Ask about this productRelated genes to: GGPS1 Blocking Peptide
- Gene:
- GGPS1 NIH gene
- Name:
- geranylgeranyl diphosphate synthase 1
- Previous symbol:
- -
- Synonyms:
- GGPPS1
- Chromosome:
- 1q42.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-26
- Date modifiied:
- 2016-10-05
Related products to: GGPS1 Blocking Peptide
Related articles to: GGPS1 Blocking Peptide
- This study evaluated the structural, electronic, pharmacokinetic, and receptor-binding properties of three bisphosphonate derivatives, alendronate, risedronate, and zoledronate, to investigate their therapeutic relevance in osteoporosis and breast cancer. Density Functional Theory (DFT) calculations at the B3LYP/6-31G(d,p) level showed that risedronate exhibited the highest kinetic stability (ΔE = 6.7468 eV), whereas zoledronate displayed greater chemical reactivity (ΔE = 2.9669 eV) and the strongest nonlinear optical response (β = 1.20 × 10 esu). ADMET analysis indicated acceptable safety profiles for all compounds, although high polarity and low lipophilicity may limit oral bioavailability. Molecular docking against 11 breast cancer- and bone metabolism-related targets revealed favorable binding affinities, particularly for zoledronate and risedronate. Zoledronate showed strong interactions with , /, , and , whereas risedronate exhibited notable affinity for and . Bioinformatics analyses identified significant dysregulation of , , , , , and in breast cancer tissues, while survival analysis linked elevated FDPS, , and expression to poor prognosis. Network analyses highlighted pathways related to mevalonate metabolism, hormone signaling, angiogenesis, extracellular matrix remodeling, and the // axis. These findings support the potential repurposing of bisphosphonates, particularly zoledronate, for breast cancer-associated bone disease. - Source: PubMed
Publication date: 2026/06/18
Dogan Sevil CeyhanGoren Kenan - Perrault syndrome is a genetically and clinically diverse autosomal recessive disorder characterized by sensorineural hearing loss in both sexes and primary ovarian insufficiency in females. This comprehensive review synthesizes data from various studies to map the genetic architecture of Perrault syndrome, highlighting mutations in fifteen principal genes: HSD17B4, HARS2, CLPP, LARS2, TWNK, ERAL1, RMND1, DAP3, PRORP, MRPL50, MRPL49, MRPS7, PEX6, GGPS1, and TFAM. Each of these genes plays a critical role either in mitochondrial function or peroxisomal processes, central to cellular energy metabolism and biosynthesis pathways. The review not only documents the spectrum of mutations found within these genes but also correlates specific genetic alterations with the range of phenotypes observed in patients, emphasizing the syndrome's allelic, locus, and clinical heterogeneity. The cohort demonstrates a distribution of 56.1% homozygous and 43.9% compound heterozygous variants, reflecting diverse ancestral backgrounds and potential selective pressures against deleterious alleles. The findings underscore the necessity for advanced genetic screening techniques in accurate diagnosis and the potential for gene-specific therapies that may mitigate some of the clinical manifestations of this complex condition. - Source: PubMed
Publication date: 2026/06/12
Tlili AbdelazizKhudeir Joudi Feras - Surface proteins enable T follicular helper (Tfh) cells' chemotactic migration toward B cells and subsequent functional interactions, underpinning effective humoral immunity. We showed that geranylgeranyl diphosphate (GGPP), a mevalonate (MVA) pathway-derived isoprenoid, was indispensable for Tfh cell function by maintaining surface protein expression. Either pharmacological inhibition or genetic depletion of geranylgeranyl diphosphate synthase (GGPS1), the enzyme responsible for GGPP biosynthesis, impaired Tfh cell generation. Mechanistically, geranylgeranyl transferase Ⅱ (GGTase Ⅱ) utilizes GGPP to geranylgeranylate RAB GTPases for surface protein expression, as exemplified by RAB35-mediated recycling of the chemokine receptor CXCR5 to the cell surface. Notably, the MVA pathway-GGPS1-GGTase Ⅱ-RAB35 axis in Tfh cells was enhanced by T cell receptor signaling and hyperactivated in autoimmunity. Conversely, the potent statin pitavastatin inhibited this axis to suppress pathogenic Tfh cells and alleviate autoimmunity. Thus, GGPP links the MVA pathway to T cell function via surface protein regulation, revealing a therapeutic target for autoimmune diseases. - Source: PubMed
Publication date: 2026/05/13
Wang LaiJiang JiaoYin HaoyuanWu JunhuiSu XiaoyuMeng LingchangWang LuluBao JingjingLi QilinWei YunboChen ZhianGong JialeiCañete Pablo FZheng MeilingLi WenruiZhou QiongqiongZhao MingYu DiLu Qianjin - Small-cell lung cancer (SCLC) responds to first-line therapy, but most patients rapidly develop resistance. This study aimed to investigate the efficacy and safety of nab-paclitaxel combined with simvastatin as second-line treatment for SCLC patients. - Source: PubMed
Publication date: 2026/04/06
Guan MaoyingZhao WenchengZhang WengangChen XuyangHuang RunzeLiu XinyueLi YujieWang HaoZhao LishuXu KandiYe LiChen ZhiminLiu YujinZhang QianqianJi HongbinHe Yayi - Intervertebral disc degeneration (IVDD) and osteoporosis (OP) are two highly prevalent degenerative diseases of the skeleton, and recent epidemiologic data have shown that the co-morbidity rate of IVDD and OP is as high as 32-45% in the elderly population, suggesting that there may be a potential molecular association. Currently, there is a lack of in-depth exploration of the co-morbidity mechanism and synergistic therapeutic targets. The aim of this study was to analyze the common pathogenic pathways of IVDD and OP and to verify the potential regulatory effects of zoledronic acid (ZOLA), a first-line anti-osteoporosis drug, on IVDD, which would provide a theoretical basis for the development of synergistic therapeutic strategies. A total of 665 co-morbid core genes were obtained from the intersection of IVDD and OP, and GO analysis showed that these genes were significantly enriched in the biological processes of inflammatory response regulation, extracellular matrix catabolism, and osteoblast differentiation, and the KEGG pathway was mainly involved in peroxisome and osteoclasts. Twelve potential targets were mapped by ZOLA, and seven core targets were obtained by intersecting with IVDD-OP co-morbid genes. Molecular docking confirmed the stable binding ability of ZOLA with FDPS, GGPS1, FDFT1, and MVD targets. This study reveals that IVDD and OP share a core molecular network of inflammation-matrix metabolic imbalance and confirms that the anti-osteoporosis drug ZOLA can intervene in the process of intervertebral disc degeneration through multi-target synergy. This finding not only provides a new perspective for the "co-treatment" of degenerative bone diseases but also lays a theoretical foundation for the clinical application of ZOLA. - Source: PubMed
Publication date: 2026/03/11
Wang LiZheng KaiyuanLuo WanhongZhang QinWang SiyuZeng LianlinWang Yinxu