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. Author manuscript; available in PMC: 2010 Oct 1.
Published in final edited form as: J Dent Res. 2009 Oct;88(10):894–903. doi: 10.1177/0022034509343143

Figure 3.

Figure 3

Putative signaling pathway involved in radiation-induced salivary gland dysfunction. In general, activation of Akt occurs through the binding of growth factors (GF) to their specific receptor (reviewed in (Manning and Cantley, 2007) and, in salivary acinar cells, requires the activation of PI-3 kinase (combined p85 and p110 subunits) (Limesand et al., 2003a). An important molecule that regulates the DNA damage response is p53, and negative regulation of p53 protein levels by Akt is mediated via activation of the Murine Double Minute Clone 2 (MDM2). p53 activation following radiation leads to apoptosis of salivary acinar cells (arrows mark activated caspase-3-positive cells) and subsequent loss of function. It is probable that other pathways (right-side icon) regulating the apoptotic response, discussed in the section “Other Pathways Involved in Radiation Damage”, could play a role in radiation-induced salivary gland dysfunction. In addition, other factors (left-side icon), such as autophagy, necrosis, senescence, etc., could be involved in DNA damage, leading to loss of function.