Browse our ABCA1 Proteins (ABCA1)

Human ATP-Binding Cassette, Sub-Family A (ABC1), Member 1 (ABCA1) interaction partners

1. Hsp27 may up-regulate the expression of ABCA1 and promotes cholesterol efflux through activation of the PI3K/PKCzeta/Sp1 signal pathway in THP-1 macrophage-derived foam cells

2. the present study revealed that overexpression of GLP1R (show GLP1R Proteins) significantly reduces proliferation, migration and cytokine release in ASM (show SMPD1 Proteins) cells from COPD (show ARCN1 Proteins) patients; this involved a significant increase in ABCA1 expression levels. This provided evidence to suggest that GLP1R (show GLP1R Proteins) may be a potential therapeutic target for the treatment of COPD (show ARCN1 Proteins).

3. Abnormal expression of ABCA1 may be associated with the dysregulation of placental lipid metabolism and the occurrence or development of spontaneous deliveries.

4. apoA-II (show APOA2 Proteins) enhanced ABCA1-mediated cholesterol efflux

5. Cholesterol efflux from THP-1 macrophages is decreased in the presence of plasma obtained from humans and rats with mild hyperbilirubinemia. A direct effect of unconjugated bilirubin on cholesterol efflux was demonstrated and is associated with decreased ABCA1 protein expression.

6. identified HuR (show ELAVL1 Proteins) as a novel posttranscriptional regulator of ABCA1 expression and cellular cholesterol homeostasis, thereby opening new avenues for increasing cholesterol efflux from atherosclerotic foam macrophages and raising circulat-ing HDL (show HSD11B1 Proteins) cholesterol levels.

7. Hepatic ABCA1 deficiency results in increased hepatic triglyceride and ANGPTL3 (show ANGPTL3 Proteins) secretion, potentially underlying the elevated plasma triglyceride levels in Tangier disease patients.

8. ABCA1-derived nascent high-density lipoprotein-apolipoprotein AI (show APOA1 Proteins) and lipids metabolically segregate.

9. Hepatic free cholesterol content was significantly increased in NASH (show SAMSN1 Proteins) as compared to non-NASH (show SAMSN1 Proteins) subjects, while ABCA1 and ABCG1 (show ABCG1 Proteins) protein levels significantly decreased with NASH (show SAMSN1 Proteins) and fibrosis progression. The relative expression of miR (show MLXIP Proteins)-33a and miR (show MLXIP Proteins)-144 correlated inversely with ABCA1 but not with ABCG1 (show ABCG1 Proteins) protein levels. miR (show MLXIP Proteins)-33a/144 and their target gene ABCA1 may contribute to the pathogenesis of NASH (show SAMSN1 Proteins) in morbidly obese subjects.

10. Understanding the relationship between cholesterol and inflammation in the lung, and the role that ABC (show ABCB6 Proteins) transporters play in this may illuminate new pathways to target for the treatment of inflammatory lung diseases

Cow (Bovine) ATP-Binding Cassette, Sub-Family A (ABC1), Member 1 (ABCA1) interaction partners

1. our results highlight the importance of the LXR (show NR1H3 Proteins)/ABCA1 system in brain pericytes and suggest a new role for these cells in brain cholesterol homeostasis.

2. The expression and distribution of the bovine ABCA1 transporter using quantitative PCR and the sequencing of the entire ABCA1 coding region, including the proximal promoter region, are reported.

3. Aortic endothelial cells transcytose high-density lipoproteins by mechanisms that involve either SR-BI (show SCARB1 Proteins) or ABCG1 (show ABCG1 Proteins) but not ABCA1.

Pig (Porcine) ATP-Binding Cassette, Sub-Family A (ABC1), Member 1 (ABCA1) interaction partners

1. ABCA1 promoter variants affect transcription activity and plasma HDL (show HSD11B1 Proteins) level in pigs

2. ABCA1 was up-regulated in monocytes of hypercholesterolemic pigs via oxidized-LDL and prior to development coronary atherosclerosis.

3. Both region-specific and ubiquitous (ABCA1) phenotype changes were identified as early prelesional responses of the endothelium to hypercholesterolemia

Rabbit ATP-Binding Cassette, Sub-Family A (ABC1), Member 1 (ABCA1) interaction partners

1. CSL112 elevation of ABCA1-dependent efflux may target atherosclerotic plaque for cholesterol removal.

Mouse (Murine) ATP-Binding Cassette, Sub-Family A (ABC1), Member 1 (ABCA1) interaction partners

1. (1) ABCA1 maintains optimal hepatocyte PM FC, through intracellular FC trafficking, for efficient insulin (show INS Proteins) signaling; and (2) hepatocyte ABCA1 deletion produces a form of selective insulin (show INS Proteins) resistance so that lipogenesis is suppressed but glucose metabolism remains normal

2. demonstrates behavior deficits caused by Abca1 deletion in APP (show APP Proteins)/PS1DeltaE9 mouse model at an early stage of amyloid pathology. The basal deficits of Abca1ko, manifested by diminished cognitive performance, prevent them from coping with additional stressors, which is in part due to the impairment of neurite morphology in the hippocampus.

3. Rutaecarpine was identified to be a candidate that protected ApoE (show APOE Proteins)(-/-) mice from developing atherosclerosis through preferentially promoting activities of ABCA1 and SR-BI (show SCARB1 Proteins) within RCT (show FOXE3 Proteins).

4. Abca1 has a protective role in atherosclerosis, it exerts detrimental effects on cardiac function after myocardial infarction

5. Caveolin-1 (show CAV1 Proteins) enhances internalization and degradation of ABCA1 by its association with ABCA1

6. ABCA1-derived nascent high-density lipoprotein-apolipoprotein AI (show APOA1 Proteins) and lipids metabolically segregate.

7. an important role for hepatic ABCA1 in regulating secretory trafficking and modulating VLDL expansion during the TG accretion phase of hepatic lipoprotein particle assembly

8. These studies showed that following brain ischemia, reactive astrocytes become phagocytic and engulf debris via the ABCA1 pathway.

9. PCSK9 (show PCSK9 Proteins) plays a direct role on Abca1-mediated cholesterol efflux through a downregulation of Abca1 gene and Abca1 protein expression. This extrahepatic effect may influence relevant steps in the pathogenesis of atherosclerosis, such as foam cell formation.

10. apoA-I (show APOA1 Proteins)/ABCA1-mediated cholesterol efflux without STAT3 (show STAT3 Proteins) activation can reduce proinflammatory cytokine expression in macrophages.