Ask about this productRelated genes to: PRKACA Blocking Peptide
- Gene:
- PRKACA NIH gene
- Name:
- protein kinase cAMP-activated catalytic subunit alpha
- Previous symbol:
- -
- Synonyms:
- PKACa
- Chromosome:
- 19p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-01-27
Related products to: PRKACA Blocking Peptide
Related articles to: PRKACA Blocking Peptide
- Fibrolamellar hepatocellular carcinoma (FLC) is a rare and distinct histologic subtype of hepatocellular carcinoma that typically arises in non-cirrhotic livers of adolescents and young adults without underlying viral hepatitis or chronic liver disease. Accounting for less than 1% of all primary liver cancers, FLC is characterized by unique clinical, radiologic, and molecular features, most notably the highly characteristic fusion. Due to its rarity and frequently nonspecific presentation, diagnosis is often delayed or misinterpreted as by benign hepatic lesions such as focal nodular hyperplasia or adenoma. This report presents a rare case of metastatic FLC in a young adult who initially presented with right upper quadrant pain, anemia, and preserved hepatic function. Imaging revealed a large hepatic mass with a central non-enhancing area suggestive of necrosis, and histopathologic evaluation aided in the diagnosis based on characteristic lamellar fibrosis, polygonal eosinophilic cells, and positive CK7 and HepPar-1 staining. Confirmatory molecular testing through fusion was not performed. Planned treatment with a combination regimen of nivolumab and neratinib was scheduled; however, the patient deteriorated rapidly, and systemic therapy could not be initiated before death. Through this case and accompanying review, we aim to highlight the diagnostic complexity, molecular underpinnings, and current therapeutic approaches of FLC. This case was notable for advanced peritoneal carcinomatosis at presentation, severe thrombocytosis, and the diagnostic and therapeutic challenges posed by metastatic fibrolamellar carcinoma without molecular confirmation. Taken together, this underscores the importance of early recognition, molecular testing, and coordinated clinical management in optimizing outcomes for this uncommon malignancy. - Source: PubMed
Publication date: 2026/05/06
El Darzi RoyAshy ChristopherKhrayzat AliChahine SallyTawil AymanTemraz Sally - Imidacloprid (IMI), a widely used neonicotinoid insecticide, has been associated with neurotoxic effects; however, the system-level mechanisms underlying these effects remain incompletely understood. Here, we integrated network toxicology with multi-omics analyses to investigate IMI-induced neurotoxicity in SH-SY5Y cells and the whole-organism model, Caenorhabditis elegans (C. elegans). Network toxicology identified 284 potential IMI-related targets, and protein-protein interaction network analysis further prioritized 45 core targets, including HSP90AA1, ESR1, MAPK3, SRC, MAPK1, IL6, BCL2, PRKACA, and MAPK8. Molecular docking suggested potential binding interactions between IMI and several core targets, while qRT-PCR provided transcript-level support for a subset of hub genes. Transcriptomic profiling revealed pronounced model-specific responses. In SH-SY5Y cells, IMI primarily induced neuron-related molecular alterations, characterized by disruption of voltage-gated calcium channel activity and enrichment of multiple synaptic pathways. In contrast, C. elegans exhibited broader organism-level transcriptomic remodeling involving developmental processes, extracellular structure organization, and stress-adaptive pathways, including the MAPK and FoxO signaling pathways. Untargeted metabolomics in SH-SY5Y cells further revealed biochemical remodeling related to the neuroactive ligand-receptor interaction pathway, glutathione metabolism, oxidative phosphorylation, and ABC transporter pathways. In addition, IMI significantly increased intracellular ROS levels and disrupted glutathione redox homeostasis, as reflected by altered GSH and GSSG levels and the GSH/GSSG ratio. Integrated analysis identified neuroactive ligand-receptor interaction and glutathione metabolism as shared pathway-level features across datasets, supporting a mechanistic model in which disruption of receptor-mediated neurotransmission is accompanied by redox imbalance. Overall, this study provides a systems-level view of IMI-induced neurotoxicity and highlights both shared pathway-level features and pronounced model-specific biological responses. - Source: PubMed
Publication date: 2026/05/05
Hou XingangWang KaiHou ZhiguangWei LipingZhang ZhengZheng XiaojiaoWang YuzhenLv MengTian JiangxinWang ZhaoyangMa ChaoZhao FanrongHan Jiajun - Carney complex (CNC) is an autosomal dominant multiple neoplasm syndrome, characterized by the presence of endocrine and non-endocrine tumors; it includes myxomas, lentigines and primary pigmented nodular adrenocortical disease, among other signs/symptoms. In CNC type 1, inactivating mutations of the PRKAR1A gene were identified as the main cause of the disease, although since 2015 variants in other genes, including PRKACA and PRKACB, have also been linked to this pathology. PKA is an enzyme involved in the G protein-coupled intracellular pathways and serves as a mediator of c-AMP actions that promote cell metabolism, proliferation and apoptosis. The penetrance of CNC due to pathogenic variants in the PRKAR1A gene is close to 100%. We present the case of a 33-year-old female patient with cutaneous and mucosal lentiginosis, blue nevus, malignant melanocytic psammomatous schwannoma, cutaneous myxoma and a novel variant in the PRKAR1A gene. - Source: PubMed
Publication date: 2026/04/15
Vázquez Ares María JoséRolón CamilaMercado Graciela - Zebrafish and neonatal mammals possess a remarkable capacity for cardiac regeneration following injury, a property that is largely absent in adult mammals. We have recently identified a cocktail of five small molecules (5SM) that promote adult cardiomyocyte (CM) proliferation and heart regeneration. However, the underlying mechanisms through which 5SM induces CM proliferation remain incompletely understood. In this study, we demonstrated an essential role for TGFβ/BMP signaling in mediating 5SM-induced heart regeneration. Harmine, one component of 5SM, plays a dominant role in upregulating TGFβ/BMP signaling by inhibiting DYRK1B. Inhibition of DYRK1B releases PRKACA, which then activates CREB phosphorylation, subsequently upregulating the expression of Tgfβ2, Tgfβ3, Bmp2, and Bmp7 in CMs. Treatment with exogenous TGFβ2, TGFβ3, BMP2, or BMP7 enabled cultured CMs to re-enter the cell cycle, while pharmacological inhibition of either the TGFβ or BMP pathways markedly diminished the effect of 5SM on CM proliferation in vitro and in vivo. CM-specific knockout of Smad4 impaired the regenerative effects of 5SM following myocardial infarction (MI) in adult mice. Based on the autocrine loop and pro-proliferative effects of TGFβ/BMP signaling, the ligands induced by 5SM ultimately bind to their receptors in CMs, leading to CM proliferation. In summary, our work establishes that TGFβ/BMP signaling mediates the effect of Harmine in promoting CM proliferation and gains novel insights into the DYRK1B-PKA-CREB axis in heart regeneration. - Source: PubMed
Publication date: 2026/04/20
Chen YuanyuanZheng LixiaXiong ConnieWang ZihaoZhu XiaojunChen Ye-GuangXiong Jing-Wei - Late-life depression (LLD) with high prevalence accelerates cognitive impairment and becomes a risk factor for dementia, yet the pathogenesis of LLD is still largely unclear. Delineating the neuromolecular mechanism of LLD is of great significance to its etiology, early diagnosis, and precision treatment. - Source: PubMed
Publication date: 2026/04/16
Chen MeilingZhang HongjiangYu XiaohuiZhang JieZhong JingmeiChen KexuanZi RongWu ZheWang ZhiyuanWu KunhuaWang JiaojianShao HengZhao YingZhu Baosheng