AMPK Activator, D942
- Known as:
- AMPK Activator, D942
- Catalog number:
- 2341-5
- Product Quantity:
- 5 mg
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- AMPK Activator D942
Related genes to: AMPK Activator, D942
- 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
- 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
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- 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 - 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 - Livsooth Authentic Herbal Formula (LAH) is a novel Chinese herbal medicine that has been previously shown to prevent non-alcoholic fatty liver disease (NAFLD). However, its efficacy in treating obesity and its underlying mechanisms remain unclear. This study uniquely investigates the therapeutic effects of LAH on high-fat diet (HFD)-induced obese mice, focusing on its multi-targeted regulation of metabolic pathways. This research highlights the potential of a multi-component herbal formula in simultaneously activating the AMPK pathway, regulating lipid metabolism, and enhancing antioxidant defenses. By integrating network pharmacology predictions with proteomics analysis, , and experiments, this study provides a comprehensive understanding of LAH's mode of action. - Source: PubMed
Publication date: 2025/03/05
Chen Yu-JuNing De-ShanWang Ching-ChiungZhao Hong-WeiWang Kun-TengLee Ming-ChungChiu Wan ChunYeh Chiu-LiJacinto Dela Vega John LouieLee Chia-Jung - Observational studies show metformin use associated with lower cancer risk, although experimental evidence is inconsistent. To provide genetic validation for repositioning of metformin in cancer prevention, we assessed genetically proxied effects of putative metformin targets on cancer outcomes using a drug-target Mendelian randomization (MR) design. - Source: PubMed
Publication date: 2026/02/27
Shen XingyuLuo ShanZheng JieChui Celine Sze LingWong Ian Chi KeiWan Eric Yuk FaiSchooling Catherine MaryAu Yeung Shiu Lun - Renal cell carcinoma (RCC) is characterized by dysregulated lipid metabolism and a high propensity for developing resistance to targeted therapies. Mitophagy is a key process involved in the progression of various cancers, including RCC. Here, using genome-wide CRISPR screening, we identified PRKAB2 as a crucial tumor suppressor in RCC. Reduced PRKAB2 expression correlated with poor prognosis and aggressive clinical features, whereas overexpression of PRKAB2 markedly inhibited RCC cell proliferation, migration, invasion, tumor growth, and metastasis both and . Mechanistically, PRKAB2 overexpression inhibited mitophagy primarily through two distinct mechanisms. First, PRKAB2 enhanced the binding between LRPPRC and PRKN/parkin, competitively reducing PRKN's interaction with PINK1 and thus suppressing ubiquitin-dependent mitophagy. Second, PRKAB2 promoted AMPK phosphorylation, which in turn suppressed SREBF1/SREBP1-mediated transcriptional activation of , leading to decreased CRLS1 expression and reduced synthesis of cardiolipin, a lipid essential for mitophagy. Importantly, PRKAB2 overexpression significantly restored sensitivity to tyrosine kinase inhibitors (TKIs) in sunitinib-resistant RCC cells. Conversely, forced PRKN expression promoted resistance to these drugs, further implicating mitophagy as a key mechanism underlying TKI resistance. Depmap analysis confirmed the association between increased mitophagy and TKI resistance. Overall, our findings identify PRKAB2 as a critical tumor suppressor in RCC, regulating both protein-protein interactions and lipid metabolism to suppress mitophagy. Targeting PRKAB2-associated pathways may provide a promising therapeutic strategy to enhance treatment efficacy and overcome drug resistance in RCC.: ACACA/ACC1: acetyl-CoA carboxylase alpha; AMPK: AMP-activated protein kinase; ATCC: American Type Culture Collection; ATP5F1A: ATP synthase F1 subunit alpha; BNIP3: BCL2 interacting protein 3; BNIP3L/NIX: BCL2 interacting protein 3 like; BRCA1: BRCA1 DNA repair associated; Cas: CRISPR-associated; CCCP: carbonyl cyanide m-chlorophenyl hydrazone; ccRCC: clear cell renal cell carcinoma; ChIP: chromatin immunoprecipitation; Co-IP: co-immunoprecipitation; COX4I1: cytochrome c oxidase subunit 4I1; CRISPR: clustered regularly interspaced short palindromic repeats; CRLS1: cardiolipin synthase 1; DNM1L/DRP1: dynamin 1 like; DOX: doxorubicin; FUNDC1: FUN14 domain containing 1; HSPA8: heat shock protein family A (Hsp70) member 8; HSPD1: heat shock protein family D (Hsp60) member 1; GO: gene ontology; IHC: immunohistochemistry; IMM: inner mitochondrial membrane; LDLR: low density lipoprotein receptor; m-SREBF1: mature sterol regulatory element binding transcriptional factor 1; LRPPRC: leucine rich pentatricopeptide repeat containing; MAP1LC3B: microtubule associated protein 1 light chain 3 beta; MFN1, mitofusin 1; MFN2: mitofusin 2; MTOR: mechanistic target of rapamycin kinase; OMM: outer mitochondrial membrane; OS: overall survival; PA: phosphatidic acid; PG: phosphatidylglycerol; PGS1: phosphatidylglycerophosphate synthase 1; PINK1: PTEN induced kinase1; PRKAA1/AMPKα1: protein kinase AMP-activated catalytic subunit alpha 1; PRKAA2/AMPKα2: protein kinase AMP-activated catalytic subunit alpha 2; PRKAB1/AMPKβ1: protein kinase AMP-activated catalytic subunit beta 1; PRKAB2/AMPKβ2: protein kinase AMP-activated non-catalytic subunit beta 2; PRKAG1/AMPKγ1: protein kinase AMP-activated non-catalytic subunit gamma 1; PRKN: parkin RBR E3 ubiquitin protein ligase; RCC: renal cell carcinoma; SASA: solvent-accessible surface areas; SUCLG1: succinate-CoA ligase GDP/ADP-forming subunit alpha; TCGA: The Cancer Genome Atlas; TKI: tyrosine kinase inhibitors; UCP1: uncoupling protein 1; ULK1: unc-51 like autophagy activating kinase 1; WCL: whole-cell lysate. - Source: PubMed
Publication date: 2026/02/18
Chen KaileiZhang YuanpengRuan HailongWei ZhihaoWang KeshanCao QiWang QiDong ZiruiWu YilongYang HongmeiLiu LeiLiu YuenanZhang Xiaoping