Ask about this productRelated genes to: PIP4K2B antibody
- Gene:
- PIP4K2B NIH gene
- Name:
- phosphatidylinositol-5-phosphate 4-kinase type 2 beta
- Previous symbol:
- PIP5K2B
- Synonyms:
- PIP5KIIB, PIP5KIIbeta
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-18
- Date modifiied:
- 2016-11-16
Related products to: PIP4K2B antibody
Related articles to: PIP4K2B antibody
- The phosphatidylinositol 5-phosphate 4-kinases (PIP4Ks) are an evolutionarily conserved family of lipid kinases that phosphorylate phosphatidylinositol 5-phosphate to generate phosphatidylinositol 4,5-bisphosphate. In mammals, the catalytically active α and β isoforms, encoded by PIP4K2A and PIP4K2B, respectively, localize to distinct cellular compartments and have been implicated in metabolism, immune regulation and tumorigenesis, prompting interest in their pharmacological inhibition. Notably, most reported small-molecule inhibitors display substantially higher potency towards the α isoform than the β isoform, suggesting intrinsic structural features that limit the effective targeting of PIP4K2B. Here, we report the crystal structure of PIP4K2A in complex with 422A, a potent dual α/β inhibitor with improved metabolic stability. The structure reveals an unexpected, water-mediated interaction in which a pyridyl nitrogen of the inhibitor engages a conserved structured water molecule in the roof of the specificity pocket, constraining the orientation of the pyridylmethyl side chain and stabilizing a rigid, high-affinity binding mode. Comparative structural analysis with the PIP4K2A-selective inhibitor BAY-091 shows that deeper penetration into the specificity pocket enhances PIP4K2A binding but is accompanied by local steric constraints that are likely to be less well tolerated in PIP4K2B. Together, these findings define structural determinants of isoform-dependent inhibitor binding within the PIP4K family and provide a framework for structure-guided optimization of lipid kinase inhibitors with improved isoform balance. - Source: PubMed
Publication date: 2026/05/12
He ZunyuChen SongMicheli FabrizioCianciulli AgostinoBeato ClaudiaEllman JonathanHa Ya - Oat grass supplementation is a promising strategy for improving meat quality in ruminants. This study investigated its effects on the meat quality of Small-tailed Han sheep. The results revealed that sheep fed oat grass displayed higher expression of key genes (, ), , and Cytochrome coxidase (Cyto) associated with muscle structure and contraction, while genes (, , ) and proteins (, , ) associated with cardiac contraction and myosin cytoskeletal regulation were downregulated. These molecular changes were likely to underpin meat tenderness and texture. Furthermore, oat grass supplementation influenced metabolic pathways linked to flavor-enhancing compounds, including amino acids and free fatty acids like alanine. These metabolic changes not only improved lamb tenderness but also enhanced its flavor and nutritional profile. This study provides evidence that oat grass supplementation is a practical and effective dietary strategy for optimizing lamb meat quality, offering dual benefits of improved sensory appeal and nutritional value. - Source: PubMed
Publication date: 2026/01/30
Wang Li-WeiLi Jian-QiangAn Jiang-HongSun HuaLiu FangZhao Meng-RanJiang Li-LiDong Xing-RanTao SarulaBayaer MengkeHe Jiang-FengLiu Yong-Bin - In the published publication [...]. - Source: PubMed
Publication date: 2025/11/14
Topchu IuliiaBychkov IgorRoshchina EkaterinaMakhov PetrBoumber Yanis - A deeper understanding of how teriparatide exerts its anabolic effects on bone tissue may open new avenues for osteoanabolic treatment. Our study aimed to identify long non-coding RNAs and messenger RNAs (mRNAs) regulated by teriparatide. Bone marrow mesenchymal stem cells (MSCs) were treated with teriparatide during osteogenic differentiation, and long RNA sequencing was performed. We identified 7 622 differentially expressed lncRNAs in both continuous and intermittent treatment groups compared to untreated MSCs. In intermittent treatment, the most upregulated lncRNAs were VCP, EMP1, OXA1L, LPP, and SCARB2, while in continuous treatment, they were XLOC_055533, SCARB2, HNRNPC, VCP, and CALM3. The most downregulated lncRNAs in intermittent treatment were KRTAP4-11, DUBR, MEG3, DIABLO, and ABI3BP, while in continuous treatment, they were XLOC_055164, SLC2A3, COPG1, and SMTN. Among mRNAs, the most upregulated in intermittent treatment were DNAJC25-GNG10, ZBTB4, SLC2A6, TMEM189-UBE2V1, and BDP1, whereas SLC2A6, ZBTB4, MX1, BDP1, and RSAD2 were the most upregulated in continuous treatment. The most downregulated mRNAs in intermittent treatment were PIP4K2B, GFI1B, ISY1-RAB43, AC010422.5, SESN2 and ISY1-RAB43, whereas ZDBF2, KLKB1, RPS10-NUDT3, and XLOC_055092 were the most downregulated mRNAs in continuous treatment. AC008622.2, MED17, and RNF213 emerged as the most critical lncRNAs for elucidating the mechanism of intermittent teriparatide therapy, while XLOC_055533, SPG7, and HOOK3 were highlighted as the most important lncRNAs in the continuous treatment. Additionally, we identified novel lncRNAs (KRTAP4-11, CEBPZOS, and CDC42SE2) that may have a role in teriparatide effects on MSCs. Identified lncRNAs and mRNAs could serve as therapeutic targets or diagnostic markers to improve osteoanabolic treatments. - Source: PubMed
Publication date: 2025/07/02
Vrščaj Lucija AnaMarc JanjaOstanek Barbara - Acute lymphoblastic leukemia (ALL), a complex malignancy, displays varying expression profiles of PIP4K2-related genes in adult patients. While PIP4K2A expression is elevated in ALL bone marrow cells compared to healthy bone marrow cells, PIP4K2B is downregulated, and PIP4K2C remains relatively unchanged. Despite the correlation between increased PIP4K2A expression and increased percentage of peripheral blood blasts, clinical outcomes do not strongly correlate with the expression of these genes. Here we investigated the therapeutic potential of three PIP4K2 inhibitors (THZ-P1-2, a131, and CC260) in ALL cell models. THZ-P1-2 emerges as the most effective inhibitor, inducing cell death and mitochondrial damage while reducing cell viability and metabolism significantly. Comparative analyses highlight the superior efficacy of THZ-P1-2 over a131 and CC260. Notably, THZ-P1-2 uniquely disrupts autophagic flux and inhibits the PI3K/AKT/mTOR pathway, indicating a distinct molecular mechanism. In summary, our findings elucidate the differential expression of PIP4K2-related genes in ALL and underscore the potential role of PIP4K2A in disease pathogenesis. The therapeutic promise of THZ-P1-2 in ALL treatment, along with its distinct effects on cell death mechanisms and signaling pathways, enriches our understanding of PIP4K2's involvement in ALL development and offers targeted therapy prospects. - Source: PubMed
Publication date: 2024/06/06
Lima KeliNogueira Frederico LisboaCipelli MarcellaCarvalho Maria Fernanda LopesPereira-Martins Diego Antonioda Silva Wellington FernandesCavaglieri Rita de CássiaNardinelli LucianaLeal Aline de MedeirosVelloso Elvira Deolinda Rodrigues PereiraBendit IsraelCâmara Niels Olsen SaraivaSchuringa Jan JacobMachado-Neto João AgostinhoRego Eduardo Magalhães