anti-ATP-Binding Cassette, Sub-Family A (ABC1), Member 7 (ABCA7) Antibodies

Mouse (Murine) ATP-Binding Cassette, Sub-Family A (ABC1), Member 7 (ABCA7) interaction partners

1. ABCA7 does not play a significant role in the regulation of cell proliferation or neurogenesis in the adult mouse.

2. This study demonstrated that novel mechanism underlying how dysfunctions of ABCA7 contribute to the risk for alzheimer disease.

3. ABCA7 has a role in Alzheimer amyloid processing

4. Theresults of this study suggested that ABCA7 plays a role in the regulation of Abeta (show APP Antibodies) homeostasis in the brain and that this may be related to altered phagocyte function.

5. ABCA7 may play a role in T cell proliferation and erythropoeisis in spleen

6. concluded that statins enhance macrophage phagocytosis through the SREBP-ABCA7 pathway.

7. Data suggest that extracellular helical apolipoproteins augment ABCA7-associated phagocytosis by stabilizing ABCA7, and show direct enhancement of the host defense system by HDL (show HSD11B1 Antibodies) components.

8. ABCA7 has the ability to bind apolipoproteins and promote efflux of cellular phospholipids without cholesterol, and has a possible role of ABCA7 in cellular phospholipid metabolism in peripheral tissues

9. genetic knockdown of ABCA7 in mouse peritoneal macrophages did not affect phospholipid or cholesterol efflux to apoA-I (show APOA1 Antibodies)

10. ABCA7 plays a novel role in lipid and fat metabolism

Human ATP-Binding Cassette, Sub-Family A (ABC1), Member 7 (ABCA7) interaction partners

1. The primary findings of this report are that abnormal ABCA7 exon 41 splicing is found in the brain of an individual carrying the minor C allele of rs200538373 and that rs200538373 is a functional SNP

2. rs3764650 ABCA7 is not associated with late-onset Alzheimer's disease.

3. Study uses targeted sequencing of ABCA7 to identify splicing, stop-gain and intronic risk variants for Alzheimer disease. Study shows that multiple variants in ABCA7 contribute to late-onset Alzheimer's disease risk.

4. ABCA7 PTC (show F9 Antibodies) mutations play a substantial role in early-onset Alzheimer disease, warranting genetic screening of ABCA7 in genetically unexplained patients.

5. This study demonstrated that Genetic Variations in ABCA7 Can Increase Secreted Levels of Amyloid-beta40 and Amyloid-beta42 Peptides and ABCA7 Transcription in Cell Culture Models.

6. The major difference in the pattern of lipid peaks between ABCA7 and ABCA1 (show ABCA1 Antibodies) was the high lysoPC/PC ratio of ABCA7.

7. Results confirm that ABCA7 loss of function variants are enriched in patients with Alzheimer disease and extend this finding to predicted damaging missense variants

8. A detailed clinicopathologic description of patients carrying an ABCA7 loss of function mutation: a classical Alzheimer disease phenotype, though with a striking wide onset age range, suggesting the influence of unknown modifying factors

9. Results suggested that ABCA7 genotypes contribute to the AD risk through involvement in amyloid-beta deposition on in vivo imaging, but not in tau pathology, brain atrophy, or decreased glucose metabolism

10. Common variants in ABCA7 and MS4A6A (show MS4A6A Antibodies) are associated with cortical and hippocampal atrophy.