ABCG1 Membrane Protein Introduction

Introduction of ABCG1

ABCG1, also known as ATP-binding cassette transporter member 1 of subfamily G, ABC8, ABC Transporter 8, WHITE1, WHT1, homolog of drosophila white, or ATP-binding cassette, sub-family G (WHITE) member 1, is a transport protein whose molecular weight is approximately 76 kDa, that is composed of 678 amino acids. In humans, it is encoded by the ABCG1 gene which is mapping at the chromosome 21q22.3. ABCG1 is a member of ATP-binding cassette (ABC) transporter and belongs to the ABCG (White) subfamily, which contains other two members, ABCG5 and ABCG8. This subfamily has been indicated to be critically implicated in the regulation of lipid-trafficking processes in macrophages, hepatocytes, and intestinal mucosa cells. ABCG1 as a product of sterol-induced genes involves in the phospholipid and cholesterol efflux.

Function of ABCG1 Membrane Protein

ABCG1 is ubiquitously expressed in various cell types including lymphocytes, myeloid cells, and endothelial cells. As a member of the ABC transporter family, it is responsible for the regulation of cellular cholesterol homeostasis. And the cholesterol homeostasis is important for the cell survival and functions. Specifically, ABCG1 has the ability to export cellular lipids to extracellular acceptors and its primary function is to efflux excess cholesterol from cells to spherical high-density lipoproteins (HDL) for reverse cholesterol transport, which is considered the only way to eliminate the cholesterol from bodies. Meanwhile, it can efflux cholesterol to low-density lipoproteins (LDL), liposomes, cyclodextrin, and export phosphatidylcholine, sphingomyelin, and oxysterols to HDL and albumin. Moreover, ABCG1 is also essential for the intracellular transport of cholesterol. As this protein is a transmembrane half-transporter, the dimerization is required for its functions. Though ABCG1 is generally acting as a homodimer, some recent studies suggested it can also form heterodimers.

Fig.1 Hypothetical model for ABCA1 and ABCG1 regulation of adipose fat storage. (Murphy, 2015)

Application of ABCG1 Membrane Protein in Literature

1. Zeng Y., et al. Dihydromyricetin ameliorates foam cell formation via LXRα-ABCA1/ABCG1-dependent cholesterol efflux in macrophages. Biomed Pharmacother. 2018, 101, 543-552. PubMed ID: 29505925
   
   

   The data from this paper suggested that the promotion of LXRα-ABCA1/ABCG1-dependent cholesterol efflux was a critical event in suppressing lipid accumulations by dihydromyricetin in the transformation of macrophage foam cells.

2. Zhao Z.W., et al. Heat shock protein 70 accelerates atherosclerosis by downregulating the expression of ABCA1 and ABCG1 through the JNK/Elk-1 pathway. Biochim Biophys Acta. 2018, 1863(8), 806-822. PubMed ID: 29678642
   
   

   Present studies had advised that heat shock protein 70 (HSP70) probably played a crucial role in cardiovascular diseases. HSP70 can promote the progression of atherosclerosis in apoE^-/- mice by inhibiting the expression of ABCA1 and ABCG1 by the JNK/Elk-1 pathway.

3. Hussain S.S., et al. Control of insulin granule formation and function by the ABC transporters ABCG1 and ABCA1 and by oxysterol binding protein OSBP. Mol Biol Cell. 2018, 29(10), 1238-1257. PubMed ID: 29540530
   
   

   This review indicated that membrane cholesterol distribution contributed to the insulin homeostasis at production, packaging, and export levels via actions of OSBP as well as ABCs G1 and A1.

4. Damen M.S.M.A., et al. Interleukin-32 upregulates the expression of ABCA1 and ABCG1 resulting in reduced intracellular lipid concentrations in primary human hepatocytes. Atherosclerosis. 2018, 271, 193-202. PubMed ID: 29524862
   
   

   Regulating IL-32 in human primary liver cell lines, HepG2 and THP-1, strongly affected the mRNA expression of ABCA1, ABCG1, LXRα and apoA1 and influenced intracellular lipid concentrations in the presence of endogenous IL-32. The data firstly showed an essential role for IL32 in cholesterol homeostases.

5. Liu X.X., et al. Kuwanon G attenuates atherosclerosis by upregulation of LXRα-ABCA1/ABCG1 and inhibition of NFκB activity in macrophages. Toxicol Appl Pharmacol. 2018, 341, 56-63. PubMed ID: 29355567
   
   

   KWG decreased intracellular lipid accumulations and mRNA levels of inflammatory cytokines in macrophages by enhancing LXRα-ABCA1/ABCG1 pathway and suppressing NFκB activation. In summary, the result highlighted that KWG can attenuate atherosclerosis by inhibiting the foam cell formation and inflammatory response.

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Reference

1. Murphy A J and Yvan-Charvet L. (2015). Adipose modulation of ABCG1 uncovers an intimate link between sphingomyelin and triglyceride storage. Diabetes. 64(3), 689-692.

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