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. 2022 Sep 2;18(9):e1010362. doi: 10.1371/journal.pgen.1010362

Fig 1. Ptprh Mutant Mouse Tumors have Increased Phosphorylation of AKT.

Fig 1

Conserved metastasis and downstream regulation of EGFR pathways is seen in PyMT tumors with Ptprh mutations. A) Protein domain map of mouse PTPRH shows the location of conserved V483M mutated Ptprh within out PyMT FVB mice. B) Exome sequencing data of PyMT FVB mice from Kent Hunter’s lab shows Ptprh mutations are not conserved to one location. Furthermore, Ptprh mutation status is conserved between primary tumors and their matched metastasis. C) Wholemount of a day 21 MMTV-PyMT mammary gland with the hyperplastic growth on the left and the lymph node embedded in the fat pad on the right. The entire gland was used for DNA extraction and sequencing of PTPRH. D) Diagram shows the main tyrosine residues capable of being phosphorylated on the c-terminal tail of EGFR. While the diagram is not comprehensive, as signaling pathways are convoluted and undergo numerous feedback mechanisms, some of the main downstream pathways that have been characterized are shown. E) Western blotting of PyMT tumor lysates shows no increased phosphorylation of STAT3 or ERK in Ptprh mutant tumors as compared to WT tumors. F) Western blotting shows increased phosphorylation of AKT within Ptprh mutant tumors as compared to WT tumors.