Ask about this productRelated genes to: IDH3A Blocking Peptide
- Gene:
- IDH3A NIH gene
- Name:
- isocitrate dehydrogenase (NAD(+)) 3 alpha
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-02
- Date modifiied:
- 2019-04-10
Related products to: IDH3A Blocking Peptide
Related articles to: IDH3A Blocking Peptide
- Adaptive thermogenesis in beige adipocytes is essential for maintaining energy homeostasis and preventing obesity. Emerging evidence suggests that human visceral adipose tissue harbors adipocytes with beige-like thermogenic features, enabling analysis of thermogenic gene regulation in humans. Isocitrate dehydrogenase 3A (IDH3A) is a rate-limiting enzyme of the tricarboxylic acid cycle, yet its function in adipocytes remains poorly defined. In this study, we examined IDH3A expression in human visceral adipose tissue and generated adipocyte-specific IDH3A knockout mice to investigate its role in beige adipocyte thermogenesis and metabolic regulation. IDH3A expression in human visceral fat was inversely associated with adiposity and adverse metabolic traits. Moreover, IDH3A expression was induced in human and mouse adipocytes following thermogenic stimulation. Adipocyte-specific IDH3A deletion in mice impaired beige fat thermogenic capacity, led to cold intolerance, and exacerbated diet-induced metabolic dysfunction. Mechanistically, IDH3A deficiency increased DNA methylation at the Bckdha promoter, resulting in the repression of this key branched-chain amino acid (BCAA) catabolic gene and impaired BCAA catabolism. Notably, restoring BCKDHA in IDH3A-deficient adipocytes rescued respiration and thermogenic function. Together, in addition to its canonical enzymatic role, our findings identify IDH3A as a critical regulator of BCAA catabolism that facilitates adaptive thermogenesis under metabolic stress conditions. - Source: PubMed
Lu XuhongBai NingningLyu JialuSun JingjingSu YingyingYe YafenHu TingtingLiu TianwenLi WenfeiLi XiaoyaMa XiaojingYang YingBao Yuqian - Heat stress significantly disrupts physiological and molecular balance in poultry, leading to oxidative damage, inflammatory responses, and metabolic dysregulation. Among emerging solutions, phytogenic adaptogens have shown promise as natural agents that enhance resilience against these environmental challenges. This exploratory study examined the transcriptomic effects of Phytocee™, a proprietary phytogenic formulation, in heat-stressed broilers, alongside in silico predictions of its phytochemical interactions with longevity-associated pathways. Phytocee™ consists of a formulation of adaptogenic medicinal plants. The primary bioactive components contributing to these adaptogenic properties include hydrolyzable tannins, withanolides, and triterpenoids. Comprehensive identification, quantification, and confirmation of these phytochemicals were conducted using liquid chromatography-mass spectrometry (LC-MS), and the formulation's integrity was validated through high-performance liquid chromatography coupled with photodiode-array detection for routine quality assurance. The transcriptomic analysis demonstrated that heat stress led to the upregulation of several vital DNA repair and cell cycle regulatory genes, including FANCF, BRCA1, and EXO1. The supplementation of Phytocee™ resulted in further increases in these genes, reaching a log2 fold change of 1.32 with a significance level of < 0.013. Additionally, resilience markers against oxidative stress such as SOD2, CAT, HSP25, HSPA2, and SOD3 along with metabolic adaptation indicators like IDH3A, ATP6V0D2, RRM2, ME1, FADS2, ALDH1L2, and DHCR7 showed significant enhancement post-treatment. There was also a restoration of several downregulated protective genes, including NFKBIA and BIRC5. DIGEP-Pred 2.0 and pathway enrichment were used in the in-silico analyses, which predicted that the key Phytocee™ phytochemicals interact with FOXO, AMPK, SIRT1, and mTOR network components. Transcriptomic patterns, such as upregulated DNA repair, oxidative resilience, and metabolic genes correlatively overlapped with this prediction. Again, no model validation or functional activation was performed. This exploratory study contributes to a hypothesis-producing framework for these associations to be tested in heat-stressed broilers but has several limitations related to the correlative nature of findings, absence of confirmation at the protein level, or functional assays, such as autophagy or pathway inhibition or direct measures of thermotolerance or production. Thus, confirmatory studies are warranted to test these implied mechanistic associations. - Source: PubMed
Publication date: 2026/03/16
Shamana KEdwin RJaishree S PPrashanth DAboli GDeepak M - Glioblastoma multiform (GBM) exhibit heterogeneity. Persistence of glioma stem cells (GSCs) are the root cause of tumor recurrence and drug resistance. So, targeting GSCs can be a better therapeutic strategy to tackle GBM. To mimic the tumor microenvironment, we have developed tumor spheroids by hanging drop method. Compared to monolayer cells spheroids had higher expression of stemness markers like CD133, CD44, PAX6 and reduced expression of differentiation marker. Cancer cells modulate the metabolic pathways to sustain high proliferation. Among the metabolic pathways, cholesterol biosynthetic pathways are mostly dysregulated in cancers, including GBM. The spheroids showed high expression of cholesterol biosynthetic genes (HMGCR, DHCR24), and Caveolin1 (CAV1). Targeting cholesterol metabolism by lovastatin resulted in depletion of cellular cholesterol levels, including in plasma membrane. Lowering of cholesterol affected membrane fluidity and hampered Hh signaling by lowering Gli1; consequently, causing downregulation of HMGCR, DHCR24, CAV1, and IDH3A, along with the loss of the stemness factors. However, there is enhanced expression of epigenetic chromatin modification enzymes, including DNMT1 and KDM5A. Tracking into the root cause of silencing of CAV1 gene, we found that CAV1 gene promoter is methylated by DNMT1, and H3K4me3 level was depleted due to enhanced KDM5A mediated demethylation. CAV1 gene silencing by siRNA validated its role in maintenance of stem-like phenotype and metabolic alterations of GBM spheroids. Collectively, this study demonstrated the regulatory role of Caveolin1 and cholesterol in maintaining stem-like characteristics of GBM spheroids and the importance of tumor models in better understanding of the molecular mechanism of GBM.Key words: Glioblastoma, cholesterol biosynthesis, stemness, Caveolin1, DNMT1, KDM5A, Gli1. - Source: PubMed
Publication date: 2026/01/28
Baral TirthankarKirtana RManna SoumenMishra JagdishChakraborty SubhajitNandi PiyasaNiharika Roy AnkanMishra PrahalladPradhan BhagyashreeDash PujariniPatra Samir Kumar - Patients who recover from cardiac arrest with autonomous circulation often have a poor prognosis due to myocardial dysfunction. Heparin, a pleiotropic drug, has not yet been identified for its myocardial protection mechanism in addition to anticoagulation. The aim of this study was to investigate the potential molecular mechanism by which heparin ameliorates cardiac injury after CA-CPR in rats via proteomic techniques. - Source: PubMed
Publication date: 2026/01/07
Wang FaTian BiyunLi NingkangGu YangLi XiaoqinZhou XiaohongLi YanLiu XinGu YinghuaWang YunYe Qingshan - Among the genes implicated in inherited retinal degenerations (IRDs), disease-causing variants in have recently been reported, although they remain exceedingly rare. In some cases, these variants are associated with macular pseudocoloboma. encodes the alpha subunit of the mitochondrial NAD-dependent isocitrate dehydrogenase 3 (IDH3) complex, a key enzyme in the tricarboxylic acid (TCA) cycle. - Source: PubMed
Publication date: 2025/11/18
Mavridou Eleftheria PMourgela AnnaPapadopoulou MargaritaKouri Agathi