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Validated All-in-One™ qPCR Primer for FASN(NM_004104.4) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
The enzyme encoded by this gene is a multifunctional protein. Its main function is to catalyze the synthesis of palmitate from acetyl-CoA and malonyl-CoA, in the presence of NADPH, into long-chain saturated fatty acids. In some cancer cell lines, this protein has been found to be fused with estrogen receptor-alpha (ER-alpha), in which the N-terminus of FAS is fused in-frame with the C-terminus of ER-alpha. [provided by RefSeq].
Gene References into function
- We present the first three-dimensional reconstruction of human fatty acid synthase obtained by electron cryomicroscopy and single-particle image processing
- regulation of expression by liver X receptors
- Domain movements in human fatty acid synthase by quantized elastic deformational model
- expression of FAS is affected by polyunsaturated fatty acids in human cells
- Fatty acid synthase in the specimens of non-small cell lung cancer patients has no correlation with most clinical factors, except that, in early lesions, it may signify poor prognosis.
- Regulation of fatty acid synthase expression in breast cancer by sterol regulatory element binding protein-1c.
- Data point to a link between fatty acid synthase overexpression and dysregulation of membrane composition and functioning in tumor cells.
- RNA interference-mediated silencing of this gene attenuates growth and induces morphological changes and apoptosis of prostate cancer cells.
- compelling evidence that human mitochondria contain a malonyl-CoA/acyl carrier protein-dependent fatty acid synthase system
- a strong association between FAS expression and prostate tumor initiation and progression
- FAS plays in important cellular processes such as apoptosis and proliferation. Because of the frequent overexpression of this enzyme prostate cancer, FAS constitutes a therapeutic target in this disease [review].
- cellular FAS activity is important for induction of immediate-early gene BZLF1 transcription from the intact latent EBV genome
- Regions responsible for hormonal regulation of the FAS gene lie in the proximal portion of the gene's 5'-flanking region, within which we identified an insulin response element.
- Val1483Ile substitution in FAS is protective against obesity in Pima Indians, an effect possibly explained by the role of this gene in the regulation of substrate oxidation.
- Data suggest that HER2 may act as the key molecular sensor of energy imbalance after the perturbation of tumor-associated fatty acid synthase hyperactivity in cancer cells.
- breast cancer-associated FAS plays an active role in human breast cancer chemosensitivity
- 2.6-A resolution structure
- study reveals for the first time that extracellular acidosis can work in an epigenetic fashion by up-regulating the transcriptional expression of FAS gene
- FAS blockade should result in a concomitant down-regulation of VEGF
- Our results indicate that the specific inhibition of fatty acid synthase (FAS) gene by siRNA leads to apoptosis of prostate tumor cells, and inhibition of PI 3-kinase pathway synergizes with FAS siRNA to enhance tumor cell death.
- increased expression in 7 of 8 patients with invasive Paget's disease of the vulva (PDV), 3 of 4 patients with microinvasive PDV & 1 of 8 patients with noninvasive PDV; statistical analysis revealed increased expression was associated with invasive PDV
- analysis of human fatty-acid synthase substrate recognition
- Fatty acid synthase (FAS) gene, encoding for a key enzyme involved in the biogenesis of membrane lipids in rapidly proliferating cells, is a conserved target of the p53 family throughout the evolution.
- Tamoxifen can modulate appetite through alterations in FAS expression and malonyl-CoA levels suggesting a link between hypothalamic sex steroid receptors, fatty acid metabolism, and feeding behavior.
- thiazolidinediones upregulate the adipocyte lipid storage genes DGAT and FAS but have no significant effect on LPL
- HCV-3a core protein has a stronger effect on fatty acid synthase activation in comparison to HCV-1b core, which could contribute to the higher prevalence and severity of steatosis in HCV-3a infections
- FASN gene expression in adipose tissue is linked to visceral fat accumulation, impaired insulin sensitivity, increased circulating fasting insulin, IL-6, leptin and RBP4
- reduced expression of the fatty acid synthase gene in adipose tissues of obese subjects.
- The crystal structure of the thioesterase domain of FAS is determined.
- the major mechanism of HER2-mediated induction of FASN and ACCalpha in the breast cancer cells used in this study is translational regulation primarily through the mTOR signaling pathway.
- By using cerulenin and C75, two known inhibitors of FAS we were able to significantly block CVB3 replication.
- Fatty acid synthase [FAS] activity levels were higher in cancer than in the corresponding normal mucosa. Tumors on the left side of the colon showed higher FAS activity; tumors from male patients showed higher activity than tumors from females.
- Surface analysis identified the ligand-binding pocket of the thioesterase domain that encompasses the catalytic triad of Ser2308, His2481, Asp2338. Docking of palmitate into this pocket revealed the ligand-binding mode
- cannot definitely establish FASN as a novel oncogene in breast cancer, but this study reveals that exacerbated endogenous FA biosynthesis in non-cancerous epithelial cells is sufficient to induce a cancer-like phenotype dependent on HER1/HER2 duo
- Dietary soy protein, by decreasing circulating insulin levels and colon FASN expression, attenuates insulin-induced DNA damage and FASN-mediated anti-apoptosis during carcinogenesis.
- FAS gene is up-regulated by hypoxia via activation of the Akt and HIF1 followed by the induction of the SREBP-1 gene, and that hypoxia-induced chemoresistance is partly due to the up-regulation of FAS.
- FASN overexpression is a new mechanism of drug resistance and may be an ideal target for chemosensitization in breast cancer chemotherapy.
- expression in squamous cell carcinoma of the tongue is associated with microscopic characteristics that determine disease progression and prognosis
- Taken together, results suggest that HCV NS2 can upregulate the transcription of SREBP-1c and FAS, and thus is probably a contributing factor for HCV-associated steatosis.
- Fatty acid synthase is overexpressed in oral or head and neck squamous cell carcinomas and hyperkeratotic oral epithelium.
- These findings suggest that FASN and Cav-1 physically and functionally interact in PCa cells.
- Proto-oncogene FBI-1 (Pokemon) and SREBP-1 synergistically activate transcription of fatty-acid synthase gene
- FASN and activated AKT pathway may be a potential target for therapeutic intervention for the treatment of papillary thyroid carcinomas.
- unique effect of inhibition of FAS results from negative regulation of the mTOR pathway via DDIT4
- Co-expression of fatty acid synthase and caveolin-1 in pancreatic ductal adenocarcinoma.
- expression did not correlate significantly with the outcome in breast cancer
- Hepatitis C virus infection directly induces FASN expression, and thus suggests a possible mechanism by which infection alters the cellular lipid profile and causes diseases such as steatosis.
- propose that cytoplasmic stabilization of beta-catenin through palmitoylation of Wnt-1 and subsequent activation of the pathway is a potential mechanism of FASN oncogenicity in prostate cancer
- Cohort study of fatty acid synthase expression and patient survival in colon cancer.
- FASN release from cancer cells is an active and controlled process that takes place by AMPK-sensed stimuli that increase the cellular AMP/ATP ratio.
