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The protein encoded by FADS2 is a member of the fatty acid desaturase (FADS) gene family. Additionally we are shipping FADS2 Kits (27) and FADS2 Proteins (10) and many more products for this protein.
Showing 10 out of 50 products:
these results implicate that Z-FADS, the sole fatty acid desaturase (show SCD Antibodies) ever been identified in zebrafish, can serve as a universal fatty acid desaturase (show SCD Antibodies) during lipogenesis.
Data (including data from studies using knockout mice) suggest that immunomodulatory effects of dietary omega-6 vs. omega-3 fatty acids are due, in part, to interconversion of the various unsaturated fatty acids consumed/administered; thus, delta-6 desaturase plays role in immunomodulatory effects of dietary unsaturated fatty acids.
Using a sample of 534 twins, study observed a trend in the moderation of brain fatty acid effects on IQ by FADS2 variation. Using of publicly available gene expression databases from both humans and mice, showed that FADS2 variants also correlate with FADS1 (show FADS1 Antibodies) brain expression
differential PUFA profiles between HET mice and human FADS SNPs suggest low expression of both FADS1 (show FADS1 Antibodies) and 2 genes in human minor haplotypes.
FADS2 deficient mice are obesity resistant.
knockdown of Elovl5 (show ELOVL5 Antibodies), Fads1 (show FADS1 Antibodies), or Fads2 decreased the level of Mead acid.
D6D activity is upregulated during melanoma and lung tumor growth and that suppressing D6D activity, either by RNAi knockdown or a specific D6D inhibitor, dramatically reduces tumor growth.
Results suggest that Fads2 is essential for spermatogenesis; Fads2-/- knockout mice develop docosahexaenoic acid deficiency and acrosome biogenesis is halted after release of proacrosomal granules.
analysis of macrophage cholesterol biosynthesis and decreased cellular paraoxonase 2 (PON2 (show PON2 Antibodies)) expression in Delta6-desaturase knockout (6-DS KO) mice
We created D6D-null mice (-/-), which enabled us to study highly unsaturated fatty acid deficiency without depleting their precursors.
methylation silencing of liver Fads2 expression and changes in liver fatty acids may contribute to the pathology of hyperhomocysteinemia.
Results show that preterm infants had as high D6D activity as term infants at birth. Thus, they have an ability to produce AA and DHA from precursor polyunsaturated fatty acids. After birth, D6D activity declined rapidly during first month.
The majority of CpG sites (117 out of 136, 86%) exhibited high levels of methylation with the greatest variability observed at three key regulatory regions-the promoter regions for FADS1 (show FADS1 Antibodies) and FADS2 and a putative enhancer site between the two genes.
FADS1 (show FADS1 Antibodies) rs174547 and FADS2 rs2727270 genotypes were significantly correlated with decreased HDL (show HSD11B1 Antibodies)-C concentrations, and D5D (show FADS1 Antibodies) /D6D activities as estimated as 20:4(n-6)/20:3 (n-6) and 18:3 (n-6)/18:2 (n-6) in a linear pattern in patients with type 2 diabetes
These data indicate that delta-6 desaturase activity might not be essential for the distinct effects of LA and ALA on NFkappaB activity.
SNP (rs1535) and 2-locus haplotypes (rs3834458-rs1535, rs1535-rs174575) in the FADS2 gene were associated with concentrations of gamma-linoleic acid (GLA (show NAT8 Antibodies)) and arachidonic acid (AA) in breast milk; the 3-locus haplotype rs3834458-rs1535-rs174575, significantly affected concentrations of GLA (show NAT8 Antibodies) but not AA
This study showed associations between FADS 1 (show FADS1 Antibodies)/2 SNPs and cognitive performance. rs1535 minor allele homozygosity and rs174448 major allele carriage associated with improved cognitive performance in 8- to 11-y-old boys but not in girls, thereby counteracting existing sex differences.
This study demonstrates for the first time that genetic variation in FADS2 is not only associated with the activity of the desaturation-elongation pathway, but also whole-body fat oxidation.
Our results demonstrate that FADS1 (show FADS1 Antibodies)-FADS2 are susceptibility genes for PCOS.
Single nucleotide polymorphisms in FADS gene (particularly rs174537) associate with plasma fatty acids and desaturase levels in patients with both type 2 diabetes and coronary artery disease.
The protein encoded by this gene is a member of the fatty acid desaturase (FADS) gene family. Desaturase enzymes regulate unsaturation of fatty acids through the introduction of double bonds between defined carbons of the fatty acyl chain. FADS family members are considered fusion products composed of an N-terminal cytochrome b5-like domain and a C-terminal multiple membrane-spanning desaturase portion, both of which are characterized by conserved histidine motifs. This gene is clustered with family members FADS1 and FADS2 at 11q12-q13.1\; this cluster is thought to have arisen evolutionarily from gene duplication based on its similar exon/intron organization.
D5D/D6D fatty acid desaturase
, delta(5)/Delta(6) fatty acid desaturase
, delta-5/Delta-6 fatty acid desaturase
, delta-6 fatty acyl desaturase
, delta(6) desaturase
, delta(6) fatty acid desaturase
, delta-6 desaturase
, delta-6 fatty acid desaturase
, linoleoyl-CoA desaturase (delta-6-desaturase)-like 2
, fatty acid desaturase 6