PTMs, such as SUMOylation, phosphorylation, and ubiquitination, have been found to regulate the tumor suppressor function of PML, but little is known about its acetylation.
Recently, PIF5, a basic helix-loop-helix (bHLH) transcription factor, was found to regulate the transcription of MEP pathway genes and function as an IPP-metabolism enhancer [ 69].
The interaction of CtIP and MRN has been found to regulate the resection of DNA ends [ 35], a process also mediated by BRCA1 [ 36, 37], thereby regulating the function of the ATR-ATRIP complex at regions of ssDNA, and so regulating the progression of the cell through the G2/M checkpoint.
Surfactants have also been found to regulate the balance of proteases/antiproteases through different pathways, SP-A may even regulate MMP-9 production and function [ 21- 24].
Other miRNAs have been found to regulate the angiogenic process by exerting an antiangiogenic function.
Various factors have been found to regulate expression and function of E-cadherin in malignant tumors and implicated in cancer progression [ 6– 14].
Autophagy proteins have recently been shown to regulate the functions of ERK, and ERK activation has been found to induce autophagy.
Prox1 was found to regulate metabolic function in hepatocytes, and to be involved in the regulation of other transcription factors [ 11].
Previously, multisite phosphorylation of proteins was found to regulate protein function in either a graded fashion, as we have found, or by a switch-like response (Nash et al., 2001; Serber and Ferrell, 2007; Strickfaden et al., 2007).
