From: The roles of nuclear focal adhesion kinase (FAK) on Cancer: a focused review
Protein | Outcome | Significant Findings |
---|---|---|
NCAM | FAK phosphorylation | NCAM induces the nuclear import of the C-terminal fragment and N-terminal fragment of FAK [59] |
PIAS1 | Post-translational modifications | PIAS1 binds to the FERM domain of FAK, affecting its post-translational modifications [51, 66] |
MBD2 | Dissociation from HDAC1 | Activate the expression of myogenic proteins and other genes that promote muscle differentiation [60] |
P53 | Degradation | FAK inhibits p53 to activate its downstream gene transcription [67, 68] |
Mdm2 | P53 ubiquitination | |
NF2 | Activation | NF2 regulates the interaction of FAK–p53 and Mdm2–p53 [69] |
PTEN | Upregulation | P53 and PTEN tumor suppressors are co-inactivated in patients and cause cancer metastasis [70] |
GATA4 | Degradation | FAK inhabits GATA4 expression and reduces the inflammatory responses [58, 65, 71] |
CHIP | GATA4 ubiquitination | The nuclear FAK interacts with GATA4 and the ubiquitin protein E3 ligase CHIP [58, 65, 72] |
IL-33 | Upregulation | |
VEGFR2 | Upregulation | VEGFR2 promotes the formation of tumor neovascularization and tumor growth [75] |
Sin3A | Activation | FAK participates in the regulation of Runx1 via Sin3A [76] |
Runx1 | Runx1 complex | The formation of the transcription factor Runx1 complex [77] |
MEF2 | Forms complex | FAK and MEF2 jointly regulate expression of Jun which is induced by load [78] |
FIP200 | FAK phosphorylation inhibition | FIP/FAK complex is associated with FAK inactivation after cell detachment [78] |
EZH2 | EZH2 phosphorylation | FAK affects the transcription and nuclear localization of EZH2 [79] |
E3 ligase | Ubiquitination | Inactive FAK coordinates with different E3 ligases, promoting transcription factor turnover [65, 71] |
Sam68 | Activation | Sam68 binds to RNA and signaling molecules to regulate multiple signaling pathways [80] |
NS | Activation | Active FAK protects the NS from proteasomal degradation [81] |