Ask about this productRelated genes to: PRKACB antibody
- Gene:
- PRKACB NIH gene
- Name:
- protein kinase cAMP-activated catalytic subunit beta
- Previous symbol:
- -
- Synonyms:
- PKACb
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: PRKACB antibody
Related articles to: PRKACB antibody
- Pulmonary hypertension (PH) involves endothelial-to-mesenchymal transition (EndMT) in vascular remodeling. Rosiglitazone (RSG), a peroxisome proliferator-activated receptor gamma agonist, alleviates PH, but its direct effect on EndMT is unclear. The study explores RSG's role and mechanism in inhibiting EndMT. - Source: PubMed
Publication date: 2026/08/22
Yuan AoxueBai YaqianJiang YuanhangSi ShengnanWang PengweiZhao FanrongChen YujingZhu Tiantian - Prenatal exposure to ambient air pollution has been associated with early-life allergic outcomes; however, underlying biological mechanisms remain incompletely understood. - Source: PubMed
Chen XiaoqinLi JunyangYang SijieHe WenjunWu JingLiu XiaohuaLi JingLi Youjin - Aflatoxin B1 (AFB1) is a widespread foodborne mycotoxin with well-established hepatotoxic and carcinogenic effects; however, its potential role in neuropsychiatric disorders remains unclear. Emerging evidence suggests that AFB1 can cross the blood-brain barrier, inducing oxidative stress and neuronal dysfunction. Whether these alterations contribute to anxiety-related molecular changes in the human brain remains poorly understood. An integrative approach combining network toxicology, brain-region-specific two-sample Mendelian randomization (MR), molecular docking, and experimental validation was employed. AFB1-associated targets were identified via STITCH, ChEMBL, and SwissTargetPrediction, and intersected with anxiety-related genes from GeneCards and GSEA. Protein-protein interaction (PPI) analysis, topological screening, and functional enrichment were used to identify hub genes and key pathways. MR analysis utilized cortex and cerebellum expression quantitative trait loci (eQTL) data from GTEx v8. Molecular docking evaluated binding interactions between AFB1 and key proteins. SH-SY5Y cells were used to validate alterations in oxidative stress and signaling. A total of 196 shared targets were identified, and 24 hub genes were screened based on the intersection of the top 40 genes ranked by degree, betweenness, and closeness centrality analyses. Enrichment analysis highlighted oxidative stress, apoptosis, MAPK, PI3K-Akt signaling, and monoaminergic synaptic pathways. MR analysis revealed region-specific associations: cortical EGFR expression positively correlated with anxiety risk, while cerebellar PPARG expression exhibited a protective effect. Additional genes (AKT1, KRAS, ABL1, PRKACB) showed positive cerebellar associations. Docking analysis indicated stable binding between AFB1 and key proteins. Experimental validation confirmed increased EGFR and AKT1 expression, reduced PPARG expression, and elevated ROS levels in SH-SY5Y cells. AFB1 promotes anxiety-related neurotoxicity in a brain-region-specific manner, supported by Mendelian randomization evidence, by inducing oxidative stress, disrupting EGFR/AKT signaling, and suppressing PPARG-mediated neuroprotection. These findings elucidate a mechanistic link between AFB1 exposure and neuropsychiatric risk, and highlight the need for stricter food safety regulation and incorporation of mycotoxin exposure into anxiety risk assessment and prevention strategies. - Source: PubMed
Publication date: 2026/07/24
Chen TingtingDu JiangBu LipingJiao Long - To evaluate the association between ICU-acquired infections and 28-day mortality in pneumonia-induced sepsis and to explore associated immune-related gene expression patterns. - Source: PubMed
Publication date: 2026/06/05
Almuntashiri SultanAlsowaida Yazed SZhang DuoAlghubayshi AliAlanazi MutebAlharby Tareq NafeaAnsari Mukhtar - Primary pigmented nodular adrenocortical disease (PPNAD) represents a rare etiology of adrenal-derived, adrenocorticotropic hormone (ACTH)-independent hypercortisolism. Its pathogenesis is primarily attributed to inactivating mutations in the , , or genes, as well as amplifications of and triploid mutations of . This report presents the case of a patient with PPNAD, who exhibited symptoms including hypertension, femoral head necrosis, anxiety and depression, nephrolithiasis, and short stature. Genetic analysis revealed a heterozygous mutation in the gene (NM_016953.4: c.2032G>A; Ala678Thr). Additionally, a review of recent literature was conducted to enhance clinicians' understanding of this condition. - Source: PubMed
Publication date: 2026/04/30
Zhen YunfengXiang HanluQi CuijuanSong Guangyao