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Gene Symbol |
ANGPTL4 |
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Aliases |
ARP4, FIAF, HARP, HFARP, NL2, PGAR, TGQTL, UNQ171, pp1158 |
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Entrez Gene ID |
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Gene Name |
Angiopoietin like 4 |
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Chromosomal Location |
19p13.2 |
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HGNC ID |
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Summary |
This gene encodes a glycosylated, secreted protein containing a C-terminal fibrinogen domain. The encoded protein is induced by peroxisome proliferation activators and functions as a serum hormone that regulates glucose homeostasis, lipid metabolism, and insulin sensitivity. This protein can also act as an apoptosis survival factor for vascular endothelial cells and can prevent metastasis by inhibiting vascular growth and tumor cell invasion. The C-terminal domain may be proteolytically-cleaved from the full-length secreted protein. Decreased expression of this gene has been associated with type 2 diabetes. Alternative splicing results in multiple transcript variants. This gene was previously referred to as ANGPTL2 but has been renamed ANGPTL4. [provided by RefSeq, Sep 2013]
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RefSeq DNA |
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RefSeq mRNA |
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e!Ensembl
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| Protein Information |
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Protein Name |
Angiopoietin-related protein 4, PPARG angiopoietin related protein, fasting-induced adipose factor, hepatic angiopoietin-related protein, hepatic fibrinogen/angiopoietin-related protein, peroxisome proliferator-activated receptor (PPAR) gamma induced angiopoietin-related protein |
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Function |
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Mediates inactivation of the lipoprotein lipase LPL, and thereby plays a role in the regulation of triglyceride clearance from the blood serum and in lipid metabolism (PubMed:19270337, PubMed:21398697, PubMed:27929370, PubMed:29899144). May also play a role in regulating glucose homeostasis and insulin sensitivity (Probable). Inhibits proliferation, migration, and tubule formation of endothelial cells and reduces vascular leakage (PubMed:14583458, PubMed:17068295). Upon heterologous expression, inhibits the adhesion of endothelial cell to the extracellular matrix (ECM), and inhibits the reorganization of the actin cytoskeleton, formation of actin stress fibers and focal adhesions in endothelial cells that have adhered to ANGPTL4-containing ECM (in vitro) (PubMed:17068295). Depending on context, may modulate tumor-related angiogenesis (By similarity). .; [ANGPTL4 N-terminal chain]: Mediates inactivation of the lipoprotein lipase LPL, and thereby plays an important role in the regulation of triglyceride clearance from the blood serum and in lipid metabolism (PubMed:19270337, PubMed:21398697, PubMed:27929370, PubMed:29899144). Has higher activity in LPL inactivation than the uncleaved protein (PubMed:19270337, PubMed:21398697). |
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UniProt |
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PDB |
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Interactions |
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| STRING |
MINT |
IntAct |
| ENSP00000288266 |
Q9UKG1 |
Q9UKG1 |
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View interactions
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Associated Diseases
| Disease group | Disease Name | References |
| Cardiovascular Diseases |
| Arteriosclerosis |
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| Ischemic Cardiomyopathy |
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| Myocardial Infarction |
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| Digestive System Diseases |
| Fatty Liver |
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| Endocrine System Diseases |
| PCOS |
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| Neoplasms |
| Breast Cancer |
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| Carcinoma |
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| Cancer Metastasis |
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| Anaplastic Carcinoma |
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| Nutritional and Metabolic Diseases |
| Obesity |
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| Dyslipidemias |
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References |
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| Gunes Meryem, Bukan Neslihan |
| a Department of Medical Biochemistry, Faculty of Health Science , Gazi University , Besevler , Ankara , Turkey and.| b Department of Medical Biochemistry, Medical Faculty , Gazi University , Besevler , Ankara , Turkey. |
| Gynecol Endocrinol. 2015;31(11):903-6. doi: 10.3109/09513590.2015.1068285. Epub |
Abstract
The pathogenesis of polycystic ovary syndrome (PCOS) and obesity is not clarified yet. But some parameters such as neuropeptide Y (NPY), angiopoietin-like protein (Angptl-4), omentin-1 are thought to be involved in this pathogenesis. In this study, we aimed to show possible effects of NPY, Angptl-4, omentin-1 throughout clinical parameters and hormones. Patients were divided into three groups. Group I; healthy volunteers, Group II; non-obese women with PCOS and group III; obese women with PCOS. Serum NPY, Angptl-4, free testosterone, total testosterone, luteinize hormone, sex hormone binding globulin, estradiol, dehydroepiandrosterone sulfate, androstenedione, triglycerides and low density lipoprotein cholesterol levels and HOMA-IR, Ferriman-Galwey scores were significantly higher in group II when compared with group I and similarly in group III when compared with group II (p < 0.005). While comparing all PCOS patients (obese + non-obese) with healthy volunteers, omentin-1 and high density lipoprotein cholesterol levels were significantly low in PCOS group (p < 0.005). As a result of this study, both in the obese and non-obese PCOS patients, there was a significant increase in levels of NPY and Angptl-4 and a significant decline in omentin-1 when compared to healthy subjects. In conclusion, insulin resistance in PCOS patients may be related to the differences of NPY, Angptl-4 and omentin-1 levels and the effects of these differences on metabolic pathways. |
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