Ask about this productRelated genes to: PRKAA2 Blocking Peptide
- Gene:
- PRKAA2 NIH gene
- Name:
- protein kinase AMP-activated catalytic subunit alpha 2
- Previous symbol:
- PRKAA
- Synonyms:
- AMPK, AMPKa2
- Chromosome:
- 1p32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-12-12
- Date modifiied:
- 2016-10-05
Related products to: PRKAA2 Blocking Peptide
Related articles to: PRKAA2 Blocking Peptide
- Vascular cognitive impairment (VCID) affects 55 million people globally but lacks effective treatments. Single-modality rehabilitation provides modest benefits; whether combining approaches yields a greater effect, and the mechanisms involved, remain undefined. - Source: PubMed
Publication date: 2026/06/17
Wu YongfeiZeng Zhuo - Diabetic peripheral neuropathy (DPN) is a common diabetic complication with unclear pathogenesis. Current therapies are limited, and resveratrol shows potential in DPN but its therapeutic mechanisms remain unclear. - Source: PubMed
Publication date: 2026/06/11
Zhang ChengMo GuokangZhang YongxingXu HaoHu XiangjunZhang Jian - Prenatal valproic acid (VPA) exposure is strongly linked to developmental cardiotoxicity, yet no targeted pharmacological countermeasure exists. Converging mechanistic evidence indicates that VPA cardiotoxicity centers on AMPK/PGC-1α suppression, positioning the AMPK activator metformin (MET) as a rational candidate for protection. We examined MET's protective effects against VPA-induced developmental cardiotoxicity in zebrafish embryos. Embryos were randomly allocated to four groups (Control, VPA 0.1 mM, MET 10 mM, VPA + MET) immediately after fertilization and chronically exposed until 96 hpf. Oxidative stress biomarkers (MDA, NO, SOD, GSH) and the expression of cardiac (), AMPK (), and mitochondrial/energy-related genes () were quantified. Compared with controls, VPA reduced (p < 0.01) and elevated (p < 0.05), triggered pericardial edema (p < 0.0001), suppressed , and (p < 0.05, p < 0.001, and p < 0.0001, respectively), upregulated (p < 0.0001), increased MDA and NO (p < 0.0001), and lowered SOD and GSH (p < 0.0001 and p < 0.001, respectively). Relative to the VPA group, MET co-treatment restored expression (p < 0.001), attenuated pericardial edema (p < 0.0001), increased (p < 0.05), (p < 0.01), and (p < 0.0001), suppressed (p < 0.0001), and normalized MDA (p < 0.05), NO (p < 0.0001), SOD, and GSH (both p < 0.0001). The restoration of , mitochondrial, and antioxidant capacity by MET suggests that the AMPK/PGC-1α axis may serve as a central target in VPA cardiotoxicity. - Source: PubMed
Publication date: 2026/06/08
Üstündağ Ünsal VeliÜstündağ Fümet DuyguAyşit Neşe - Atherosclerosis (AS) is a chronic inflammatory vascular disorder in which endoplasmic reticulum stress (ERS) plays a crucial regulatory role. However, the biological and translational relevance of ERS-related gene networks in AS remains largely unexplored. This study aimed to identify a robust ERS-related gene signature for AS. We integrated multiple GEO datasets and applied machine learning algorithms, including least absolute shrinkage and selection operator (LASSO) regression, support vector machine-recursive feature elimination (SVM-RFE), and random forest (RF). Five ERS-related signature genes (TRIM25, CYBB, CYBA, MYOC, and PRKAA2) were identified and showed favorable discriminatory performance in the integrated discovery cohort (combined AUC = 0.946). The expression patterns of these genes were further examined at both the mRNA and protein levels by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting (WB) in an oxidized low-density lipoprotein (ox-LDL)-induced endothelial injury model. Gene set enrichment analysis and immune infiltration analysis indicated that the identified genes were primarily involved in oxidative stress and immune-related pathways. Collectively, this study identifies a machine learning-derived ERS gene signature associated with AS. These findings improve our understanding of ERS-related vascular injury in AS and provide candidate biomarkers for further tissue-level and mechanistic validation. - Source: PubMed
Publication date: 2026/06/01
Qu XiaomengShao YimingLi HanBao YuhanSun ZhenYu Shuhua - Previous studies demonstrate that the protein kinase AMP-activated catalytic subunit alpha 2 (AMPKα2), one of two isoforms of catalytic subunit of AMPK encoded by PRKAA2, is highly expressed and contributes to cell survival and chemo-resistance in TNBC. However, the mechanisms underlying AMPKα2 upregulation is poorly understood. Here, we found that AMPKα2 expression was decreased in primary TNBC but paradoxically increased in doxorubicin (DOX) resistant TNBC cancer stem cells (TBCSCs). DOX treatment led to an enrichment of TBCSCs and a concomitant increase in AMPKα2 expression. Mechanistically, enhanced AMPKα2 expression in TBCSCs was driven by H3K27 acetylation at PRKAA2 promoter. This epigenetic modification was facilitated by the histone acetyltransferases CBP/p300. Moreover, CITED2 was essential for CBP/p300-mediated H3K27 acetylation. Loss of CITED2 disrupted CBP/p300 localization and reduced H3K27 acetylation at PRKAA2 promoter. CITED2 directly bound to p300 via its C-terminal LPEL domain, promoting the formation and localization of the CBP/p300/CITED2 complex at PRKAA2 promoter. Disruption of CITED2/p300/CBP complex using an exogenous LPEL peptide inhibited H3K27 acetylation at the PRKAA2 promoter, decreasing AMPKα2 expression. Up-regulation of AMPKα2 promoted stemness properties and conferred DOX resistance in both cell line-derived and patient-derived TBCSCs. Further, we found LPEL peptide significantly suppressing TBCSCs stemness properties. Importantly, this approach sensitized DOX-resistant TBCSCs to DOX treatment. Our findings revealed a critical role of CITED2-dependent p300/CBP mediated H3K27 acetylation in promoting AMPKα2 expression within TBCSCs and contributing to DOX resistance. Targeting the CITED2/p300/CBP complex with an exogenous LPEL peptide represents a promising strategy to overcome DOX resistance in TNBC. - Source: PubMed
Publication date: 2026/05/15
Liu XinjunSi ZizhenLi LinboZhou MiaoPeng ShangmingLee Ki-YoungWang Xidi