Heart-type fatty acid binding protein

1G5W, 1HMR, 1HMS, 1HMT, 2HMB, 3RSW, 3WBG, 3WVM, 3WXQ, 4TJZ, 4TKB, 4TKH, 4TKJ, 4WBK, 5CE4217014077ENSG00000121769ENSMUSG00000028773P05413P11404NM_004102NM_001320996NM_010174NP_001307925NP_004093NP_034304Heart-type fatty acid binding protein (hFABP) also known as mammary-derived growth inhibitor is a protein that in humans is encoded by the FABP3 gene.1g5w: SOLUTION STRUCTURE OF HUMAN HEART-TYPE FATTY ACID BINDING PROTEIN1hmr: 1.4 ANGSTROMS STRUCTURAL STUDIES ON HUMAN MUSCLE FATTY ACID BINDING PROTEIN: BINDING INTERACTIONS WITH THREE SATURATED AND UNSATURATED C18 FATTY ACIDS1hms: 1.4 ANGSTROMS STRUCTURAL STUDIES ON HUMAN MUSCLE FATTY ACID BINDING PROTEIN: BINDING INTERACTIONS WITH THREE SATURATED AND UNSATURATED C18 FATTY ACIDS1hmt: 1.4 ANGSTROMS STRUCTURAL STUDIES ON HUMAN MUSCLE FATTY ACID BINDING PROTEIN: BINDING INTERACTIONS WITH THREE SATURATED AND UNSATURATED C18 FATTY ACIDS2hmb: THREE-DIMENSIONAL STRUCTURE OF RECOMBINANT HUMAN MUSCLE FATTY ACID-BINDING PROTEIN Heart-type fatty acid binding protein (hFABP) also known as mammary-derived growth inhibitor is a protein that in humans is encoded by the FABP3 gene. The HADHB gene is located on chromosome 1, with its specific location being 1p33-p32. The gene contains 5 exons. HADHB encodes a 51.2 kDa protein that is composed of 133 amino acids; 124 peptides have been observed through mass spectrometry data. Heart-type Fatty Acid-Binding Protein (H-FABP) is a small cytoplasmic protein (15 kDa) released from cardiac myocytes following an ischemic episode. Like the nine other distinct FABPs that have been identified, H-FABP is involved in active fatty acid metabolism where it transports fatty acids from the cell membrane to mitochondria for oxidation. See FABP3 for biochemical details. The intracellular fatty acid-binding proteins (FABPs) belongs to a multigene family. FABPs are divided into at least three distinct types, namely the hepatic-, intestinal- and cardiac-type. They form 14-15 kDa proteins and are thought to participate in the uptake, intracellular metabolism and/or transport of long-chain fatty acids. They may also be responsible in the modulation of cell growth and proliferation. Fatty acid-binding protein 3 gene contains four exons and its function is to arrest growth of mammary epithelial cells. This gene is also a candidate tumor suppressor gene for human breast cancer. FABP3 is known to interact with TNNI3K in the context of interacting with cardiac troponin I. The protein also interacts with, VPS28, KIAA159,NUP62, PLK1, UBC, and Xpo1. In HIV, a synthetic peptide corresponding to the immunosuppressive domain (amino acids 574-592) of HIV-1 gp41 downregulates the expression of fatty acid binding protein 3 (FABP3) in peptide-treated PBMCs. H-FABP is a sensitive biomarker for myocardial infarction and can be detected in the blood within one to three hours of the pain. The diagnostic potential of the biomarker H-FABP for heart injury was discovered in 1988 by Professor Jan Glatz (Maastricht, Netherlands). H-FABP is 20 times more specific to cardiac muscle than myoglobin, it is found at 10-fold lower levels in skeletal muscle than heart muscle and the amounts in the kidney, liver and small intestine are even lower again. H-FABP is recommended to be measured with troponin to identify myocardial infarction and acute coronary syndrome in patients presenting with chest pain. H-FABP measured with troponin shows increased sensitivity of 20.6% over troponin at 3–6 hours following chest pain onset. This sensitivity may be explained by the high concentration of H-FABP in myocardium compared to other tissues, the stability and solubility of H-FABP, its low molecular weight; 15kDa compared to 18, 80 and 37kDa for MYO, CK-MB and cTnT respectively, its rapid release into plasma after myocardial injury - 60 minutes after an ischemic episode, and its relative tissue specificity. Similarly this study showed that measuring H-FABP in combination with troponin increased the diagnostic accuracy and with a negative predictive value of 98% could be used to identify those not suffering from MI at the early time point of 3–6 hours post chest pain onset. The effectiveness of using the combination of H-FABP with troponin to diagnose MI within 6 hours is well reported.