AKAP1 expression levels in tumor and matched non-tumor tissues were evaluated using reverse transcription-quantitative polymerase chain reaction and immunohistochemical staining.
Several studies from primary cancers have reported individual AKAP genes to be associated with cancer risk and metastatic relapses as well as direct involvement in cellular invasion and migration processes.
Several studies from primary cancers have reported individual AKAP genes to be associated with cancer risk and metastatic relapses as well as direct involvement in cellular invasion and migration processes.
Furthermore, we used gene expression from the metastatic lesions and a primary breast cancer data set to study the gene expression of the AKAP gene family.
However, loss of <i>Akap1</i> exacerbated LVH and cardiomyocyte hypertrophy induced by pressure overload and accelerated the progression toward HF in TAC mice, and these changes were not observed upon prevention of AKAP121 degradation in seven <i>in absentia</i> homolog 2 (<i>Siah2</i>) knockout mice (<i>Siah2</i><sup>-/-</sup>).
However, loss of <i>Akap1</i> exacerbated LVH and cardiomyocyte hypertrophy induced by pressure overload and accelerated the progression toward HF in TAC mice, and these changes were not observed upon prevention of AKAP121 degradation in seven <i>in absentia</i> homolog 2 (<i>Siah2</i>) knockout mice (<i>Siah2</i><sup>-/-</sup>).
Selective targeting of AKAP protein-protein interactions may be a means to uncouple pathologically active signaling pathways in neurological disorders with a greater degree of specificity.
Our report is timely and highly impactful because it provides the first evidence that genetic disinhibition of Drp1 via knock-out of the mitochondrial protein kinase A (PKA) scaffold AKAP1 exacerbates stroke injury in mice.
However, loss of <i>Akap1</i> exacerbated LVH and cardiomyocyte hypertrophy induced by pressure overload and accelerated the progression toward HF in TAC mice, and these changes were not observed upon prevention of AKAP121 degradation in seven <i>in absentia</i> homolog 2 (<i>Siah2</i>) knockout mice (<i>Siah2</i><sup>-/-</sup>).
We found that AKAP1 protein expression was increased in HCC tissues, and high AKAP1 expression was associated with tumor size (P=0.024), Tumor-Node-Metastasis stage (P=0.0296) and portal vein thrombosis (P=0.00498).
Mechanistically, lipid-induced changes in mitochondrial redox status increased mitochondrial fission by increased ubiquitination of AKAP121 (A-kinase anchor protein 121) leading to reduced phosphorylation of DRP1 (dynamin-related protein 1) at Ser637 and altered proteolytic processing of OPA1 (optic atrophy 1).
Furthermore, we used gene expression from the metastatic lesions and a primary breast cancer data set to study the gene expression of the AKAP gene family.
Here we describe that male mice lacking the mitochondrial A-kinase anchoring protein 1 (AKAP1) exhibit increased sensitivity in the transient middle cerebral artery occlusion model of focal ischemia.
Our results indicate that inhibition of Drp1-dependent mitochondrial fission by the outer mitochondrial AKAP1/PKA complex protects neurons from ischemic stroke by maintaining respiratory chain activity, inhibiting superoxide production, and delaying Ca<sup>2+</sup> deregulation.
Several studies from primary cancers have reported individual AKAP genes to be associated with cancer risk and metastatic relapses as well as direct involvement in cellular invasion and migration processes.
These findings reveal an essential role for α1<sub>C</sub> phosphorylation at Ser<sup>1928</sup> in stimulating Ca<sub>V</sub>1.2 channel activity and vasoconstriction by AKAP-targeted PKA upon exposure to increased glucose and in diabetes.