Ask about this productRelated genes to: PRKAA1 antibody
- Gene:
- PRKAA1 NIH gene
- Name:
- protein kinase AMP-activated catalytic subunit alpha 1
- Previous symbol:
- -
- Synonyms:
- AMPKa1
- Chromosome:
- 5p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-09
- Date modifiied:
- 2016-01-27
Related products to: PRKAA1 antibody
Related articles to: PRKAA1 antibody
- AMP-activated protein kinase (AMPK) serves as a crucial energy sensor, maintaining organismal energy homeostasis through the regulation of diverse metabolic pathways. However, the association between the AMPK signaling pathway and hypoxia adaptation in yak lung tissue has not yet been elucidated. Consequently, this study focused on the lung tissues of yaks and cattle residing at the same altitude (2600 m). Morphological analysis demonstrated that, compared to cattle, yak lung tissue possessed significantly thicker alveolar septa (P < 0.05), a greater abundance of elastic fibers (P < 0.05), and a reduced blood-air barrier thickness (P < 0.05), suggesting substantial structural adaptations in the yak lung under identical altitudinal conditions. RNA-seq analysis identified 3684 genes with significant differential expression between yaks and cattle. KEGG pathway enrichment analysis showed significant enrichment for the AMPK signaling pathway under the "Environmental Information Processing" category, and Gene Set Enrichment Analysis (GSEA) further confirmed the activation of the AMPK signaling pathway in yak lung tissue. Despite qRT-PCR indicating reduced mRNA levels of key AMPK pathway genes (PRKAA1, PRKAA2, PRKAB1, PRKAG2) in yak lung tissue, Western blot analysis demonstrated a marked upregulation in the relative abundance of phosphorylated AMPK (P-AMPK α1 + α2), implying potential activation of the AMPK signaling pathway via phosphorylation in yak lung tissue. Further analysis of downstream gene expression within the AMPK signaling pathway indicated significant downregulation of genes associated with glucose metabolism (PCK2, G6PC1), lipid metabolism (FASN, ACACA), protein metabolism (MAPKAPK5, MTOR), cell proliferation and apoptosis (RPTOR, MTOR), and autophagy (TXNIP, NLRP3) in yak lung tissue. These findings suggest that, relative to cattle, the yak lung may adapt to hypoxic conditions by minimizing energy expenditure, suppressing aberrant cell proliferation, mitigating oxidative stress, and reducing inflammatory responses. In summary, the activation of the AMPK signaling pathway in yak lung tissue may play a crucial role in hypoxic adaptation by enhancing oxygen utilization and energy supply capacity. - Source: PubMed
Publication date: 2026/04/04
Zhang XunDing WeiqinWang HuizhenLi JingyiChen JiaruiWei Qing - The present study explored the effects of dietary supplementation with hot water extract of Juncao-substrate Ganoderma lucidum residue (HWE-JGLR) on growth performance, carcass traits, meat quality, and antioxidant capacity of Liancheng white ducks. A total of 288 one-day-old male Liancheng white ducks were randomly allocated into 4 groups with 6 replicates of 12 ducks each. The control group was fed a corn-soybean meal basal diet, while the test groups were fed a basal diet supplemented with either 0.25%, 0.5%, or 1% HWE-JGLR, designated as HJ-I, HJ-Ⅱ, and HJ-Ⅲ groups, respectively, for 63 days. No significant differences were observed in growth performance or carcass traits among the groups. Regarding meat quality, the primary beneficial effect was the mitigation of pH decline in breast muscles (P < 0.05); no significant effects were observed in shear force, drip loss, or meat color of both breast and leg muscles. In breast muscle, the expression levels of genes CPT-1 and PRKAA1 were elevated by HWE-JGLR supplementation (P < 0.05). In contrast, a marked suppression was observed in the expression of SREBP-1C (P < 0.05). Additionally, compared with the control group, the serum T-SOD and GSH-Px activities in ducks fed HJ-Ⅱ and HJ-Ⅲ diets were found to be increased (P < 0.05). Besides, ducks fed HJ-I and HJ-Ⅲ diets reduced serum MDA concentration (P < 0.05). In liver and breast muscle, HJ-Ⅱ and HJ-Ⅲ groups increased the expression of CAT, SOD, TXN, GCLC, NRF2 and NQO1 (P < 0.05). Meanwhile, the activity of liver GSH-Px and breast muscle CAT was also enhanced (P < 0.05). In summary, diet supplemented with HWE-JGLR has been shown to improve the meat quality of breast muscle and suppress the expression levels of fat-related genes. Meanwhile, HWE-JGLR promoted the antioxidant capacity of Liancheng through a coordinated increase in antioxidant enzyme activities and upregulation of associated gene expression. Based on the results of various measurement indicators, it is appropriate to add 0.5% HWE-JGLR in feed. - Source: PubMed
Publication date: 2026/03/18
Cai Zai-XingLv Hai-XuanYang YunGu Xiao-MingLiu Xiao-PingJin LingGao Yu-Yun - TNIK (Traf2- and Nck-interacting kinase) is a serine/threonine kinase that plays a crucial role in cytoskeletal organization, Wnt pathway activation, and cancer progression. Recent studies have implicated the role of TNIK in oncogenic signaling pathways and neuropsychiatric regulation. However, the phosphosignaling dynamics of TNIK remain largely unknown. - Source: PubMed
Publication date: 2026/03/13
Sheela AkhilaSubair SuhailUmmar SamseeraMahin AlthafGopalakrishnan Athira PerunellyRaju RajeshSoman Sowmya - Ventromedial hypothalamic nucleus/dorsomedial division (VMNdm) metabolic-sensory growth hormone-releasing hormone (Ghrh) neurons operate within the brain circuitry that maintains systemic glucostasis. Sex-specific counterregulatory hormone adaptation to recurrent insulin-induced hypoglycemia (RIIH) entails undiscovered CNS mechanisms. Combinative single-cell immunocytochemistry/laser-microdissection/multiplex qPCR methods were employed here to determine if RIIH alters VMNdm Ghrh neuron neurotransmission according to sex. Precedent insulin administration resulted in attenuated hypoglycemic up-regulation of male rat Ghrh neuron glucose sensor gene expression. Females exposed to RIIH acquired negative glucose transporter-2 and positive glucokinase transcriptional reactivity to dysglycemia. VMNdm Ghrh neurons express mRNAs for 5'-AMP-activated protein kinase catalytic subunit variants. Hypoglycemia-associated amplification of those transcripts in the male was exacerbated (PRKAA1) or reversed (PRKAA2) by RIIH; meanwhile females showed transcript up-regulation during recurring but not singular hypoglycemia. RIIH caused opposite, sex-specific adaptation of VMNdm Ghrh neuron Ghrh and Ghrh receptor gene transcription. Ghrh neuron transcripts for counterregulation-enhancing glutamate and nitric oxide marker proteins showed diminution or amplification of transcriptional responses, respectively, in males, but did not habituate to RIIH in females. Hypoglycemic inhibition of glutamate decarboxylase (GAD)-1 and - 2 mRNAs, markers for counterregulatory inhibitor γ-aminobutyric acid size variants, in male Ghrh neurons was correspondingly unaffected or attenuated by RIIH. Meanwhile, negative GAD2 transcriptional reactivity in the female was exacerbated following precedent hypoglycemia. Ongoing research aims to establish, for each sex, whether and how VMNdm Ghrh neuron metabolic sensor functional acclimation to RIIH may affect counterregulatory neurotransmitter release and to determine how adjustments in integrated neurochemical discharge may affect brain glucostatic network function. - Source: PubMed
Publication date: 2026/03/22
Yadav RajeshSapkota SubashBriski Karen P - Oxidative stress (OS) plays a critical role in the pathogenesis of Alzheimer's disease (AD), yet its genetic and epigenetic regulatory mechanisms remain unclear. In this study, we applied a three-step summary-based Mendelian randomization (SMR) framework to integrate Alzheimer's disease (AD) GWAS summary statistics with peripheral-blood eQTL and mQTL datasets, and further evaluated brain-tissue relevance using GTEx v8 and AMP-AD resources. Across the three-step SMR analyses, we prioritized multiple OS-related candidate genes (e.g., CRLS1, PRKAA1, CYP2E1, GPX1, and APP) associated with AD risk, and brain-tissue analyses further highlighted KEAP1, SIRT1, and PRDX5 as region-relevant signals. Functional enrichment analyses highlighted critical pathways such as "Nrf2-mediated antioxidant response" and "PI3K-AKT signaling," emphasizing the roles of oxidative stress, mitochondrial function, and neuroinflammation in AD. Novel regulatory mechanisms were uncovered at methylation sites (e.g., cg20211653 associated with ABCA1), linking epigenetic regulation to transcriptional mechanisms and providing candidates for brain-tissue follow-up. This study provides new insights into the molecular underpinnings of AD, bridging genetic variation, epigenetic regulation, and transcription, and identifies potential therapeutic targets for mitigating oxidative damage and neurodegeneration. - Source: PubMed
Publication date: 2026/03/16
Wu LiuDong Yu-TingMu XinLuo XiaoChen Ze-Jun