
-   AKIP1 enhances NF-kappaB-dependent gene expression by promoting the nuclear retention and phosphorylation of p65. AKIP1 serves as a molecular bridge between p65 and PKAc, promoting their interaction and subsequent p65 phosphorylation at Ser-276, thus enhancing NF-kappaB signaling [PMID: 18178962, PMID: 20562110].
-   The impact of AKIP1 on TSCC cell malignant behavior might be related to its effect on activating the mTOR, PI3K-Akt, MAPK, Hippo, and Wnt signaling pathways [PMID: 34956456].
-   AKIP1 promotes angiogenesis and tumor growth by upregulating the levels of the NF-kappaB-dependent chemokines (e.g., CXCL1, CXCL2, and CXCL8) in cervical cancer, AML, and prostate cancer [PMID: 29520695, PMID: 31617252, PMID: 32339056].
-   AKIP1 interacted with and sustained beta-catenin in the nuclear by blocking its interaction with adenomatous polyposis coli protein (APC). AKIP1 enhanced the protein kinase A catalytic subunit (PKAc)-mediated phosphorylation of beta-catenin, leading to recruitment of cyclic AMP response element-binding protein (CBP) and activation of beta-catenin downstream transcription [PMID: 30936461].

## Summary

The AKIP1 gene plays a crucial role in the heart's response to stress and injury, as evidenced by its upregulation in conditions like heart failure, hypertrophy, and cardiac stress [CS: 8]. AKIP1 facilitates activation of cellular survival mechanisms and tissue repair by increasing NF-kappa-B transcriptional activity through promoting nuclear retention and phosphorylation of p65 [CS: 7]. The enhanced NF-kappa-B signaling aids in cellular survival and repair processes, countering the effects of the initial cardiac stress [CS: 7].

Furthermore, AKIP1's role in promoting cardiomyocyte growth via the Akt pathway is critical during cardiac stress [CS: 7]. In hypertrophic conditions, where the heart muscle enlarges to compensate for increased workload or damage, AKIP1's upregulation supports this adaptive growth [CS: 7]. By stimulating cardiomyocyte growth, AKIP1 assists in maintaining cardiac output and function, counteracting the detrimental effects of sustained stress, such as pressure overload or myocardial infarction [CS: 7].
