Guest guest Posted March 5, 2011 Report Share Posted March 5, 2011 Dr. Hamblin's old lab is looking into GA-101 and how it works. Mark Cragg and Tim Illidge et al have found that certain type II anti-CD20 mAbs, like GA-101, efficiently induce programmed cell death, whereas rituximab-like type I anti-CD20 mAbs do not. Further, they demonstrated that GA101-induced cell death is dependent on actin reorganization, can be abrogated by inhibitors of actin polymerization and is independent of BCL-2 over-expression and caspase activation. GA101-induced programmed cell death is executed by lysosomes which disperse their contents into the cytoplasm and surrounding environment. In conclusion it is felt that GA101 is able to potently elicit actin-dependent, lysosomal cell death, which may potentially lead to improved clearance of B-cell malignancies in vivo. Abstract: http://bloodjournal.hematologylibrary.org/cgi/content/abstract/blood-2010-07-296\ 913v1 ~chris Quote Link to comment Share on other sites More sharing options...
Recommended Posts
Join the conversation
You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.