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Formiminotransferase cyclodeaminase

formiminotransferase cyclodeaminase, FTCD
The protein encoded by this gene is a bifunctional enzyme that channels 1-carbon units from formiminoglutamate, a metabolite of the histidine degradation pathway, to the folate pool. Mutations in this gene are associated with glutamate formiminotransferase deficiency. Alternatively spliced transcript variants have been found for this gene.[provided by RefSeq, Dec 2009] (from NCBI)
Top mentioned proteins: ACID, CAN, Autoantigen, HAD, V1a
Papers on formiminotransferase cyclodeaminase
A novel "humanized mouse" model for autoimmune hepatitis and the association of gut microbiota with liver inflammation.
Wen et al., Gent, Belgium. In Hepatology, Nov 2015
Cytochrome P4502D6 is the antigenic target of anti-liver kidney microsomal type 1, and formiminotransferase cyclodeaminase is the antigenic target of anti-liver cytosol type 1.
Nicotine Dependence, Nicotine Metabolism, and the Extent of Compensation in Response to Reduced Nicotine Content Cigarettes.
Benowitz et al., San Francisco, United States. In Nicotine Tob Res, Sep 2015
RESULTS: Higher baseline FTCD predicted smoking more cigarettes per day (CPD), higher cotinine and smoke toxicant levels while smoking RNC throughout the study, with no interaction by RNC level.
Extending the limits of quantitative proteome profiling with data-independent acquisition and application to acetaminophen-treated three-dimensional liver microtissues.
Reiter et al., China. In Mol Cell Proteomics, May 2015
The adducts were identified on four mitochondrial oxidative stress related proteins (GATM, PARK7, PRDX6, and VDAC2) and two other proteins (ANXA2 and FTCD).
Using a yeast two-hybrid system to identify FTCD as a new regulator for HIF-1α in HepG2 cells.
Huang et al., Shanghai, China. In Cell Signal, 2014
We identified 53 genes, including formiminotransferase cyclodeaminase (FTCD), which was confirmed by co-immunoprecipitation.
Mood, mood regulation, and frontal systems functioning in current smokers, long-term abstinent ex-smokers, and never-smokers.
Edwards et al., Australia. In J Psychoactive Drugs, 2014
All participants completed the following measures online: Depression Anxiety Stress Scales (DASS-21), the Negative Mood Regulation (NMR) scale, the Frontal Systems Behavior Scale (FrSBe), the Fagerström Test for Cigarette Dependence (FTCD), and the Alcohol Use Disorders Identification Test (AUDIT).
Genetic predisposition and environmental danger signals initiate chronic autoimmune hepatitis driven by CD4+ T cells.
Jaeckel et al., Hannover, Germany. In Hepatology, 2013
We developed a new model of experimental murine AIH (emAIH) by a self-limited adenoviral infection with the hepatic autoantigen formiminotransferase cyclodeaminase (FTCD).
Adoptive transfer of ex vivo expanded regulatory T cells in an autoimmune hepatitis murine model restores peripheral tolerance.
Alvarez et al., Montréal, Canada. In Hepatology, 2013
An increased ectopic expression of a liver autoantigen (FTCD) in the thymus leading to reduced numbers of circulating autoreactive T cells was sufficient to prevent development of AIH in mice.
Effect of maternal folic acid supplementation on hepatic proteome in newborn piglets.
Chen et al., China. In Nutrition, 2013
FS during gestation increased the content of proteins that regulate the immune response (90-kDa heat shock protein), energy metabolism (aconitase and succinate dehydrogenase), and intermediary metabolism (formiminotransferase cyclodeaminase and abhydrolase).
The genetic landscape of mutations in Burkitt lymphoma.
Dave et al., Durham, United States. In Nat Genet, 2012
Our data implicate a number of genes in cancer for the first time, including CCT6B, SALL3, FTCD and PC.
Update and new concepts in vitamin responsive disorders of folate transport and metabolism.
Rosenblatt et al., Montréal, Canada. In J Inherit Metab Dis, 2012
Derivatives of folic acid are involved in transfer of one-carbon units in cellular metabolism, playing a role in synthesis of purines and thymidylate and in the remethylation of homocysteine to form methionine. Five inborn errors affecting folate transport and metabolism have been well studied: hereditary folate malabsorption, caused by mutations in the gene encoding the proton-coupled folate transporter (SLC46A1); glutamate formiminotransferase deficiency, caused by mutations in the FTCD gene; methylenetetrahydrofolate reductase deficiency, caused by mutations in the MTHFR gene; and functional methionine synthase deficiency, either as the result of mutations affecting methionine synthase itself (cblG, caused by mutations in the MTR gene) or affecting the accessory protein methionine synthase reductase (cblE, caused by mutations in the MTRR gene).
Upregulated and downregulated proteins in hepatocellular carcinoma: a systematic review of proteomic profiling studies.
Qin et al., Shanghai, China. In Omics, 2011
One upregulated protein, heat-shock 70-kDa protein, and four downregulated proteins, fructose-1,6-bisphosphatase 1, formiminotransferase cyclodeaminase, alcohol dehydrogenase, and fructose-bisphosphate aldolase B were identified as potential biomarkers for HCC.
Folate network genetic variation, plasma homocysteine, and global genomic methylation content: a genetic association study.
Cassano et al., Ithaca, United States. In Bmc Med Genet, 2010
Using a more stringent false discovery rate threshold, SNPs in FTCD, SLC19A1, and SLC19A3 genes remained associated with plasma homocysteine.
Functional analysis and identification of cis-regulatory elements of human chromosome 21 gene promoters.
Yaspo et al., Berlin, Germany. In Nucleic Acids Res, 2010
The FTCD promoter is activated by serum depletion according to promoter reporter assays in HEK 293 cells.
Advances in the diagnosis, pathogenesis, and management of autoimmune hepatitis.
Manns et al., Rochester, United States. In Gastroenterology, 2010
AIH has been associated with autoantibodies against members of the cytochrome P450 superfamily of enzymes, transfer RNA selenocysteine synthase, formiminotransferase cyclodeaminase, and the uridine diphosphate glucuronosyltransferases, whereas alleles such as DRB1*0301 and DRB1*0401 are genetic risk factors in white North American and northern European populations.
Forkhead box p3+ regulatory T cell underlies male resistance to experimental type 2 autoimmune hepatitis.
Alvarez et al., Montréal, Canada. In Hepatology, 2010
Autoreactive B cell response against formiminotransferase-cyclodeaminase correlated with disease activity, possibly linking B-cell autoreactivity and AIH pathogenesis
Scyl1 regulates Golgi morphology.
McPherson et al., Montréal, Canada. In Plos One, 2009
Scyl1 interacts with 58K/formiminotransferase cyclodeaminase (FTCD) and golgin p115, and is required for the maintenance of Golgi morphology
Structure of the bifunctional and Golgi-associated formiminotransferase cyclodeaminase octamer.
Quiocho et al., Houston, United States. In Embo J, 2004
Determination of the FTCD structure by X-ray crystallography and electron cryomicroscopy revealed that the eight subunits, each composed of distinct FT and CD domains, are arranged like a square doughnut
Autoimmune hepatitis: evolving concepts.
Boumpas et al., Irákleion, Greece. In Autoimmun Rev, 2004
To date, several putative hepatocellular surface antigens have been identified: P450-IID6 (recognized by the anti-LKM-1 autoantibodies) a membrane bound asialoglycoprotein receptor (a liver-specific membrane protein), a cytosolic UGA-suppressor tRNA associated protein (recognized by anti-SMA and anti-LP antibodies) and argininosuccinate lysate and formiminotransferase cyclodeaminase (recognized by ant-LC1 antibodies).
The molecular basis of glutamate formiminotransferase deficiency.
Rosenblatt et al., Montréal, Canada. In Hum Mutat, 2003
Disease-causing mutations have been identified in the FTCD gene in three patients with the putative autosomal recessive disorder glutamate formiminotransferase deficiency.
Congenital errors of folate metabolism.
Zittoun, Créteil, France. In Baillieres Clin Haematol, 1995
Glutamate formiminotransferase-cyclodeaminase deficiency is responsible for massive excretion of formiminoglutamic acid but megaloblastic anaemia is not constant.
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