anti-ATP-Binding Cassette, Sub-Family A (ABC1), Member 2 (ABCA2) Antibodies

Human ATP-Binding Cassette, Sub-Family A (ABC1), Member 2 (ABCA2) interaction partners

1. The analyses results suggested ABCA2 mRNA expression was upregulated significantly in AD compared with controls in all datasets.

2. Our findings indicate a considerable and direct relationship between mRNA expression levels of ABCA2, ABCA3, MDR1, and MRP1 genes and positive minimal residual disease (MRD) measured after one year of treatment.

3. Down-regulation of the ATP-binding cassette transporter 2 (Abca2) reduces amyloid-beta production by altering Nicastrin maturation and intracellular localization.

4. SLC2A1/GLUT1, SLC1A3/EAAT1, and SLC1A2/EAAT2 were the main SLC proteins whereas ABCG2/BCRP, ABCB1/MDR1, ABCA2 and ABCA8 were the main ABC quantified in isolated brain microvessels

5. A possible biochemical mechanism links ABCA2 expression, amyloid precursor protein processing, and Alzheimer's disease.

6. we demonstrate that ABCA2-deficiency inhibits prostate tumor metastasis in vivo and decreases chemotactic potential of cells

7. roles for this largest known ABC protein in neural transmembrane lipid export

8. Reciprocal regulation of expression of the ABCA2 promoter by the early growth response-1 and Sp-family transcription factors.

9. It is likely that expression of ABCA2 by two independent promoters constitutes locus of regulation controlling expression of the protein to meet requirements in different tissues.

10. Increased expression of ABCA2 may be causally linked with altered expression of genes associated with the pathogenesis of Alzheimer disease.

11. Among the 45 ABCA2 single nucleotide polymorphisms(SNPs) we tested, one synonymous SNP (rs908832) was found significantly associated with AD in both samples.

12. the expression patterns of ABCA2 in combination with other markers showed phenotypic heterogeneity in schwannomas

13. Data suggest that ABCA2 may exert population-dependent effects on the genetic risk for sporadic Alzheimer's disease and support a role of ABC lipid transporters in the pathogenesis of this disease.

14. No association of ABCA2 Single Nucleotide Polymorphism on chromosome 9 with Alzheimer's disease.

Mouse (Murine) ATP-Binding Cassette, Sub-Family A (ABC1), Member 2 (ABCA2) interaction partners

1. Study suggests that ABCA2 modulation of sphingolipid metabolism activates a signaling pathway that regulates amyloid precursor protein transcription

2. control of ABCA2 expression level may be a key locus of regulation for esterification of plasma membrane-derived cholesterol through modulation of sphingolipid metabolism.

3. Data from knockout mice suggest that Abca2 functions in penile erection; Abca2 knockout mice are more susceptible to estrogen-induced convulsions than wildtype mice; Abca2 appears to be involved in biotransformation of therapeutic estrogens.

4. Lack of ABCA2 generates abnormalities in intracellular lipid distribution/trafficking in macrophages, increasing susceptibility to apoptosis in response to oxidized lipids and reduced atherosclerotic lesion development in LDL receptor knockout mice.

5. The ATP-binding cassette transporter-2 (ABCA2) is a key regulator of cholesterol homeostasis and low-density lipoprotein receptor metabolism in neuronal cells.

6. Down-regulation of the ATP-binding cassette transporter 2 (Abca2) reduces amyloid-beta production by altering Nicastrin maturation and intracellular localization.

7. ABC-me is a novel gene that determines the ability to tolerate cardiac ischemia/reperfusion.

8. ABCA2 has a role in myelin compaction in spinal cord and cerebrum, and in phenotypic tremor

9. ABCA2 is expressed in non-myelin-forming as well as in myelin-forming Schwann cells. ABCA2 may be involved in transport of a substance associated with cellular maturation rather than initial myelin formation in both types of Schwann cells.

10. ABCA2 is involved in the intracellular metabolism of sphingolipids in the brain, particularly SM and gangliosides in oligodendrocytes and certain neurons.