Mouse SAA reference serum (DAGA-671)

Mouse SAA reference serum, native protein

Alternative Names
Mouse; SAA; Serum
Batch dependent - please inquire should you have specific requirements
0.1% Sodium Azide
Frozen -20°C
Antigen Description
Serum amyloid A (SAA)proteins are a family of apolipoproteins associated with high-densitylipoprotein (HDL) in plasma. Different isoforms of SAA are expressedconstitutively (constitutive SAAs) at different levels or in response toinflammatory stimuli (acute phase SAAs). These proteins are producedpredominantly by the liver. The conservation of these proteins throughoutinvertebrates and vertebrates suggests that SAAs play a highly essential rolein all animals.


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Foldable paper-based analytical device for membraneless gas-separation and determination of iodate based on fluorescence quenching of gold nanoclusters


Authors: Lert-itthiporn, Aurachat; Srikritsadawong, Pongpichet; Choengchan, Nathawut

A new design of a paper-based analytical device (PAD) for membraneless gas-separation with subsequent determination of iodate is presented. The rectangular PAD was invented as the folded pattern, where two circular reservoirs: the donor reservoir and the acceptor reservoir were situated in "a single paper" for convenient use. The hydrophobic barrier of each reservoir was easily fabricated by painting with a permanent marker. The PAD was demonstrated for the quantitative analysis of iodate, based on the fluorescence quenching of the bovine serum albumin-stabilized gold nanoclusters (BSA-AuNCs). The BSA-AuNCs were fast prepared by a microwave-assisted approach. The nanoclusters solution was applied into the acceptor reservoir, while the sample, iodide and sulfuric acid were sequentially aliquoted into the donor reservoir. After folding the PAD, the donor and the acceptor were mounted together via a two-sided mounting tape. The headspace between the two reservoirs allows membraneless gas-separation of free iodine from the donor to diffuse into the acceptor. Etching of gold core of the nanoclusters in the acceptor resulted in quenching of the red emission, was monitored by two methods, i.e. "fluorometric detection" (lambda(ex): 490 nm, lambda(em): 630 nm) and "image capture" of the acceptor under the UV irradiation by a smart phone's camera. Two calibrations were plotted accordingly to their detections and good linearities (r(2) > 0.98) were observed from 0.005 to 0.1 mmol L-1 iodate. High accuracy (mean recovery: 95.1 (+/- 4.6) %) and high precision (RSD < 3%) were obtained. The lower limits of detection were 0.005 mmol L-1 (with fluorometric detection) and 0.01 mmol L-1 (with image capture). The method was effectively applied for the measurement of iodate in iodized salts and fish sauces without prior sample pre-treatment.

ABCB1, ABCG2 and CYP2D6 polymorphism effects on disposition and response to long-acting risperidone


Authors: Ganoci, Lana; Trkulja, Vladimir; Zivkovic, Maja; Bozina, Tamara; Sagud, Marina; Lovric, Mila; Bozina, Nada

The relevance of the multidrug resistance (ABCB1) and breast cancer resistance (ABCG2) protein transporter polymorphisms for treatment with long-acting intramuscular (LAI) risperidone is largely unknown. We explored the relationship between these polymorphisms and cytochrome P450 (CYP) 2D6 genotype-predicted phenotype in their effects on drug disposition and clinical outcomes in adults with schizophrenia. In a 24-week observational study, patients initiated on LAI-risperidone (n = 101) were genotyped [enzymes (CYP2D6 dupl,*3,*4,*5,*6,*41; CYP3A4*22, CYP3A5*3), transporters (ABCG2 421C > A; ABCB1 1236C > T, 2677G > T/A, 3435C > T)] and evaluated for steady-state (weeks 6-8) serum levels of dose-corrected risperidone, 9-OH-risperidone, risperidone + 9-OH-risperidone (active moiety), and for response to treatment (PANSS, reduction vs. baseline 30% at week 12 and 45% at week 24). CYP2D6 normal/ultrarapid metabolizers (NM/UM) (vs. other) had lower risperidone (29%) and active moiety levels (24%) (9-OH-risperidone not affected). The effect on the three analytes was mild (0 to 23% reduction) in ABCG2 wild-type homozygotes and pronounced (44-55% reduction) in ABCG2 variant allele carriers. ABCG2 variant had no effect on disposition in CYP2D6 "other" phenotypes, while the effect was pronounced in CYP2D6 NM/UM subjects (31-37% reduction). ABCB1 polymorphisms had no effect on exposure to risperidone. CYP2D6 NM/UM phenotype tended to lower odds of PANSS response, ABCG2 variant was associated with 4-fold higher odds and ABCB1 (1236C > T, 2677G > T/A, 3435C > 7) overall mainly wild-type genotype was associated with around 4-fold lower odds of response. In patients treated with LAI-risperidone, CYP2D6 phenotype effect on systemic exposure is conditional on the ABCG2 421C > A polymorphism. ABCG2 and ABCB1 polymorphisms affect clinical response independently of systemic risperidone disposition.

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