Ask about this productRelated genes to: FDFT1 Blocking Peptide
- Gene:
- FDFT1 NIH gene
- Name:
- farnesyl-diphosphate farnesyltransferase 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-26
- Date modifiied:
- 2016-10-05
Related products to: FDFT1 Blocking Peptide
Related articles to: FDFT1 Blocking Peptide
- The human lipidome comprises numerous complex lipids, dysregulation of which can contribute to the pathogenesis of a wide range of diseases. Despite the high heritability of parts of the lipidome, the genetic architecture of many circulating lipid species and their structure remains mostly unknown. Thus, we perform genome-wide association studies on 970 lipid species and 267 fatty acid composite measures using samples from the population-based Rhineland Study (n = 6096). We validate our findings using corresponding data from two other independent cohorts, including FinnGen (n = 7266) and EPIC-Potsdam (n = 1188). Out of 217 lead genomic loci, we find 136 to be novel, such as FDFT1. Using mendelian randomization and individual-level gene expression data, we identify 43 possible causal associations between candidate genes and corresponding lipid species, including FDFT1 - diacylglycerol (16:0/18:0). Our findings provide new insights into the intricate genetic underpinnings of lipid metabolism, which may facilitate risk stratification and discovery of new therapeutic targets. - Source: PubMed
Publication date: 2026/05/02
Landstra Elvire NImtiaz Mohammed ATalevi ValentinaEichelmann FabianSchulze Matthias BAziz N AhmadBreteler Monique M B - Macrophage anti-tumor efficacy requires coordinated inflammatory activation and phagocytic function, whether a tumor-intrinsic metabolic regulator simultaneously determines both macrophage anti-tumor mechanisms remains unclear. Here, we screened and identified that farnesyl-diphosphate farnesyltransferase 1 (FDFT1) drives the dual inhibition of macrophage activation and phagocytic function and promotes tumor progression. Mechanistically, tumor-intrinsic FDFT1 directly binds to STAT3 and facilitates the later phosphorylation, which induces PD-L1-dependent suppression of macrophage phagocytosis. Concurrently, FDFT1 binds to and stabilizes cholesterol 25-hydroxylase (CH25H) to promote the secretion of 25-hydroxycholesterol (25HC), suppressing proinflammatory activation of macrophages. Furthermore, FDFT1-mediated dual anti-tumor pathways were validated in mouse tumor models and correlated with clinical pathophysiology. Notably, a small-molecule drug FDFT1-I (2123) targeting FDFT1 inhibits both STAT3-PD-L1 and CH25H/25HC pathways and improves anti-tumor immunity. Collectively, our findings highlight FDFT1 as a tumor-intrinsic metabolic factor promoting tumor development via dual macrophage-dependent mechanisms, suggesting FDFT1 as a promising target for tumor therapy. - Source: PubMed
Publication date: 2026/04/29
Shi RongchenHuang YulanZheng PengfeiZhang DapengQin QingZhang FanWang MengZhao KunYang MinliGuan XuDeng RenchaoMiao Hongming - Autophagy is a conserved catabolic process that degrades proteins and damaged organelles to maintain cellular homeostasis, and its role in cancer depends on stage and context. Farnesyl-diphosphate farnesyltransferase 1 (FDFT1) is an essential enzyme in the sterol branch of the mevalonate pathway, but its functions in hepatocellular carcinoma (HCC) and in the regulation of autophagy remain poorly understood. In this study, we show that FDFT1 acts as a negative regulator of autophagy in HCC cells. Loss of FDFT1 led to increased autophagosome formation and fusion with lysosomes, whereas its overexpression suppressed both basal and induced autophagy. These changes were associated with AMPK-ULK1 signaling, suggesting that FDFT1 influences a central pathway controlling autophagy. Our findings connect cholesterol metabolism with autophagy regulation and tumor growth, highlighting FDFT1 as a potential prognostic marker and therapeutic target in liver cancer. - Source: PubMed
Publication date: 2025/04/30
Nguyen Thi HaLee YongookNguyen Minh TuanChoi Seoung GyuNguyen Phuong NganKim BoramKim Eun JiKang Gyeoung JinPark Mi KyungLee Sung HoonKim Sang GeonLee Chang Hoon - -Aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the central nervous system and is involved in the development of neural tissue as well as the regulation of its functions. Meanwhile, GABA has also been demonstrated to confer multiple physiological benefits, including alleviating stress and improving metabolic homeostasis. This study investigated GABA effects on proliferation, differentiation, and temperature stress protection of bovine skeletal muscle satellite cells (BSCs). - Source: PubMed
Publication date: 2026/04/14
Manzoor AbidNaseem SajidaFu ZhiqiRuan ChaohuiLiu XuYan ChunriChoi SeonghoLi Xiangzi - Abdominal fat thickness (AFT) is a crucial indicator for assessing fat deposition in White Feather broilers. Previous genome-wide association studies (GWAS) have primarily focused on single-point measurements of abdominal fat, with limited attention given to longitudinal phenotype records. Compared to traditional GWAS models, the longitudinal data-based GWAS (LONG-GWAS) model accounts for temporal phase effects, thereby more effectively controlling the false positive rate. This study conducted a genome-wide association analysis on 1654 White Feather broilers at four distinct ages during the laying period of broiler breeders (25, 27, 35, and 43 weeks). Three SNP loci associated with fat were identified (rs16341267, rs740644432, and rs15049519), which were annotated to three candidate genes: FDFT1, HTR2C, and ALDH3A2. These genes are involved in regulating lipid metabolism, energy balance, and fat deposition. This study provides new insights into the genetic basis of abdominal fat thickness in White Feather broilers and offers stage-specific marker information that can accelerate precision breeding for abdominal fat control in white feathered broilers. - Source: PubMed
Li PenghaoLuo NaYing FanZhu DanLiu DaweiSong XianyiWen JieZhao GuipingAn Bingxing