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- Table of Contents
Facts about Fatty acid-binding protein, heart.
Human | |
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Gene Name: | FABP3 |
Uniprot: | P05413 |
Entrez: | 2170 |
Belongs to: |
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calycin superfamily |
FABP11; FABP3; fatty acid binding protein 11; fatty acid binding protein 3, muscle and heart (mammary-derived growthinhibitor); Fatty acid-binding protein 3; Fatty acid-binding protein 3, muscle; fatty acid-binding protein, heart; Heart-type fatty acid-binding protein; HFABP; H-FABP; H-FABPM-FABP; Mammary-derived growth inhibitor; MDGI; Muscle fatty acid-binding protein; O-FABP
Mass (kDA):
14.858 kDA
Human | |
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Location: | 1p35.2 |
Sequence: | 1; NC_000001.11 (31359595..31373618, complement) |
Cytoplasm.
The newly discovered marker FABP3 could be a game changer for diagnostics. This gene has three main applications: Diagnostics, Research and Development. This article will examine the potential of this marker in each of these areas. Let's begin with diagnosticsfirst, then move on to research and development. This article will discuss the various phases of research and development and will conclude with commercialization.
The performance of FABP3 for diagnosing Alzheimer's disease (AD) is lower than Ab42 or tau, and/or p-tau181. The reason for this variation is not entirely understood. Research suggests that this difference may be due to a lipid-related function in neurodegenerative process. In addition the increased expression of the protein is linked to an increase in Tau levels, a marker for Alzheimer's disease.
Although a-Syn has been associated with neurodegenerative diseases, it has also been linked with a-Syn accumulation. FABP3 is an intracellular carrier of lipids. Recent research has linked FABP3 to neurodegeneration and amyloid plaques. It is not clear why FABP3 is so widespread however it is crucial to remember that FABP3 is found in the CSFs of a variety of patients suffering from neurodegenerative disorders.
Clinically, FABP3 levels were inversely associated with baseline MMSE scores for the MCI cohort. However, the correlation was not statistically significant. Although FABP3 level was higher in MCI patients than healthy controls, the opposite relationship between FABP3 and the baseline MMSE score was found. In a recent study FABP3 levels were shown to be associated with a higher amount of t-tau levels in MCI patients than in the group of controls.
FABP3 is expressed in many neuronal tissues of the human body. This marker is often associated with synucleinopathies, and AD in which it is co-localized. It was not found in PD brain tissue deposits of p-aSyn. If you're interested in finding out more about this marker, read the complete review of studies published to date.
Researchers have found that people with aortic-valve disease (Aortic Stenosis) are at a higher risk for cardiac hypertrophy , if they are carriers of the FABP3 marker. This is an intriguing finding since FABP3 is vital for the maintenance of the cardiac FAO and glucose homeostasis in both pathological and physiological conditions. Research is still incomplete regarding the role FABP3 plays in the physiology of the heart.
The a-Syn gene group regulates the metabolism of cellular lipids as well as turnover of fatty acids. FABP3 is found in CSF from patients suffering from neurodegenerative diseases and has been proposed as a biomarker. Recent studies have revealed that FABP3 could be linked to the synucleinopathies the a-Syn accumulation pathway. The transporter of fatty acids is also associated with amyloid plaques.
Although FABP3 has its limitations It is nevertheless a promising biomarker to be used in clinical use. FABP3 can be used to detect disease because it alters the cell membrane fluidity. FABP3 is also linked to pathological alterations in the Ab gene and aSynuclein. Further studies are necessary to establish whether FABP3 interacts with tau protein in the brain. Patients with Parkinson's disease as well as vascular dementia also have elevated FABP3.
The following areas of study are possible using the FABP3 marker: mitochondrial processes epigenetic modifications to Blimp-1 expression, control of B-cell cycle and mitochondrial processes. It also regulates B cell differentiation. It also plays a role in the development of IgM secretion. The study suggests that FABP3 is involved in the immune system and host-defense processes. Although its future looks promising it is still a need to conduct more research.
The FABP3 gene has been recently identified as a potential biomarker in synucleinopathies. FABP3 has been linked to synucleinopathies, a-Syn accumulating, and the deregulation of the dopaminergic system. Neuropsychiatric disorders have been linked to FABP3's interaction with long-isoform D2 receptor receptor cells as well as co-localization with D2 positive cells.
PPARa is responsible for transcriptional activation in FABP genes. FABP3 interacts with PPARa to regulate its transcriptional activity. This interaction could contribute to the hypertrophic response of cells. FABP3 reduces PPARa degradation activity and boosts the luciferase activity of PPRE-driven luciferas. This interaction could be involved in the regulation of FAO or glycolysis.
FABP3 overexpression in cardiac hypertrophies helps to restore PPARa levels. FABP3's protection effects were eliminated through siRNA-based methods of knocking down PPARa. The resultant cell size is greater, with an increase of Bnp and Anp. In addition, the neutral lipid (CNP) content increases, indicating that FABP3 is responsible for the hypertrophy of the heart.
Cardiovascular disease and cardiac hypertrophy are closely connected. However, Fabp3 deficiency blunts FA boxidation , and causes the accumulation of toxic lipids inside the heart. The Fabp3 gene was identified as an indicator of metabolic activity in cardiomyopathy. Additionally, FABP3 is linked to the biosynthesis of lipids. FABP3 also plays a role in the regulation of extracellular structures.
As we have already noted that the cause of cardiac hypertrophy is the FABP3 gene. To identify this gene researchers employed a knockout strategy. Mice were fertile and F3-KO, which allowed direct observation of the effects of FABP3 on hypertrophy. The findings of the knockout strategy confirm that FABP3 is a key role in the hypertrophy of the cardiac. The effects of neurohormonal stimulation are blocked by FABP3's increased expression in cardiac hypertrophy.
The biomarker FABP3 has been in the spotlight for years. Its high affinity to fatty acids makes it simple to detect in animal and human samples. It is being increasingly used in a variety of diagnostic and therapeutic applications, including banking on blood and tissue. Commercialization is an ideal time for commercialization of the FABP3 marker. Here's a brief overview of the present status of this marker.
The FABP3 marker could be described as a protein. It is linked to CKD and may be influenced by renal damage. Although further research is required to determine the mechanism of action, it has the potential to be commercialized. In the meantime, it may be used to determine the severity of CKD and albuminuria, two important outcomes of kidney disease. The FABP3 marker is a possibility to be commercialized to help doctors determine the severity of the disease and could be a standard of practice.
The FABP3 marker isn't necessary for B-cell formation. The FABP3 marker may be a factor in dietary cholesterol intake. Further research is required to understand the role FABP3 plays in metabolic processes. The commercialization of the FABP3 marker will enable researchers to develop novel therapies for diseases that involve the immune system. It may also be useful for evaluating the health risks associated with certain fatty acid intakes.
The FABP3 marker has also been linked to podocytes inside the glomeruli. This suggests that FABP3 might be an agent in the induction of MCP-1 by kidneys. The urinary FABP3 marker was found to be associated with eGFR independently of albuminuria. Because of these findings, FABP3 might prove to be an excellent urinary DKD marker. And it is a promising way to measure the development of DKD.
The FABP3 gene encodes a protein that has numerous physiological and clinical applications. It is involved in cardiac hypertrophy and cellular metabolic balance. Additionally, FABP3 regulates cardiac metabolism and is a factor in the development of cardiovascular disease and hypertension. We examine the most recent research using the FABP3 marker. Read on for more information on its applications. While FABP3 is present in all tissues but its expression is highly variable.
A variety of studies have evaluated the utility of FABP3 in diagnostic tests. The Fabp3 marker has been demonstrated to be the most useful individual biomarker, and has the most accurate positive and negative predictive value. The Fabp3 marker was also shown to be superior in terms of diagnostic value to the AST creatine kinase metabolite, also known as the MM isoenzyme.
Studies have also revealed that FABP3 is responsible for PPARa activation, and inhibits its degrading. The capability of FABP3 to regulate PPARa levels in cardiac tissue is demonstrated through double staining using immunofluorescence. FABP3 also regulates transcriptional activity of PPARa which is a major element in the metabolic reprogramming and the reprogramming of the heart. The mechanism by which FABP3 targets PPARa is still unknown.
Another study looked at the capacity of FABP3 to regulate the PPARg activity. HCAECs that had FABP3 knockouts had lower levels of ANP proteins in the nucleus. The results indicated that FABP3 knockouts slowed the process of lipogenesis in HCAECs and are associated with increased ANP mRNA expression. Future studies are planned to study the function FABP3 is playing in imaging using cells.
PMID: 1710107 by Peeter R.A., et al. Cloning of the cDNA encoding human skeletal-muscle fatty-acid-binding protein, its peptide sequence and chromosomal localization.
PMID: 3421901 by Offner G.D., et al. Characterization and amino acid sequence of a fatty acid-binding protein from human heart.