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Figure 4 | Molecular Cancer

Figure 4

From: MutS homologue hMSH5: role in cisplatin-induced DNA damage response

Figure 4

Identification of hMSH5 tyrosine residues that could be phosphorylated by c-Abl. (A) Six hMSH5 cp-1 mutants, harboring various Tyr-to-Phe mutations, were co-expressed with c-Abl in BL21 cells. The effects of these mutations on tyrosine phosphorylation were examined by immunoblotting analysis of affinity-purified hMSH5 cp-1 proteins with an α-p-Tyr antibody. (B) Tyr742 on hMSH5 was targeted by c-Abl kinase in response to cisplatin treatment, and hMSH5 tyrosine phosphorylation led to the dissociation of hMSH5 from c-Abl. 293T/f-hMSH5 and 293T/f-hMSH5Y742F cells were transfected with myc-c-Abl and treated with 20 μM cisplatin 48 hrs post-transfection. Cell lysates were prepared 6 hrs after cisplatin treatment, and α-Flag immunoprecipitates were analyzed by α-p-Tyr and α-c-Abl immunoblots. Four μM imatinib was used to inhibit c-Abl kinase activity.

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