Mechanisms of Cisplatin-Induced Apoptosis and of Cisplatin Sensitivity: Potential of BIN1 to Act as a Potent Predictor of Cisplatin Sensitivity in Gastric Cancer Treatment

Figure 2

Molecular model of the NER system. Quoted from [7] and modified. (i) XPC-hHR23B (XC-23) binds and senses DNA distorting NER lesions in global NER, resulting in conformational alterations of the DNA. In transcriptional-coupled repair (NER), lesions are detected by elongating RNA polymerase II (Pol II). (ii) (left) XPC-hHR23B attracts TFIIH together with XPG (XG). TFIIH creates a 10- to 20-nucleotide open DNA complex. XPC-hHR23B is released. (right) CSA, CSB, TFIIH, XG, and possibly cofactors displace the stalled Pol II and then bind to the lesions. (iii) XPA (XA) and RPA bind and stabilize the open DNA complex. (iv) XG that is positioned by TFIIH and RPA cuts the damaged nucleotides at the 3′ site and ERCC-XPF (XF) that is positioned by RPA and XPA cuts them at the 5′ site. (v) DNA polymerase fills the gap and ligase seals the nick. Normal nucleotide sequence is consequently restored. Contacts drawn between molecules reflect reported protein-protein interactions.