Ask about this productRelated genes to: OGDH antibody
- Gene:
- OGDH NIH gene
- Name:
- oxoglutarate dehydrogenase
- Previous symbol:
- -
- Synonyms:
- E1k
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2016-10-05
Related products to: OGDH antibody
Related articles to: OGDH antibody
- Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide. Current treatments offer limited efficacy and no definitive cure, underscoring the urgent need for more selective and effective therapeutic strategies. This study investigated the synthetic lethality caused by co-targeting two metabolic genes, ATP citrate lyase ( ) and oxoglutarate dehydrogenase ( ), in HCC cells. Using valproic acid (VPA) and bempedoic acid (BA) as pharmacological inhibitors of and , respectively, we observed a strong synergistic effect in inhibiting the proliferation of HCC cell lines (Hep3B and Huh7), compared to using these drugs individually. Importantly, this combination treatment exhibited little increased cytotoxicity in the non-cancerous liver cell line THLE-2, indicating a degree of selectivity. Our findings are consistent with previous reports implicating as a metabolic regulator of and in various cancers, suggesting that the inhibition of may prevent HCC cell proliferation primarily through its downstream effects on and . By directly co-targeting and , our approach may offer a more precise and safer alternative to inhibition. Additionally, while both VPA and BA have been individually associated with beneficial effects in liver disease, their combined application in the context of HCC has not been previously investigated. Limitations include the reliance on cell line models, highlighting the need for validation in more physiologically relevant systems such as human organoids and animal models. Overall, this study provides a compelling rationale for further investigation into and as a synthetic lethal pair and the therapeutic potential of the VPA-BA combination treatment in HCC. - Source: PubMed
Publication date: 2026/04/22
Manshadi Mehdi DehghanPanchal Nagesh KishanSun Lu-ZheSetoodeh PayamZare Habil - Fresh-cut lettuce suffers diminished market value due to surface color degradation. This experiment investigated how sodium dehydroacetate (SD) delays discoloration in fresh-cut lettuce by analyzing its effects on chlorophyll content and energy metabolism. - Source: PubMed
Publication date: 2026/05/01
Feng TianyuanCheng HongyingLi YuleDu HuayingZuo XiaoxiaShen YonggenWang JingZhang WeiCai ZhipengZhu Liqin - Robust microalgal activity is critical for the microalgal-bacterial symbiosis system (MBSS) to enable wastewater resource recovery, but microalgal performance can be affected by high concentrations of sludge. Ca may regulate microalgal performance. Nevertheless, the mechanism of Ca-mediated regulation, particularly under high concentrations of sludge, remains unclear. This study integrated physiological and genomic analyses to investigate microalgal responses to sludge (100-800 mg/L) and Ca supplementation (10-50 mM). Results showed that high-concentration sludge (400-800 mg/L) reduced microalgal growth, pigment synthesis, and photosynthetic efficiency by 65.6%-86.6%, 20.1%-39.2%, and 1.6%-7.0%, respectively, while Ca restored these parameters by up to 39.9%, 39.7%, and 8.5%. At the genetic level, Ca activated microalgal Ca signaling pathways (43.9%-226.4% increase in CaM, CDPK, and CBL). It upregulated antioxidant enzyme genes (76.1%-373.0% increase in SOD, CAT, and POD) to mitigate cell damage and photosynthetic genes (e.g. 95.0%-260.9% increase in psbA and rbcL) to restore chloroplast function. Concurrently, Ca promoted bacterial central carbon metabolism genes (e.g., 1.6%-26.2% increase in CS, IDH and OGDH) to increase CO release for microalgal carbon fixation and recruited siderophore-producing bacteria (e.g., 120.6%-154.3% increase in Sphingopyxis) to improve iron bioavailability for microalgal photosynthesis. Therefore, a positive feedback loop was formed through the supplementation of Ca. Microalgal photosynthesis supplied organic carbon/O for bacteria, while bacterial metabolism provided CO and iron for microalgae. Collectively, Ca optimized microalgal activity via cross-kingdom coordination of carbon-iron metabolism, offering a mechanistic basis for optimizing MBSS applications in wastewater treatment and biological resource recovery by using Ca as an effective regulator. - Source: PubMed
Publication date: 2026/04/25
Zhang YiYang XinyueLiu XudongFeng JiaXie ShulianLv Junping - The aim of this study is to explore how porcine epidemic diarrhea virus (PEDV) infection induces reprogramming of glucose metabolism in host cells and its impact on viral replication. We designed a control group and an infection group [infection of porcine intestinal epithelial cells (IPEC-J2) with PEDV]. First, we determined the infection time and dose of the virus by observing the PEDV titer and the expression of the N protein. Then, through proteomic comparative analysis, we studied the enriched differentially expressed proteins, key proteins, and key metabolic pathways in PEDV-infected cells. RT-qPCR and Western blotting were employed to verify the protein or gene expression of key enzymes in the glycolysis and tricarboxylic acid (TCA) cycle pathways in PEDV-infected cells. Finally, we clarified the impact of PEDV-induced glycolytic changes on viral replication by measuring the content of glucose, ATP, and lactic acid, as well as the expression of glucose transporters (SGLT-1 and GLUT-2) and PEDV N protein in cells. The results indicated that the optimal infection time of PEDV in IPEC-J2 was 48 h and the optimal multiplicity of infection was 1. Proteomics results showed that 342 differentially expressed proteins were screened out and mainly enriched in pathways such as glycolysis, digestion and absorption of carbohydrates, and lipid metabolism. PEDV infection upregulated the protein levels of key glycolysis enzymes HKII (<0.05), LDHA, and PKM (<0.01) in IPEC-J2 and the gene transcription level of (<0.01), while downregulating the gene transcription levels of key enzymes CS, OGDH, and IDH in the TCA cycle pathway (<0.01). In addition, PEDV infection increased intracellular lactate content (<0.01), decreased the ATP content (<0.01), upregulated the expression levels of SGLT-1 and GLUT-2 (<0.05, <0.01). Pre-treatment of IPEC-J2 with the glycolysis inhibitor 2-deoxy- d-glucose (2-DG) reduced the intracellular expression of PEDV N protein (<0.05). In conclusion, PEDV infection can induce reprogramming of glucose metabolism in host cells and enhance the replication of the virus. This is manifested as the activation of the glycolysis pathway and the obstruction of the TCA cycle and oxidative phosphorylation. PEDV promotes glucose uptake and up-regulate the expression of key enzymes in the glycolysis pathway to induce reprogramming of glucose metabolism, thus promote its efficient replication in host cells. This study confirms that PEDV infection can induce reprogramming of host cell glucose metabolism and promote viral replication by activating aerobic glycolysis, providing new insights and approaches for the targeted treatment and prevention of PEDV infection. - Source: PubMed
Chen XueqingWang GongminMa ChangWu GangXu JiajingChen XiwenZhang Yuanshu - - Source: PubMed
Publication date: 2026/04/10
Huang EnyuanZhou JingyuHu MengtingZhang LiuhongShao JiahaoLv MengMiao FenJiang YaoLi NianLi JiaqiYuan Xiaolong