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A database built with INDRA combining content from numerous readers and databases. This page allows you to curate the loaded statements. For more information please see the manual.

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INDRA is developed by indralabs, a part of the Harvard Medical School Laboratory of Systems Pharmacology.

This project, indra_db, is also developed by the indralab team. For more information on how we procure our sources, you can go here. This work was funded by ARO grant W911NF‐15‐1‐0544 under the DARPA Communicating with Computers program.

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Mutated TP53 leads to the phosphorylation of STAT3. 3 / 3

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"Similar to previous studies, we observed that wild-type p53 inhibited phosphorylation of STAT-3 in response to OSM, and mutant p53 promoted the phosphorylation of STAT-3."

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"Upon expression of various p53 hotspot missense mutants in TP53 -/- H1299 and HCT116 cells, some p53 mutants augmented Stat3 phosphorylation."

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"Further, mutant p53 has been reported to activate STAT-3 phosphorylation in human colorectal cancer cells, resulting in EMT and cell migration [XREF_BIBR]."

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Mutated TP53 leads to the phosphorylation of STAT3. 3 / 3

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