ARV1 Membrane Protein Introduction

Introduction of ARV1

Acyl-coA acyltransferase-related enzyme 2 required for viability is a protein that in humans is encoded by the ARV1 gene. ARV1 is ubiquitously expressed in higher eukaryotes, and in Saccharomyces cerevisiae yeast. It is a transmembrane protein of the endoplasmic reticulum (ER) that is conserved between plants, yeast, and mammals. ARV1 protein contains a conserved N-terminal zinc ribbon motif known as the ‘Arv1 homology domain' (AHD) which is followed by several transmembrane regions. The predicted and experimentally defined topology of the yeast Arv1p indicates the AHD is cytosolic.

Basic Information of ARV1
Protein Name ARV1
Gene Name ARV1
Aliases hARV1, HT035
Organism Homo sapiens (Human)
UniProt ID Q9H2C2
Transmembrane Times 3
Length (aa) 271

Function of ARV1 Membrane Protein

ARV1 has been revealed to function a role as a putative lipid transporter. It was first characterized in yeast ARV1-mutants, showing changes in intracellular cholesterol distribution and abnormal phospholipid, sphingolipid, and glycosylphosphatidylinositol-metabolism. ARV1 knockout mice displayed a striking metabolic phenotype including major reductions in white adipose tissue mass, improved glucose tolerance, and increased energy expenditure. These findings suggest an important role for ARV1 in fatty acid homeostasis. Besides, ARV1 is also involved in the regulation of body composition and energy expenditure in mice. Antisense oligonucleotide targeting ARV1 transcripts causes accumulation of cholesterol in the endoplasmic reticulum at the expense of cholesterol levels in the plasma membrane. Germline deletion of ARV1 in mice leads to a lean phenotype with increased energy expenditure and improved glucose tolerance.

ARV1 Membrane Protein Introduction Fig.1 Experimentally determined membrane topology of ARV1.

Application of ARV1 Membrane Protein in Literature

  1. Gallo-Ebert C., et al. Mice lacking ARV1 have reduced signs of metabolic syndrome and non-alcoholic fatty liver disease. J Biol Chem. 2018, 293(16): 5956-5974. PubMed ID: 29491146

    This article hypothesized that ARV1 may be a key regulator for initiating events associated with the progression of diseases associated with MetS and NAFLD.

  2. Palmer E.E., et al. Neuronal deficiency of ARV1 causes an autosomal recessive epileptic encephalopathy. Hum Mol Genet. 2016, 25(14): 3042-3054. PubMed ID: 27270415

    This study suggested lacking ARV1 as a cause of autosomal recessive epileptic encephalopathy.

  3. Sundvold H., et al. Arv1 promotes cell division by recruiting IQGAP1 and myosin to the cleavage furrow. Cell Cycle. 2016, 15(5): 628-643. PubMed ID: 27104745

    Authors identified a novel function for Arv1 in regulation of cell division through promotion of the contractile actomyosin ring, which was independent of its lipid transporter activity.

  4. Ikeda A., et al. Complementation analysis reveals a potential role of human ARV1 in GPI anchor biosynthesis. Yeast. 2016, 33(2): 37-42. PubMed ID: 26460143

    This investigation indicated that Arv1 function in GPI biosynthesis may be conserved in all eukaryotes, from yeast to humans.

  5. Lagor W.R., et al. Deletion of murine Arv1 results in a lean phenotype with increased energy expenditure. Nutr Diabetes. 2015, 5: e181. PubMed ID: 26479315

    Authors indicated ARV1 as an important regulator in mammalian lipid metabolism and whole-body energy homeostasis.

ARV1 Preparation Options

To obtain the soluble and functional target protein, the versatile Magic™ membrane protein production platform in Creative Biolabs enables many flexible options, from which you can always find a better match for your particular project. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-ARV1 antibody development services.

Creative Biolabs' skillful scientists are glad to leverage our expertise and advanced technologies to help you with the member protein research. If you are interested, please feel free to contact us for more details.

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