Comparison Of Parthenolide And STAT
All MAPKs are activated by dual phosphorylation of threonine and tyrosine motifs within the sub-domain VIII of activation loop. Once activated, they translocate to the nucleus and phosphorylate target transcription factors, such as c-Jun. JNK involved in apoptosis, neurodegeneration, cell differentiation, proliferation and inflammatory conditions [50]. Won et al. (2004) showed that PN inhibited JNK activation and led to UVB-induced apoptosis of JB6 murine epidermal cells [51]. But Zhang et al. (2004) demonstrated that inhibition of NF-kappaB activation and sustained JNK activation contribute to the sensitization of PN effect on TNF- induced apoptosis in human cancer cells [39]. The authors reported that PN sensitizes human nasopharyngeal carcinoma (CNE1) cells to TNF-α induced apoptosis. Tang et al. (2001) and Varfolomeev et al. (2004) concluded that sustained JNK activation had resulted from NF-κB inhibition [52, 53]. Furthermore, it downregulates the phosphorylated form of NF-κB, p38MAPK, and ERK1/2 protein level [Popiolek-Barczyk et al., 2015 Neural Plast]. Based on the literature data, it is evident that in normal cells, PN protects cells from apoptosis whereas in cancer cells, it supports apoptotic cell death