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Aldehyde dehydrogenase 4 family, member A1

ALDH4, ALDH4A1, aldehyde dehydrogenase 4A1
This protein belongs to the aldehyde dehydrogenase family of proteins. This enzyme is a mitochondrial matrix NAD-dependent dehydrogenase which catalyzes the second step of the proline degradation pathway, converting pyrroline-5-carboxylate to glutamate. Deficiency of this enzyme is associated with type II hyperprolinemia, an autosomal recessive disorder characterized by accumulation of delta-1-pyrroline-5-carboxylate (P5C) and proline. Alternatively spliced transcript variants encoding different isoforms have been identified for this gene. [provided by RefSeq, Jun 2009] (from NCBI)
Top mentioned proteins: Aldehyde Dehydrogenase, ACID, ALD3, Raldh3, fibrillin-1
Papers on ALDH4
SAXS fingerprints of aldehyde dehydrogenase oligomers.
Tanner, Columbia, United States. In Data Brief, Dec 2015
Mutations in genes encoding ALDHs cause metabolic disorders, including alcohol flush reaction (ALDH2), Sjögren-Larsson syndrome (ALDH3A2), hyperprolinemia type II (ALDH4A1), γ-hydroxybutyric aciduria (ALDH5A1), methylmalonic aciduria (ALDH6A1), pyridoxine dependent epilepsy (ALDH7A1), and hyperammonemia (ALDH18A1).
Structural Basis of Substrate Recognition by Aldehyde Dehydrogenase 7A1.
Tanner et al., Columbia, United States. In Biochemistry, Oct 2015
This binding mode resembles that of glutamate bound to the proline catabolic enzyme ALDH4A1.
Discovery of a series of aromatic lactones as ALDH1/2-directed inhibitors.
Hurley et al., Indianapolis, United States. In Chem Biol Interact, Jul 2015
Single concentration measurements at 10μM compound were performed using ALDH1A1, ALDH1A2, ALDH1A3, ALDH2, ALDH1B1, ALDH3A1, ALDH4A1, and/or ALDH5A1 to determine the selectivity of these 12 compounds toward ALDH2.
N,N-diethylaminobenzaldehyde (DEAB) as a substrate and mechanism-based inhibitor for human ALDH isoenzymes.
Hurley et al., Indianapolis, United States. In Chem Biol Interact, Jul 2015
We sought to determine the selectivity of DEAB toward ALDH1A1, ALDH1A2, ALDH1A3, ALDH1B1, ALDH1L1, ALDH2, ALDH3A1, ALDH4A1 and ALDH5A1 isoenzymes and determine the mechanism by which DEAB exerts its inhibitory action.
Target discovery of acivicin in cancer cells elucidates its mechanism of growth inhibition†Electronic supplementary information (ESI) available: Synthesis, cloning, protein expression, purification and biochemical assays. See DOI: 10.1039/c4sc02339k.
Sieber et al., Garching bei München, Germany. In Chem Sci, 2015
Further in depth target validation confirmed that acivicin inhibits ALDH4A1 activity by binding to the catalytic site.
In Vivo Exposures to Particulate Matter Collected from Saudi Arabia or Nickel Chloride Display Similar Dysregulation of Metabolic Syndrome Genes.
Costa et al., New York City, United States. In J Toxicol Environ Health A, 2014
Many of the 107 genes are involved in metabolic syndrome and include ALDH4A1, BCO2, CYP1A, CYP2U, TOP2A.
Long-term clinical outcome, therapy and mild mitochondrial dysfunction in hyperprolinemia.
Morava et al., Nijmegen, Netherlands. In J Inherit Metab Dis, 2014
Due to the mitochondrial localization of both ALDH4A1 and PRODH mitochondrial enzyme complex activity was evaluated and oxygen consumption was measured to assess ATP production in patient-fibroblasts.
Structural studies of yeast Δ(1)-pyrroline-5-carboxylate dehydrogenase (ALDH4A1): active site flexibility and oligomeric state.
Tanner et al., Columbia, United States. In Biochemistry, 2014
The proline catabolic enzyme Δ(1)-pyrroline-5-carboxylate dehydrogenase (ALDH4A1) catalyzes the NAD(+)-dependent oxidation of γ-glutamate semialdehyde to l-glutamate.
Proteomic investigation of cultivated fibroblasts from patients with mitochondrial short-chain acyl-CoA dehydrogenase deficiency.
Palmfeldt et al., Århus, Denmark. In Mol Genet Metab, 2014
Three proteins were found significantly regulated in both patient groups: adenylate kinase 4 (AK4), nucleoside diphosphate kinase A (NME1) and aldehyde dehydrogenase family 4 member A1 (ALDH4A1).
Effect of zinc oxide nanomaterials-induced oxidative stress on the p53 pathway.
Leong et al., Singapore, Singapore. In Biomaterials, 2013
At low level of ZnO NMs induced ROS, p53 triggers expression of antioxidant genes such as SOD2, GPX1, SESN1, SESN2 and ALDH4A1 to restore oxidative homeostasis while at high concentration of ZnO NMs, the elevated level of intracellular ROS activated the apoptotic pathway through p53.
SKN-1 and Nrf2 couples proline catabolism with lipid metabolism during nutrient deprivation.
Curran et al., Los Angeles, United States. In Nat Commun, 2013
In human cells, an orthologous alh-6 enzyme, ALDH4A1, is also linked to the activity of Nrf2, the human orthologue of SKN-1, and regulates the expression of lipid metabolic genes.
Structural basis of substrate selectivity of Δ(1)-pyrroline-5-carboxylate dehydrogenase (ALDH4A1): semialdehyde chain length.
Tanner et al., Columbia, United States. In Arch Biochem Biophys, 2013
The enzyme Δ(1)-pyrroline-5-carboxylate (P5C) dehydrogenase (aka P5CDH and ALDH4A1) is an aldehyde dehydrogenase that catalyzes the oxidation of γ-glutamate semialdehyde to l-glutamate.
The three-dimensional structural basis of type II hyperprolinemia.
Tanner et al., Columbia, United States. In J Mol Biol, 2012
the impact of the hyperprolinemia-associated mutation of Ser352 to Leu on the structure and catalytic properties of the P5CDH
T-DNA insertion mutants reveal complex expression patterns of the aldehyde dehydrogenase 3H1 locus in Arabidopsis thaliana.
Bartels et al., Bonn, Germany. In J Exp Bot, 2012
ALDH3H1 locus generates at least five alternative transcript variants.
Aldehyde dehydrogenases and cell proliferation.
Canuto et al., Torino, Italy. In Free Radic Biol Med, 2012
Noteworthy is the fact that elevated activity of various ALDHs, namely ALDH1A2, ALDH1A3, ALDH1A7, ALDH2*2, ALDH3A1, ALDH4A1, ALDH5A1, ALDH6, and ALDH9A1, has been observed in normal and cancer stem cells.
Identification of ALDH4 as a p53-inducible gene and its protective role in cellular stresses.
Arakawa et al., Tokyo, Japan. In J Hum Genet, 2003
ALDH4 is transcriptionally induced by p53.
Polymorphisms of human aldehyde dehydrogenases. Consequences for drug metabolism and disease.
Pappa et al., Denver, United States. In Pharmacology, 2000
Polymorphisms in ALDH3A2, ALDH4A1, ALDH5A1 and ALDH6A1 are associated with metabolic diseases generally characterized by neurologic complications.
Human aldehyde dehydrogenase gene family.
Chang et al., Duarte, United States. In Eur J Biochem, 1998
Metabolic disorders and clinical problems associated with mutations of ALDH1, ALDH2, ALDH4, ALDH10 and succinic semialdehyde (SSDH) genes have been emerged.
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