𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Contribution of BCR–ABL-independent activation of ERK1/2 to acquired imatinib resistance in K562 chronic myeloid leukemia cells

✍ Scribed by Takeru Nambu; Norie Araki; Aiko Nakagawa; Akihiko Kuniyasu; Tatsuya Kawaguchi; Akinobu Hamada; Hideyuki Saito


Book ID
108586546
Publisher
John Wiley and Sons
Year
2010
Tongue
English
Weight
502 KB
Volume
101
Category
Article
ISSN
1347-9032

No coin nor oath required. For personal study only.


📜 SIMILAR VOLUMES


Bcr-Abl-induced tyrosine phosphorylation
✍ Jing-Yi Chen; Ming-Chung Wang; Wen-Chun Hung 📂 Article 📅 2010 🏛 John Wiley and Sons 🌐 English ⚖ 227 KB

## Abstract Our previous study demonstrates that Bcr‐Abl fusion oncogene frequently found in chronic myeloid leukemia (CML) cells can up‐regulate Skp2 expression via transcriptional activation. However, Bcr‐Abl also modulates Skp2 protein stability in these cells. Treatment of Bcr‐Abl kinase inhibi

JNK1/c-Jun and p38α MAPK/ATF-2 pathways
✍ Ku-Chung Chen; Yi-Ling Chiou; Long-Sen Chang 📂 Article 📅 2009 🏛 John Wiley and Sons 🌐 English ⚖ 421 KB

## Abstract Fas and FasL expression upregulation was found in human leukemia K562 cells upon exposure to __Naja naja atra__ phospholipase A~2~ (PLA~2~). PLA~2~ treatment induced an increase in intracellular Ca^2+^ ([Ca^2+^]i) and ROS generation levels, leading to activation of p38 MAPK and JNK. Sup