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Validated All-in-One™ qPCR Primer for FTO(NM_001080432.2) Search again
Product ID:
HQP018895
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ALKBH9, BMIQ14, GDFD, IFEX9
Gene Description:
FTO alpha-ketoglutarate dependent dioxygenase
Target Gene Accession:
NM_001080432.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
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:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- A genome-wide search for type 2 diabetes-susceptibility genes identified a common variant in the FTO gene that predisposes to diabetes through an effect on body mass index
- Association with obesity in adult and childre. Interestingly, this association receives clear confirmation under a Transmission Disequilibrium Test design which is robust to population stratification.
- FTO-meediaated weight gain does not predispose individuals to type 1 diabetes as it does for type 2 diabetes.
- common genetic variants in the FTO gene are associated with substantial changes in BMI, hip circumference, and body weight
- Variation in the FTO gene locus is associated with cerebrocortical insulin resistance in humans.
- Our study of the FTO polymorphisms has generated no evidence to support the thrifty genotype hypothesis for Oceanic populations
- Variation in FTO is associated with type 2 diabetes when not adjusted for body mass index and with an overall increase in body fat mass.
- Data do not support that the FTO common variants are major contributors of obesity or type 2 diabetes in a Chinese Han population.
- Amino acid conservation of FTO protein suggests that it is a member of the non-heme dioxygenase superfamily.
- Subcutaneous adipose tissue biopsies were taken for fat cell metabolism studies and FTO genotype analysis
- SNP rs1421085 has a MAF of 0.41 and rs9939609 of 0.40 in our control population and the calculated ORs are 1.31 and 1.28, respectively
- common variability in FTO is associated with increased obesity risk or resistance and may in part account for differences between closely related individuals
- BMI increases associated with FTO genotypes begin in youth and are maintained throughout adulthood
- This study suggests that FTO may have an important role for gender specific development of severe obesity and insulin resistance in children.
- Expression of adipose tissue FTO mRNA is fat depot-specific and negatively correlates with measures of obesity.
- a role of the common rs9939609 SNP in FTO gene in the early stages of fat accretion in humans and disclose novel associations between this SNP and both serum visfatin and abdominal fat mass in neonates.
- Discuss Fto/Ftm gene expression regulation via CUTL1.
- revuew of genomic analyses of FTO in adipocytes and obesity-related genetic variation
- Genetic variation at the FTO locus contributes to the etiology of obesity, insulin resistance, and increased plasma leptin levels.
- variants in the FTO gene confer a similar magnitude of risk of obesity to children as to their adult counterparts and appear to have a global impact
- Neither our parental comparisons nor the use of FTO genotype as an instrumental variable, suggest that greater maternal BMI during offspring development has a marked effect on offspring fat mass at age 9-11 y.
- FTO rs9939609 SNP was associated with an increased risk for metabolic syndrome in a multi-ethnic sample.
- FTO genotype is associated with metabolic traits to an extent entirely consistent with its effect on body mass index.
- Increased BMI in morbid obesity is associated with a combination of FTO and INSIG2 SNPs.
- 15 SNPs, including rs9939609 and rs1121980, in a linkage disequilibrium (LD) block of approximately 50 kb demonstrated significant associations with obesity
- FTO is a common obesity susceptibility gene in Filipinos, with an effect size similar to that seen in samples of European origin.
- The AA-genotype of FTO rs9939609 had higher resting energy expenditure in the age-adjusted model, but the association was eliminated when adjusting for fat mass and lean body mass.
- The predominant effect of FTO variants on polycystic ovary syndrome susceptibility is probably mediated through adiposity
- Genetic variation in the FTO gene is strongly associated with obesity and BMI in the Chinese population.
- During lifestyle intervention, there was also no influence of the FTO polymorphism on changes in body weight or fat distribution.
- FTO genotype probably affects obesity via effects on food intake rather than energy expenditure.
- Two SNPs in the FTO gene (rs1421085 and rs17817449) were genotyped using the TaqMan method in a Korean population (n = 1,733). The two SNPs were then used for an association study with BMI through statistical analyses.
- FTO is a strong influential gene in polycystic ovary syndrome and correlated to various components of MetS including obesity, IFG, glucose intolerance and insulin resistance.
- The commonest known risk allele for obesity is likely to exert at least some of its effects by influencing appetite.
- FTO SNPs revealed a significant association with type 2 diabetes
- Data show that FTO single nucleotide polymorphisms are associated with obesity in the Chinese and Malay populations in Singapore.
- Data show that the association between FTO SNP rs9939609 and obesity risk may decline at older age. The variant affects circulating adiponectin and leptin levels through the changes in BMI.
- Fatness induced by FTO rs9939609 in early childhood is sustained until early adulthood, where further weight gain may occur. FTO rs9939609 may, however, also be associated with linear growth and LBM mainly through the effect on fat mass
- Study show that polymorphisms in FTO were associated with type 2 diabetes risk in the studied population.
- Association of FTO single nucleotide polymorphism(SNP) to fatness throughout the range of fatness was confirmed, explaininng the relation between the SNP and body fat distribution and decreased insulin sensitivity.
- FTO is a major risk factor for obesity (particularly class III) in the Mexican-Mestizo population, and is upregulated in subcutaneous fat tissue of obese individuals.
- FTO can catalyze the demethylation of 3-meU in ssRNA with a slightly higher efficiency over that of 3-meT in ssDNA, suggesting that methylated RNAs are the preferred substrates for FTO.
- Our results strongly suggest that the increased risk of obesity owing to genetic susceptibility by FTO variants can be blunted through physical activity
- Common genetic variants in the intron 1 of FTO gene may confer a modest susceptibility to obesity in an ethnicity-specific manner, but may be unlikely to contribute to a clinically significant diabetes risk.
- the rs9939609 A-allele is a risk factor for early onset obesity whereas its impact on weight loss or on serum levels of glucose, triglycerides and cholesterol could not be detected in our samples
- common variants in FTO and INSIG2 are nominally associated with quantitative measures of obesity
- persons carrying minor variants at rs9939609 were consuming more fat and total energy than were those not carrying such variants. They also suggest that this difference was not simply dependent on having higher average BMIs among the former group.
- The FTO variant that confers a predisposition to obesity does not appear to be involved in the regulation of energy expenditure but may have a role in the control of food intake and food choice.
- In addition to FTO and MC4R, we detected significant association of obesity with three new risk loci in NPC1 (endosomal/lysosomal Niemann-Pick C1 gene), near MAF (encoding the transcription factor c-MAF) and near PTER (phosphotriesterase-related gene).
- data support a statistically significant association of the rs9939609 polymorphism with obesity for the Uyghur population
- Independent of fatness, the A-allele of the FTO SNP appears to increase mortality of a magnitude similar to smoking, but without a particular underlying disease pattern barring an increase in the risk of diseases of the nervous system.