Ask about this productRelated genes to: PANK1 antibody
- Gene:
- PANK1 NIH gene
- Name:
- pantothenate kinase 1
- Previous symbol:
- PANK
- Synonyms:
- MGC24596, PANK1a, PANK1b
- Chromosome:
- 10q23.31
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-02
- Date modifiied:
- 2014-11-19
Related products to: PANK1 antibody
Related articles to: PANK1 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 - 1,3,6,8-Tetrabromocarbazole (1368-BCZ), an emerging dioxin-like persistent organic pollutant, can enter the body through multiple routes including dietary intake, inhalation, and dermal contact. Growing concerns have been raised about its potential toxicity, particularly regarding its poorly characterized neurotoxic effects. This study aims to elucidate the neurotoxic effects of the emerging pollutant 1368-BCZ by establishing a subchronic exposure mouse model, and to investigate the underlying metabolic disruption mechanisms in the hippocampus that contribute to neurodegenerative damage, through an integrated approach combining neurobehavioral, histopathological, and multi-omics analyses. Neurobehavioral assessments revealed significant neurodegenerative damage in exposed mice, as evidenced by a decreased recognition index (∼10 %), prolonged escape latency (∼20 s), reduced time spent in the target quadrant (5-10 s), and fewer platform crossings (1-2 times) in behavioral tests. Histopathological examination demonstrated distinct damage in the hippocampus, a brain region crucial for episodic memory formation and spatial navigation. Furthermore, 1368-BCZ exposure significantly upregulated neurodegenerative-related proteins in hippocampal tissues, including Aβ (∼3-fold) and phosphorylated Tau (p-Tau, ∼1.5-2.0 fold) relative to the control group. Untargeted metabolomic analyses revealed that 1368-BCZ exposure-induced significant metabolic disturbances in mouse hippocampus, including the downregulation of 602 metabolites and upregulation of 78 metabolites. Integrated transcriptomic and untargeted metabolomic analyses revealed that 1368-BCZ exposure-induced the downregulation of Dpys, Mlycd, and Pank1 mediated the disruption and the cross-talk of the pantothenate and CoA biosynthesis pathway and the β-alanine metabolism pathway might be primarily contributed to neurodegenerative damage in mice. Collectively, our findings demonstrate that subchronic 1368-BCZ exposure induces significant neurotoxicity by disrupting hippocampal metabolic networks, ultimately leading to neurodegenerative damage in mice. This study not only characterizes the neurotoxic effects of 1368-BCZ but also establishes a link between its subchronic exposure and neurodegeneration in vivo, thereby firstly providing mechanistic insights into the neurotoxicity of this emerging persistent pollutant and underscoring its potential environmental health risks. - Source: PubMed
Publication date: 2026/01/19
Wu JingHuang HuiminLi JingXu TongLiao JingLiu PeifangLiu YifeiLi GuofengWu ChuanchengXiang JianjunJiang Yu - Humans have 3 different PANK enzymes (PANK1-3) that catalyze the first step in the synthesis of Coenzyme A (CoA). All PANKs are feedback inhibited by acyl-CoAs but only PANK2 can overcome this inhibition by binding palmitoyl-carnitine. Previous studies, conducted under glucose-replete conditions, have failed to detect a PANK2-mediated contribution to CoA synthesis. We found that exposure to BSA-conjugated palmitate (PAL-BSA) led to activation of fatty acid oxidation (FAO) and the accumulation of both palmitoyl-carnitine and palmitoyl-CoA in HEK293T cells, suggesting that PANK2 is active under these conditions. Isotope tracing experiments with CN-pantothenate showed that PANK2 uniquely sustains CoA synthesis and high production of Acetyl-CoA in the presence of long-chain fatty acids, indicating that FAO is limited by CoA availability in these conditions. Consistent with this mechanism, fibroblasts from PKAN patients exhibited impaired oxidation of palmitoyl-carnitine, confirming the functional relevance of our results in a disease context. - Source: PubMed
Publication date: 2025/11/18
Nordlie Sandra MSchafer RobertRauckhorst AdamSantos-Exposito Ana MPrieto-Rodriguez AndresWilson Bryce AEvans Idil AHadziamehtovic UnaNowlen FrancesSantos-Ocaña CarlosTaylor Eric BKruer Michael CPadilla-Lopez Sergio - Kidney renal clear cell carcinoma (KIRC) lacks sensitive early diagnostic markers and effective therapeutic guidance. Given the tight crosstalk between tumor metabolism and immunity, we investigated immunometabolism for biomarker discovery. Transcriptomes from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus were integrated. Immunometabolism-related genes were screened by weighted gene co-expression network analysis and differential expression, followed by three machine learning algorithms (least absolute shrinkage and selection operator, Support Vector Machine-Recursive Feature Elimination (SVM-RFE), and random forest) to select features and build a diagnostic model. Performance was validated in external cohorts. Multi-omics correlation, immune infiltration, drug-sensitivity, and survival analyses were conducted. Functional assays were performed in vitro and in vivo. Six biomarkers-ABCB1, Acyl-CoA Dehydrogenase Short/Branched Chain (ACADSB), PLA2G6, AKR1C3, PANK1, and Lactate Dehydrogenase B (LDHB)-were identified. The model showed strong discrimination (AUC 0.976 in TCGA; 0.902 in GSE126964; and 0.916 in GSE36895). The genes correlated with immune checkpoints, cytokine signaling, T-cell infiltration, and clinical parameters. Drug analyses suggested cisplatin and sunitinib downregulated oncogenic targets. Silencing ABCB1 or AKR1C3, or overexpressing LDHB, suppressed KIRC cell proliferation and migration in vitro; LDHB overexpression combined with sorafenib significantly reduced tumor growth in vivo. We propose a robust immunometabolism-based diagnostic model and six experimentally supported biomarkers for KIRC, providing mechanistic insight into tumor-immune interactions and potential avenues for personalized therapy. - Source: PubMed
Publication date: 2025/09/17
Hu GuofanLiang JianFeng MeilingLin HanshengHe Jingwei - Coenzyme A (CoA), derived from Vitamin B5 (VB5), is essential for lipid metabolism, energy production, and cell proliferation. While the intracellular functions of CoA are well characterized, its tissue-specific regulation and systemic physiological roles remain poorly understood. Here, using , we uncover a gut-renal circuit in which dietary VB5 stimulates CoA biosynthesis specifically in the Malpighian tubules (MTs, the fly kidney), non-autonomously impacting gut homeostasis. We show that Myc boosts renal CoA production by directly upregulating ( homolog) and downregulating in the MTs. Elevated CoA biosynthesis enhances the 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, 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: 2025/08/11
Miao TingLiu YingQadiri MujeebAsara John MHu YanhuiSun XiaomeiDibble ChristianPerrimon Norbert