Human ABCA7 (ATP-binding cassette sub-family A member 7) ELISA Kit (DEIA-FN08)

Regulatory status: For research use only, not for use in diagnostic procedures.

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serum, plasma, cell culture supernatants, tissue homogenate
Species Reactivity
Intended Use
For quantitative detection of Human ABCA7 (ATP-binding cassette sub-family A member 7) in serum, plasma, tissue homogenates and other biological fluids.
Contents of Kit
1. 96-well strip plate (Dismountable), 1 plate
2. Lyophilized Standard, 2 vials
3. Sample/Standard dilution buffer, 20 mL
4. Biotin-detection antibody (Concentrated), 120 uL
5. Antibody dilution buffer, 10 mL
6. HRP-Streptavidin Conjugate(SABC), 120 uL
7. SABC dilution buffer, 10 mL
8. TMB substrate, 10 mL
9. Stop solution, 10 mL
10. Wash buffer (25X), 30 mL
11. Plate Sealer, 5 pieces
12. Product Manual, 1 copy
Store the unopened product at 2 - 8 °C. Do not use past expiration date.
Intra-Assay: CV<8%
Inter-Assay: CV<10%
Detection Range
0.156-10 ng/mL
0.094 ng/mL
Standard Curve


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Updated Meta-Analysis of BIN1, CR1, MS4A6A, CLU, and ABCA7 Variants in Alzheimer's Disease


Authors: Figueiredo Almeida, Jucimara Ferreira; dos Santos, Ligia Ramos; Trancozo, Maira; de Paula, Flavia

Genome-wide association studies (GWAS) have associated several genetic variants with late-onset Alzheimer's disease (LOAD), a neurodegenerative disease. Among those, rs3764650 ABCA7, rs6656401 CR1, and rs744373 BIN1 were associated as risk factors for LOAD, while rs11136000 CLU and rs610932 MS4A6A were protective. Recently, several case-control studies have investigated the association of these polymorphisms with AD. However, not all meta-analyses analyzed these variants across different ethnic groups. Therefore, we performed an updated meta-analysis of rs3764650 ABCA7, rs6656401 CR1, rs744373 BIN1, rs11136000 CLU, and rs610932 MS4A6A variants associated with LOAD, considering different ethnic populations. We utilized samples from 38 articles, comprising a total of 24,771 patients and 35,324 controls obtained through the PubMed database. Odds ratios (ORs) with 95% confidence intervals (CI) for polymorphisms were calculated by allelic comparison as an additive genetic model. We validated the risk for LOAD with BIN1 (rs744373), CR1 (rs6656401), and ABCA7 (rs376465), as well as the protective association for MS4A6A (rs610932) and CLU (rs11136000) variants.

Expression of Novel Alzheimer's Disease Risk Genes in Control and Alzheimer's Disease Brains


Authors: Karch, Celeste M.; Jeng, Amanda T.; Nowotny, Petra; Cady, Janet; Cruchaga, Carlos; Goate, Alison M.

Late onset Alzheimer's disease (LOAD) etiology is influenced by complex interactions between genetic and environmental risk factors. Large-scale genome wide association studies (GWAS) for LOAD have identified 10 novel risk genes: ABCA7, BIN1, CD2AP, CD33, CLU, CR1, EPHA1, MS4A6A, MS4A6E, and PICALM. We sought to measure the influence of GWAS single nucleotide polymorphisms (SNPs) and gene expression levels on clinical and pathological measures of AD in brain tissue from the parietal lobe of AD cases and age-matched, cognitively normal controls. We found that ABCA7, CD33, and CR1 expression levels were associated with clinical dementia rating (CDR), with higher expression being associated with more advanced cognitive decline. BIN1 expression levels were associated with disease progression, where higher expression was associated with a delayed age at onset. CD33, CLU, and CR1 expression levels were associated with disease status, where elevated expression levels were associated with AD. Additionally, MS4A6A expression levels were associated with Braak tangle and Braak plaque scores, with elevated expression levels being associated with more advanced brain pathology. We failed to detect an association between GWAS SNPs and gene expression levels in our brain series. The minor allele of rs3764650 in ABCA7 is associated with age at onset and disease duration, and the minor allele of rs670139 in MS4A6E was associated with Braak tangle and Braak plaque score. These findings suggest that expression of some GWAS genes, namely ABCA7, BIN1, CD33, CLU, CR1 and the MS4A family, are altered in AD brains.

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