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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Bile acid CoA: amino acid N-acyltransferase

The protein encoded by this gene is a liver enzyme that catalyzes the transfer of C24 bile acids from the acyl-CoA thioester to either glycine or taurine, the second step in the formation of bile acid-amino acid conjugates. The bile acid conjugates then act as a detergent in the gastrointestinal tract, which enhances lipid and fat-soluble vitamin absorption. Defects in this gene are a cause of familial hypercholanemia (FHCA). Two transcript variants encoding the same protein have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: UCP1, CAN, HAD, Insulin, fibrillin-1
Papers using BAT antibodies
An Analysis of Pressure-Volume Characteristics of the Lungs.
Whitsett Jeffrey A., In PLoS ONE, 1963
... mice to produce BAT-gal transgenic ...
Papers on BAT
Effects of dietary phosphate on glucose and lipid metabolism.
Taketani et al., Tokushima, Japan. In Am J Physiol Endocrinol Metab, Feb 2016
On the other hand, uncoupling protein 1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator alpha (PGC1α) expression were significantly increased in the brown adipose tissue (BAT) of HP group.
mTORC2 sustains thermogenesis via Akt-induced glucose uptake and glycolysis in brown adipose tissue.
Hall et al., Basel, Switzerland. In Embo Mol Med, Feb 2016
UNASSIGNED: Activation of non-shivering thermogenesis (NST) in brown adipose tissue (BAT) has been proposed as an anti-obesity treatment.
Endocannabinoid regulation in white and brown adipose tissue following thermogenic activation.
Di Marzo et al., Hamburg, Germany. In J Lipid Res, Feb 2016
CB1 agonists and blockers have been reported to influence the thermogenic function of white and brown adipose tissue (WAT and BAT), affecting body weight through the inhibition and stimulation of energy expenditure, respectively.
Autophagy in the CNS and Periphery Coordinate Lipophagy and Lipolysis in the Brown Adipose Tissue and Liver.
Singh et al., United States. In Cell Metab, Feb 2016
Here, we show that cold induces autophagy in proopiomelanocortin (POMC) neurons and activates lipophagy in brown adipose tissue (BAT) and liver in mice.
Nanoparticle-allergen interactions mediate human allergic responses: protein corona characterization and cellular responses.
Duschl et al., Salzburg, Austria. In Part Fibre Toxicol, Dec 2015
Differences in the activation of human basophil cells derived from birch/grass pollen- and house dust mite-allergic patients in response to free allergen and AuNP-allergen conjugates were determined using the basophil activation assay (BAT).
Thyroid Hormone Activates Brown Adipose Tissue and Increases Non-Shivering Thermogenesis - A Cohort Study in a Group of Thyroid Carcinoma Patients.
van Marken Lichtenbelt et al., Maastricht, Netherlands. In Plos One, Dec 2015
BACKGROUND/OBJECTIVES: Thyroid hormone receptors are present on brown adipose tissue (BAT), indicating a role for thyroid hormone in the regulation of BAT activation.
Brown and Beige Fat: Physiological Roles beyond Heat Generation.
Seale et al., San Francisco, United States. In Cell Metab, Nov 2015
Since brown adipose tissue (BAT) dissipates energy through UCP1, BAT has garnered attention as a therapeutic intervention for obesity and metabolic diseases including type 2 diabetes.
The Bile Acid Chenodeoxycholic Acid Increases Human Brown Adipose Tissue Activity.
Schrauwen et al., Maastricht, Netherlands. In Cell Metab, Oct 2015
The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans.
Browning of Subcutaneous White Adipose Tissue in Humans after Severe Adrenergic Stress.
Herndon et al., Galveston, United States. In Cell Metab, Sep 2015
Since the presence of brown adipose tissue (BAT) was confirmed in adult humans, BAT has become a therapeutic target for obesity and insulin resistance.
Short-term cold acclimation improves insulin sensitivity in patients with type 2 diabetes mellitus.
Schrauwen et al., Maastricht, Netherlands. In Nat Med, Aug 2015
Cold exposure may be a potential therapy for diabetes by increasing brown adipose tissue (BAT) mass and activity.
Review: Miglitol has potential as a therapeutic drug against obesity.
Hosoi et al., Ayabe, Japan. In Nutr Metab (lond), 2014
Miglitol has been shown to inhibit adipogenesis of white adipocytes in vitro, activate brown adipose tissue (BAT) in mice, influence bile acid metabolism in mice, and regulate the secretion of incretin hormones in humans.
Capsaicin and Related Food Ingredients Reducing Body Fat Through the Activation of TRP and Brown Fat Thermogenesis.
Saito, Sapporo, Japan. In Adv Food Nutr Res, 2014
Brown adipose tissue (BAT) is a site of sympathetically activated adaptive nonshivering thermogenesis, thereby being involved in the regulation of energy balance and body fatness.
Hypothalamic control of brown adipose tissue thermogenesis.
Richard et al., Québec, Canada. In Front Syst Neurosci, 2014
It has long been known, in large part from animal studies, that the control of brown adipose tissue (BAT) thermogenesis is insured by the central nervous system (CNS), which integrates several stimuli in order to control BAT activation through the sympathetic nervous system (SNS).
Bioengineering Beige Adipose Tissue Therapeutics.
Stahl et al., Berkeley, United States. In Front Endocrinol (lausanne), 2014
The recent discovery that brown adipose tissue (BAT)-derived secreted factors positively alter whole body metabolism further expands potential benefits of brown or beige/brite adipose expansion.
Unlock the Thermogenic Potential of Adipose Tissue: Pharmacological Modulation and Implications for Treatment of Diabetes and Obesity.
Bartesaghi et al., Mölndal, Sweden. In Front Endocrinol (lausanne), 2014
Brown adipose tissue (BAT) is considered an interesting target organ for the treatment of metabolic disease due to its high metabolic capacity.
Diagnosis in bile acid-CoA: amino acid N-acyltransferase deficiency.
Knisely et al., London, United Kingdom. In World J Gastroenterol, 2012
Case Report: mmunostaining may facilitate diagnosis in bile-acid amidation defects in bile acid-CoA: amino acid N-acyltransferase deficiency.
Retinoid X receptor alpha participation in dexamethasone-induced rat bile acid coenzyme A-amino acid N-acyltransferase expression in septic liver.
Hsu et al., Kao-hsiung, Taiwan. In Shock, 2009
Dex restored the expression of rBAT in septic rats by enhancing RXR[alpha], a process that might explain the mechanism underlying Dex's anticholestatic effect.
High-resolution mass spectrometry analysis of protein oxidations and resultant loss of function.
Renfrow et al., Birmingham, United States. In Biochem Soc Trans, 2008
Data show that dose-response inactivation by 4HNE (4-hydroxynonenal) of hBAT (human bile acid CoA:amino acid N-acyltransferase) and CKBB (cytosolic brain isoform of creatine kinase) is associated with site-specific modifications.
Role of retinoid-X receptor-alpha in the suppression of rat bile acid coenzyme A-amino acid N-acyltransferase in liver during sepsis.
Hsu et al., Kao-hsiung, Taiwan. In Shock, 2007
mechanisms of RXR-alpha-mediated BAAT regulation during polymicrobial sepsis
Genetic polymorphism of bile acid CoA: amino acid N-acyltransferase in Japanese individuals.
Azuma et al., Ōsaka, Japan. In Drug Metab Pharmacokinet, 2007
identification of 3 novel SNPs, 147C>T in exon 2 (silent), 602G>C in exon 3 (Arg201Pro) & 1134C>T in exon 4 (silent), in the BAAT gene by resequencing the entire coding region and the exon-intron junctions of 100 Japanese individuals
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