Ask about this productRelated genes to: PANK4 Blocking Peptide
- Gene:
- PANK4 NIH gene
- Name:
- pantothenate kinase 4
- Previous symbol:
- -
- Synonyms:
- FLJ10782
- Chromosome:
- 1p36.32
- Locus Type:
- gene with protein product
- Date approved:
- 2002-10-11
- Date modifiied:
- 2015-08-25
Related products to: PANK4 Blocking Peptide
Related articles to: PANK4 Blocking Peptide
- Propionic acidemia (PA) is a rare autosomal recessive metabolic disorder caused by a deficiency of mitochondrial propionyl-CoA carboxylase, leading to the accumulation of propionyl-CoA and toxic metabolites that disrupt TCA cycle flux and ammonia detoxification. Propionyl-CoA is generated from gut microbiome-derived propionate, propiogenic amino acids, odd-chain fatty acids, and cholesterol side chains. Its accumulation produces downstream metabolites such as propionylcarnitine and methylcitrate and promotes histone propionylation. These alterations collectively contribute to mitochondrial dysfunction, oxidative stress, and multi-organ pathology. Current clinical management focuses on reducing propionyl-CoA burden through dietary restriction and supportive therapies, but long-term outcomes remain suboptimal due to poor tolerability and progressive complications. Although liver transplantation improves hepatic metabolism, it does not fully correct extrahepatic disease. Gene-based approaches, including mRNA-based enzyme replacement and viral vector-mediated gene delivery, show promise but face challenges related to delivery efficiency, durability of expression, and immune responses. Emerging small-molecule strategies aim to reprogram metabolism by restoring the balance between propionyl-CoA and acetyl-CoA while replenishing cellular CoA pools. Precision metabolic therapy may combine acetate supplementation and NRF2 activation to enhance acetyl-CoA production and mitochondrial resilience, while suppressing propionyl-CoA formation through ACSS3 inhibition and propiogenic amino acid restriction. In parallel, CoA availability may be increased through activation of PANK1-3, inhibition of PANK4, and supplementation with CoA precursor compounds. We propose that rational combination therapy targeting multiple nodes of short-chain fatty-acid metabolism and CoA homeostasis will provide a more effective strategy than single-agent approaches for correcting metabolic imbalance in PA. - Source: PubMed
Publication date: 2026/06/24
Subramaniyan BoopathiLu FangLi HuanPaiboonrungruang ChorladaLi YahuiXiong ZhaohuiZhang Guo-FangChen Xiaoxin - Mild cognitive impairment (MCI), a condition that falls somewhere between normal aging and severe cognitive dysfunction (e.g., Alzheimer's disease), is a common manifestation of the neurocognitive function decline that seniors encounter as they age. The fundamental processes causing its beginning are still not well understood yet. - Source: PubMed
Publication date: 2026/05/13
Wang BoZhang JingLi Chang-HongHuang XiaoGao Ruo-BingPeng YanXie QingNing Ya-LeiZhao YanYang NanChen XingXie Yang-LiZhou Yuan-GuoLin SenChen LinLi Ping - Lens epithelial cell-mesenchymal transition (LEC-EMT) is the key process in diabetic cataract (DC). Although PANK4 is known to suppress LEC-EMT, its mechanism remains unclear. This study aims to elucidate the role of PANK4 in DC pathogenesis through the YAP/TAZ pathway. - Source: PubMed
Li XueLuo LinlinChen SiSun YuanruiLi ChengLiu XuemeiHu QiumeiHu ZegangLiu WeiLiu Ting - 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 - Dizziness/vertigo is a multifactorial neurological disorder with complex ge-netic and cellular bases, yet its molecular mechanisms remain unclear. Understanding how gene regulation contributes to dizziness/vertigo may reveal novel neurobiological and therapeutic insights. - Source: PubMed
Publication date: 2026/02/11
Shan DingduoLi ShuoZhang LiliBai JiaqiWang Henglin