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
- 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 - During T-cell-mediated inflammatory responses, T cells are activated upon recognizing specific antigens presented by antigen-presenting cells. This recognition initiates signaling through the TCR and CD28, leading to their activation and subsequent clonal expansion. Within the signaling cascades triggered by TCR and CD28 engagement, the CD28-PI3K pathway serves as a central regulator of metabolic reprogramming in T cells, supporting the biosynthetic needs essential for their effective proliferation. In this study, we found that the regulation of PANK4 plays a role in TCR/CD28-mediated CD4 T-cell proliferation by regulating de novo lipid synthesis. The CD28 signaling pathway negatively regulates PANK4 through direct binding with PDK1, thereby controlling de novo lipid synthesis for CD4 T-cell proliferation. Interestingly, we found that Pank4-deficient CD4 T cells enhance coenzyme A synthesis and glutaminolysis, whereby glutamine contributes carbon for fatty acid synthesis and provides nitrogen for coenzyme A biosynthesis. The regulatory role of PANK4 in CD4 T-cell proliferation was confirmed in models of experimental colitis and influenza A virus infection, where Pank4-deficient CD4 T cells exhibited greater expansion than their wild-type counterparts when co-transferred. Our findings suggest that PANK4 regulation of de novo lipid synthesis is crucial for TCR/CD28-induced CD4 T-cell proliferation and represents a potential target for modulating general CD4 T-cell responses. - Source: PubMed
Publication date: 2025/09/18
Hwang Jeong-RyulNguyen Chi Thi NgocKo GwanghoonKang Jung-AhByeon YeongseonPark SeowooChang RyunhaJung DawoonJeon Mi YeonSung Young HoonLee Cho-RongNam Ki-HoanSeong Je KyungGhosh SankarKang Yun PyoPark Sung-Gyoo - Pantothenate kinases (PANKs), which regulate the first and rate-limiting step of coenzyme A (CoA) biosynthesis, have emerged as therapeutic targets for various human diseases. PANKs family consists of PANK1, PANK2, PANK3, and PANK4. We summarized the research progress of the PANK family in the last two decades. Notably, PANKs play critical roles in diverse pathophysiological mechanisms underlying human diseases, including pantothenate kinase-associated neurodegeneration (PKAN), propionic acidemia (PA), lipid metabolic disorders, Parkinson's disease (PD), glioma, clear cell renal cell carcinoma (ccRCC), and insulin resistance (IR). Nevertheless, the precise relationship between PANKs and human diseases remained ambiguous. Therefore, this review provides a comprehensive summary of the structural properties, molecular mechanisms, and relevant modulators that govern PANK activity. In conclusion, targeting PANKs as regulators of CoA biosynthesis and disease pathogenesis contributes to connecting biochemistry with pharmacotherapy. - Source: PubMed
Publication date: 2025/08/05
Zhang XinnanZhang BoLi XinzeQiu FengZhang QiangKang Ning