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Table 1 Proteins interacting with nuclear FAK

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

P53 proteosomal degradation in the nucleus [31, 69]

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

IL-33 regulates CCL5 expression [73, 74]

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]