PDK2 antibody - middle region (ARP31778_P050)
- Known as:
- PDK2 (anti-) - middle region (ARP31778_P050)
- Catalog number:
- arp31778_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PDK2 antibody - middle region (ARP31778_P050)
Related genes to: PDK2 antibody - middle region (ARP31778_P050)
- Gene:
- PDK2 NIH gene
- Name:
- pyruvate dehydrogenase kinase 2
- Previous symbol:
- -
- Synonyms:
- PDHK2
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-14
- Date modifiied:
- 2016-01-06
Related products to: PDK2 antibody - middle region (ARP31778_P050)
Related articles to: PDK2 antibody - middle region (ARP31778_P050)
- Autosomal dominant polycystic kidney disease (ADPKD) is mainly caused by mutations in PKD1 or PKD2 genes, but a subgroup of patients has no detectable mutation and remains understudied. We profiled microRNAs (miRNAs) in this mutation-negative group and compared them with PKD1, PKD2, and healthy controls. - Source: PubMed
Publication date: 2026/04/02
De Felice BrunaNigro ErsiliaAmicone MariaPisani AntonioDaniele AuroraFarinella Federica - Fluorinated liquid crystal monomers (FLCMs), emerging contaminants from electronic waste, exhibit environmental persistence and bioaccumulative potential. Despite their growing detection in humans and aquatic systems, the subcellular mechanisms of their metabolic toxicity remain poorly understood. Here, zebrafish (Danio rerio) embryos and larvae were exposed to five representative FLCMs (0.05-50 µg/L) to investigate mitochondrial and metabolic disruption. Exposure to environmentally relevant concentrations significantly reduced basal respiration by 25.0-49.8 %, ATP-linked oxygen consumption by 25.0-65.5 %, NAD⁺/NADH ratio by 32.8-84.4 %, and membrane potential by 2.5-10.8 %, indicating oxidative phosphorylation dysfunction. Concurrent upregulation of cytoplasmic isocitrate dehydrogenase (ICDHc) and α-ketoglutarate dehydrogenase (α-KGDH) activities suggested compensatory activation of the tricarboxylic acid (TCA) cycle. Targeted gene expression analysis revealed downregulation of pdk2 (-24.6 %), accompanied by increased expression of gls (+40.6 %) and mt-nd1 (+72.1 %), consistent with an AMPK-associated metabolic shift. Co-exposure with the AMPK inhibitor Compound C reversed these alterations, restoring acetyl-CoA, NAD⁺, and TCA intermediates. Targeted metabolomics and KEGG enrichment further confirmed AMPK- associated rerouting of carbon flux toward amino acid-driven anaplerosis. Overall, these findings identify FLCMs as sublethal mitochondrial toxicants and highlight the AMPK-glutamate-TCA axis as a mechanistic hallmark of metabolic disruption, raising concern that such reprogramming may increase susceptibility to metabolic disorders. - Source: PubMed
Publication date: 2026/02/17
Wang JunjieMa SiyingLi SiyiHe ShanWei KunyuGuo XingyuHe JiaWu Fengchang - Beef cattle during the finishing phase are predominately fed with high-cereal diets to promote rapid growth, which commonly caused surplus energy supply and nitrogen deficiency, disrupted rumen energy and nitrogen balance (RENB), and reduced feed efficiency. This study aims to determine the effects of small peptide (SP) supplement on reciprocal patterns between rumen microbiota and epithelial genes in regulating nutrient metabolism and feed efficiency of beef cattle. - Source: PubMed
Publication date: 2026/01/08
Liu EnSun ShujunDeng YawenLiu JiajiaXue JintaoLi MengmengXue Fuguang - Perfluorooctanoic Acid (PFOA), widely recognized as an enduring environmental pollutant, is associated with immune system disruption and potential cancer-causing effects. Epidemiological findings show that serum power is significantly associated with inflammatory bowel disease (IBD). However, the specific mechanisms driving these effects remain poorly understood. - Source: PubMed
Publication date: 2025/12/15
Chen GangYuan HangLi XiaoPengChen ShihuiSun XuejunYu Junhui - Pyruvate dehydrogenase kinase 2 (PDK2) regulates glucose metabolism; however, its role in liver injury development is unknown. Therefore, this study aimed to explore the effects of PDK2 on liver injury using a concanavalin A (Con A)-induced acute liver injury mouse model. To understand the mechanisms by which PDK2 affects liver injury pathogenesis, network pharmacology analysis was performed to pinpoint the potential target genes and signaling pathways involved. Con A was used to induce acute liver injury in mice. Thereafter, PDK2 differential expression levels in the liver tissue of normal and liver injury mice were analyzed, and the effects of PDK2 inhibition on Con A-induced liver damage were assessed through biochemical analysis and observation of hepatic histopathological changes. Enzyme-linked immunosorbent assay, quantitative polymerase chain reaction, flow cytometry, and western blotting were used to explore the possible mechanisms by which PDK2 affects liver injury. PDK2 was involved in liver injury progression, and pharmacological inhibition of PDK2 notably increased mouse survival, decreased serum alanine transaminase and aspartate aminotransferase levels, attenuated hepatic histopathological damage and apoptosis, and inhibited pro-inflammatory cytokine secretion and the activation of the mitogen-activated protein kinase/nuclear factor kappa B (MAPK/NF-κB) signaling pathway. Pharmacological inhibition of PDK2 markedly alleviated hepatic oxidative stress and elevated myeloid-derived suppressor cells (MDSCs) in the livers of acute liver injury mice. Overall, inhibiting PDK2 ameliorates Con A-induced acute liver injury by enhancing MDSCs accumulation and suppressing oxidative stress, the MAPK/NF-κB signaling pathway, and inflammation. These findings identify PDK2 as a promising therapeutic target for immune-mediated hepatitis. - Source: PubMed
Publication date: 2025/10/15
Li ChunxiaLi ChenyuZhai WeiweiYu RuihanXu XinyiYan FenglianZhang HuiZhang JunfengZhao MingshengWang LinZhu YuanboLiu ZhihongYang ZhuoqunLi WenboXiong Huabao