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Fig. 2 | Acta Neuropathologica Communications

Fig. 2

From: The complement system in glioblastoma multiforme

Fig. 2

Proposed interaction of complement C3a and C5a with GSC regulatory mechanisms. C5a-C5aR interaction activates PI3K/Akt/mTOR signaling and PKCĪ¶ but suppresses p21 with subsequent OCT-4 activation. Intracellular activation of C3a by cathepsin-L may occur, thereby sustaining basal mTOR activation. Either intracellular or extracellular derived C3a phosphorylates STAT-3 and causes an increase of SOX-2 expression

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