mediated G2/M arrest and apoptosis in K562 cells [14]. Although it appears that CTX III can induce cytotoxicity and apoptotic cell death, the underlying mechanism of this process has not been well characterized.…”

Involvement of p38 and c-Jun N-Terminal Protein Kinase in Cardiotoxin III-Induced Apoptosis of K562 Cells

“…JNK specifically phosphorylates the transcription factor c-Jun on its N-terminal transcactivation domain at two serine residues, Ser63 and Ser73, which mediates the proapoptotic function of JNK via modulating the proapoptotic Bcl-2 family protein BIM. 28) Yang et al (2007) have shown that only the JNK signaling pathway is critically involved in the CTX III-mediated apoptosis of K562 cells.…”

Biomimetic affinity purification of cardiotoxin and its pharmacological effects on the nervous system

“…Further studies showed that cardiotoxin has various pharmacological functions such as hemolysis, cytolysis, membrane depolarization (Harvey, 1985), muscle contraction (Markert et al, 2006), and selective death of tumor cells (Yang et al, 2007). Cardiotoxin's target sites include phospholipids, glycosaminoglycans, the Na þ /K þ ATPase, ion channels and protein kinase C (Wang et al, 2005).…”