Akap7
- Known as:
- Akap7
- Catalog number:
- 064296A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Akap7
Related genes to: Akap7
- Gene:
- AKAP7 NIH gene
- Name:
- A-kinase anchoring protein 7
- Previous symbol:
- -
- Synonyms:
- AKAP18, AKAP15
- Chromosome:
- 6q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-16
- Date modifiied:
- 2018-05-03
Related products to: Akap7
Related articles to: Akap7
- Bladder urothelial carcinoma (BLCA) is a common urinary malignancy, and the identification of appropriate biomarkers remains a significant challenge. AKAP7 is a molecular scaffolding protein that plays a crucial role in spatially regulating cyclic adenosine monophosphate (cAMP) signaling through its ability to anchor protein kinase A (PKA) to the cytoskeleton. This study aims to explore the expression level, prognostic implications and immune characteristics of AKAP7 in BLCA. - Source: PubMed
Publication date: 2026/03/10
Liu HongquanMao QianchengWang XiaofengTang GonglinDing GuixinWang TianqiLiu ChuMa XiaohongCui YuanshanWu Jitao - Clozapine is an effective antipsychotic medication for the management of treatment-resistant schizophrenia. However, the use of clozapine is limited due to severe and sometimes fatal adverse events, including cardiac inflammation (myocarditis). To date, studies of clozapine dosing and genetic studies have not identified robust risk markers. Our study aimed to identify potential epigenetic markers for clozapine-induced myocarditis using genome-wide profiling of DNA methylation and RNA sequencing in a novel in vitro model using patient-derived cells. Induced pluripotent stem cells (iPSCs) from treatment-resistant schizophrenia patients with (case) and without (control) a history of clozapine-induced myocarditis were differentiated into beating cardiomyocytes (iPSC-CMs). These cells were exposed to clozapine at a physiologically relevant concentration (2.8 µmol/L) for 24 h. Before and after clozapine treatment, RNA from the iPSC-CMs was sequenced (RNA-seq), and DNA was assessed for methylation using the EPIC array. Our analysis revealed that hypermethylation at the promoter regions of and is associated with reduced gene expression in cases relative to controls, regardless of clozapine exposure. Additionally, hypermethylation in the gene bodies of and was associated with increased expression in cases relative to controls. Conversely, hypomethylation in the gene bodies of and correlated with lowered gene expression in cases relative to controls. These findings highlight a potential involvement of DNA methylation in gene expression regulation and its putative impact on clozapine-induced myocarditis. Additional studies are warranted to validate our findings and further elucidate a potential mechanism. - Source: PubMed
Publication date: 2025/10/24
Marques Diogo FSpindola Leticia MNarang AnkitaVaziri NazaninStavrum Anne-KristinJayaram MaheshThomas NaveenPantelis ChristosLe Hellard StephanieHemberger MyriamDean WendyGreenway Steven CBousman Chad - Subcellular targeting of signaling enzymes influences where and when various modes of intracellular communication operate. Macromolecular complexes of signal transduction and signal termination elements favor reversible control of repetitive processes. This includes adrenergic stimulation of excitation-contraction coupling in the heart. Long isoforms of A-kinase anchoring protein 18 (AKAP18γ and δ) modulate this process via regulation of calcium uptake into the sarcoplasmic reticulum through the CaATPase 2a (SERCA2a). AKAP18 proximity-proteomic screening in cardiomyocytes identifies networks for protein kinase A (PKA) and ubiquitin-specific proteinases (USPs). A 2'phosphoesterase domain on AKAP18 interfaces with the USP4 isoform at the Z bands of sarcomeres. PKA stimulates USP4 activity in the presence of the anchoring protein. AKAP18 anchored PKA phosphorylates serine 829 on USP4, a conserved residue near the active site of this deubiquitinase. Antibodies against the pSer motif show that adrenergic stimulation enhances phosphorylation of USP4 in mouse adult cardiomyocytes. In related studies, elevated USP4 phosphorylation at Ser is detected in human post myocardial infraction tissue as compared to healthy tissue. Thus, phosphorylation of sarcoplasmic USP4 may be a cardioprotective response. Pharmacological inhibition of PKA or deletion of the AKAP7/18 gene in mice decreases calcium flux through the exchanger. This suggests that loss of the anchoring protein impacts SERCA2 action. Thus, AKAP18/PKA/USP4 complexes are well positioned to influence the rate and magnitude of calcium reuptake during the cardiac cycle. - Source: PubMed
Publication date: 2025/05/29
Park TaeyeopForbush KatherineLi YongVivas OscarRosenthal Kacey JFalcone JeromeWong Cassandra JBruce James EMoreno ClaudiaDessauer Carmen WScott John D - To investigate the preclinical efficacy and identify predictive biomarkers of polo-like kinase 1 (PLK1) inhibitors in small cell lung cancer (SCLC) models. We tested the cytotoxicity of selective PLK1 inhibitors (rigosertib, volasertib, and onvansertib) in a panel of SCLC cell lines. We confirmed the therapeutic efficacy of subcutaneous xenografts of representative cell lines and in four patient-derived xenograft models generated from patients with platinum-sensitive and platinum-resistant SCLC. We employed an integrated analysis of genomic and transcriptomic sequencing data to identify potential biomarkers of the activity and mechanisms of resistance in laboratory-derived resistance models. Volasertib, rigosertib, and onvansertib showed strong in vitro cytotoxicity at nanomolar concentrations in human SCLC cell lines. Rigosertib, volasertib, and onvansertib showed equivalent efficacy to that of standard care agents (irinotecan and cisplatin) in vivo with significant growth inhibition superior to cisplatin in PDX models of platinum-sensitive and platinum-resistant SCLC. There was an association between expression and disruptive or inactivation gene mutations, with greater efficacy of PLK1 inhibitors. Comparison of lab-derived onvansertib-resistant H526 cells to parental cells revealed differential gene expression with upregulation of , , , and and downregulation of , , , and highlighting the potential mechanisms of resistance in the clinical setting. We established the efficacy of PLK1 inhibitors in vitro and in vivo using PDX models of platinum-sensitive and resistant relapsed SCLC. An ongoing phase II trial is currently testing the efficacy of onvansertib in patients with SCLC (NCT05450965). - Source: PubMed
Publication date: 2025/01/28
Zhang GuojingPannucci AbbeIvanov Andrey ASwitchenko JeffreySun Shi-YongSica Gabriel LLiu ZhentaoHuang YufeiSchmitz John COwonikoko Taofeek K - Coronaviruses exhibit many mechanisms of genetic innovation, including the acquisition of accessory genes that originate by capture of cellular genes or through duplication of existing viral genes. Accessory genes influence viral host range and cellular tropism, but little is known about how selection acts on these variable regions of virus genomes. We used experimental evolution of mouse hepatitis virus (MHV) encoding a cellular AKAP7 phosphodiesterase and an inactive native phosphodiesterase, NS2, to model the evolutionary fate of accessory genes. After courses of serial infection, the gene encoding inactive NS2, ORF2, unexpectedly remained intact, suggesting it is under cryptic constraint uncoupled from the function of NS2. By contrast, AKAP7 was retained under strong selection but rapidly lost under relaxed selection. Experimental evolution also led to altered viral replication in a cell-type-specific manner and changed the relative proportions of subgenomic viral RNA in plaque-purified viral isolates, revealing additional mechanisms of adaptation. Guided by the retention of MHV ORF2 and similar patterns in related betacoronaviruses, we analyzed ORF8 of SARS-CoV-2, which is proposed to have arisen via gene duplication and contains premature stop codons in several globally successful lineages. As with MHV ORF2, the coding-defective SARS-CoV-2 ORF8 gene remained largely intact in these lineages, mirroring patterns observed during MHV experimental evolution, challenging assumptions on the dynamics of gene loss in virus genomes, and extending these findings to viruses currently adapting to humans. - Source: PubMed
Publication date: 2024/11/19
Goldstein Stephen AFeeley Teagan MBabler Kristina MHilbert Zoë ADownhour Diane MMoshiri NiemaElde Nels C