Ask about this productRelated genes to: PANK2 antibody
- Gene:
- PANK2 NIH gene
- Name:
- pantothenate kinase 2
- Previous symbol:
- C20orf48, NBIA1
- Synonyms:
- HSS, FLJ11729, PKAN, HARP
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-21
- Date modifiied:
- 2019-04-23
Related products to: PANK2 antibody
Related articles to: PANK2 antibody
- Coenzyme A (CoA), derived from Vitamin B5 (VB5; also called pantothenate), is essential for lipid metabolism, energy production, and cell proliferation. While the intracellular functions of CoA are well-characterized, much less is known about its tissue‑specific regulation and systemic physiological roles. Here, using Drosophila melanogaster, we uncover a gut-renal circuit in which dietary VB5 fuels CoA biosynthesis specifically in the Malpighian tubules (MTs, the fly kidney), non‑autonomously impacting gut homeostasis. We show that, in the MTs, Myc boosts renal CoA production by directly upregulating the pantothenate kinase Fbl (human PANK1-3 ortholog) and downregulating CG5828, which we characterize as the functional ortholog of the metabolite phosphatase and CoA synthesis suppressor PANK4 (dPANK4). Elevated CoA biosynthesis enhances mevalonate-isoprenoid pathway activity in the gut, promoting intestinal stem cell proliferation. We further demonstrate that renal CoA production is required for gut tumor growth in a fly model. Consistently, MYC and genes within the CoA-isoprenoid axis display strong association with clinical outcomes in human cancers. Together, our findings establish that Myc-driven CoA metabolism generates an inter‑organ signal that couples VB5 availability to stem cell control and tumor growth, and identify the CoA-isoprenoid axis as a targetable metabolic vulnerability in cancer. - Source: PubMed
Publication date: 2026/04/18
Miao TingLiu YingQadiri MujeebDasseux AmauryAsara John MHu YanhuiSun XiaomeiPliego-Alcántara Luz Del CarmenDibble Christian CPerrimon Norbert - Coenzyme A (CoA) is a vital cofactor involved in energy metabolism, lipid biosynthesis, protein modification, and epigenetic regulation. Disruptions in CoA biosynthesis have been implicated in neurometabolic disorders such as pantothenate kinase-associated neurodegeneration (PKAN) and COASY protein-associated neurodegeneration (CoPAN), both within the heterogeneous spectrum of Neurodegeneration with Brain Iron Accumulation (NBIA). Specifically, CoPAN results from recessive variants in the COASY gene, encoding the bifunctional CoA synthase enzyme, leading to progressive neurodegeneration, motor impairment, and metabolic abnormalities. To investigate the neuronal impact of CoA deficiency, we developed an inducible, neuron-specific Coasy deleted mouse model. Unlike previous constitutive models, this system faithfully recapitulates key clinical and molecular features of CoPAN, including motor deficits, neurodegeneration, iron dyshomeostasis, and reduced survival. Strikingly, conditional neuronal Coasy ablation triggered extensive and progressive neuroinflammation, highlighting a neglected pathogenic component and potential therapeutic target. This model thus represents a robust platform to dissect disease mechanisms and evaluate candidate treatments. Given the established neuroprotective role of peroxisome proliferator-activated receptor gamma (PPARγ), we tested leriglitazone, a novel brain-penetrant full and selective PPARγ agonist effective in other rare neurodegenerative models. Leriglitazone treatment significantly improved motor performance, restored iron homeostasis, and attenuated both neuroinflammation and neurodegeneration. This study advances our understanding of the mechanism driving CoA-related neurodegeneration, highlights neuroinflammation as a pivotal pathogenic process, and demonstrates the therapeutic potential of PPARγ activation, underscoring leriglitazone as a promising candidate for CoPAN and potentially for the broader NBIA spectrum. - Source: PubMed
Publication date: 2026/04/13
Cavestro ChiaraCascone FlorianaLegati AndreaIzzo RossellaCatania MarcellaVergara CristinaRodríguez-Pascau LauraPizcueta PilarTiranti ValeriaDi Meo Ivano - Neurodegeneration with brain iron accumulation (NBIA) is a group of inherited disorders characterized by iron accumulation in the basal ganglia. Although the prevalence is estimated at 0.1-0.3 per 100,000,000 individuals, epidemiological data remain limited. - Source: PubMed
Publication date: 2026/04/13
Ozturk HasanBas HasanYapici ZuhalDevrez FatmaYilmaz M BurakOcal MineCakir Rana BBal HarunCeylaner Serdar - SUMMARYFungal infections are the leading cause of mortality among eukaryotic pathogens. They are responsible for approximately 150 million cases of severe illness and 3.8 million deaths annually. This global health threat is exacerbated by the limited arsenal of clinically approved antifungal drugs, particularly for the treatment of life-threatening invasive infections. The rise of multidrug-resistant fungal strains further underscores the urgent need for new classes of antifungals with novel mechanisms of action. In this context, the fungal coenzyme A (CoA) biosynthesis pathway has emerged as a promising therapeutic target due to its essential role in fungal physiology and key differences from its human counterpart. This review explores the critical role of CoA biosynthesis in fungal metabolism and highlights recent advances in the discovery and characterization of novel compounds targeting this pathway. Some of these emerging candidates act both as standalone inhibitors and as broad-spectrum potentiators of existing antifungals through their ability to enhance strain susceptibility and counteract mechanisms of drug detoxification and multidrug resistance. Collectively, these findings establish CoA metabolism as a compelling target for the next generation of antifungal therapies, offering a multipronged strategy to overcome the limitations of current treatment options and reduce fungal-related mortality. - Source: PubMed
Publication date: 2026/03/31
Choi Jae-YeonChiang AbigailBen Mamoun Choukri - - Source: PubMed
Publication date: 2026/03/12
Van Opstal JolienClaeys Kristl GDermaut BartDemaerel PhilippeVandenberghe Wim