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

Aldehyde dehydrogenase 7 family, member A1

The protein encoded by this gene is a member of subfamily 7 in the aldehyde dehydrogenase gene family. These enzymes are thought to play a major role in the detoxification of aldehydes generated by alcohol metabolism and lipid peroxidation. This particular member has homology to a previously described protein from the green garden pea, the 26g pea turgor protein. It is also involved in lysine catabolism that is known to occur in the mitochondrial matrix. Recent reports show that this protein is found both in the cytosol and the mitochondria, and the two forms likely arise from the use of alternative translation initiation sites. An additional variant encoding a different isoform has also been found for this gene. Mutations in this gene are associated with pyridoxine-dependent epilepsy. Several related pseudogenes have also been identified. [provided by RefSeq, Jan 2011] (from NCBI)
Top mentioned proteins: Phosphodiesterase, PDE5, CAN, V1a, HAD
Papers using PDE antibodies
The phosphodiesterase inhibitor, pentoxifylline, alters rat intestinal epithelial cell proliferation via changes in the expression of transforming growth factors.
Morty Rory Edward, In PLoS ONE, 2001
... PDE activity was assayed in human ASM cell lysates using a colorimetric assay method from Biomol (Enzo life science, Plymouth ...
Papers on PDE
Discovery of Potent and Selective Inhibitors of Phosphodiesterase 1 for the Treatment of Cognitive Impairment Associated with Neurodegenerative and Neuropsychiatric Diseases.
Wennogle et al., In J Med Chem, Feb 2016
Systematic optimizations of this novel scaffold culminated in the identification of a clinical candidate, (6aR,9aS)-2-(4-(6-fluoropyridin-2-yl)benzyl)-5-methyl-3-(phenylamino)-5,6a,7,8,9,9a-hexahydrocyclopenta[4,5]imidazo[1,2-a]pyrazolo[4,3-e]pyrimidin-4-(2H)-one phosphate (ITI-214), which exhibited picomolar inhibitory potency for PDE1, demonstrated excellent selectivity against all other PDE families, and showed good efficacy in vivo.
Cyclic nucleotide phosphodiesterase isoforms in human basophils and mast cells.
Peachell et al., Eşfahān, Iran. In Int J Immunopathol Pharmacol, Feb 2016
UNASSIGNED: Cyclic nucleotide phosphodiesterase (PDE) exists as multiple molecular forms.
Overexpression of Bcl-2, SOCS 1, 3 and Cdh 1, 2 are associated with the early neoplasic changes in modified 4-nitroquinoline 1-oxide-induced murine oral cancer model.
Spolidorio et al., Paulista, Brazil. In J Oral Pathol Med, Feb 2016
BACKGROUND: The objective was to assess histopathological changes and the expression of proliferating cell nuclear antigen (PCNA), Bcl-2, suppressor of cytokine signaling (SOCS) 1 and 3, Vimentin, TWIST1, and Cdh 1 and 2 in early stages of experimental oral carcinogenesis process using a shorter period of exposure to 4-nitroquinoline oxide (4-NQO) model.
Roles of phosphodiesterases in the regulation of the cardiac cyclic nucleotide cross-talk signaling network.
Winslow et al., Baltimore, United States. In J Mol Cell Cardiol, Feb 2016
However, the cross-talk response and the individual roles of each PDE isoenzyme in shaping this response remain to be fully characterized.
An emerging role of cGMP in the treatment of schizophrenia: A review.
Duncan et al., Atlanta, United States. In Schizophr Res, Jan 2016
cGMP is also regulated by phosphodiesterase (PDE), the enzyme hydrolyzing cGMP.
Pentoxifylline for Diabetic Nephropathy: an Important Opportunity to Re-purpose an Old Drug?
Leehey et al., Washington, D.C., United States. In Curr Hypertens Rep, Jan 2016
It competitively inhibits phosphodiesterase (PDE), resulting in increased intracellular cyclic AMP (cAMP), activation of protein kinase A (PKA), inhibition of interleukin (IL) and tumor necrosis factor (TNF) synthesis, and reduced inflammation.
Protein kinase G signaling in cardiac pathophysiology:Impact of proteomics on clinical trials.
Van Eyk et al., Maywood, United States. In Proteomics, Jan 2016
Phosphodiesterases (PDEs) degrade cGMP, thus PDE inhibitors that can increase PKG are of translational interest and the subject of ongoing human trials.
BMI1, ALDH1A1, and CD133 Transcripts Connect Epithelial-Mesenchymal Transition to Cancer Stem Cells in Lung Carcinoma.
Cufer et al., Slovenia. In Stem Cells Int, Dec 2015
In this study, we assessed mRNA expression levels of EMT-inducing transcription factors (BMI1, TWIST1), CSC (CD133, ALDH1A1), and epithelial (EpCAM) markers in primary tumor and whole blood samples obtained from 57 patients with operable non-small-cell lung cancer (NSCLC) as well as in circulating tumor cells (CTCs) of 13 patients with metastatic disease; then possible associations between marker expressions were evaluated.
Psychiatric aspects of phosphodiesterases: An overview.
Mangot et al., Sātāra, India. In Indian J Pharmacol, Nov 2015
Phosphodiesterases (PDE) are exciting new targets in medical sciences.
Epigenetic Regulation of Phosphodiesterases 2A and 3A Underlies Compromised β-Adrenergic Signaling in an iPSC Model of Dilated Cardiomyopathy.
Wu et al., Stanford, United States. In Cell Stem Cell, Aug 2015
We further discovered increased nuclear localization of mutant TNNT2 and epigenetic modifications of PDE genes in both DCM iPSC-CMs and patient tissue.
Matrix stiffness drives epithelial-mesenchymal transition and tumour metastasis through a TWIST1-G3BP2 mechanotransduction pathway.
Yang et al., San Diego, United States. In Nat Cell Biol, May 2015
Here we report that TWIST1 is an essential mechanomediator that promotes epithelial-mesenchymal transition (EMT) in response to increasing matrix stiffness.
Phosphodiesterase 9A controls nitric-oxide-independent cGMP and hypertrophic heart disease.
Kass et al., Baltimore, United States. In Nature, Apr 2015
However, cGMP stimulation alone is limited by counter-adaptions including PDE upregulation.
The limits of oral therapy in pulmonary arterial hypertension management.
Jing et al., Shanghai, China. In Ther Clin Risk Manag, 2014
Over the past decade, new treatments for PAH, such as the use of ERAs, PDE-5 inhibitors and prostacyclin analogs, have brought about dramatic improvements in clinical outcomes.
Advances in targeting cyclic nucleotide phosphodiesterases.
Manganiello et al., Kingston, Canada. In Nat Rev Drug Discov, 2014
Currently, a small number of PDE inhibitors are used clinically for treating the pathophysiological dysregulation of cyclic nucleotide signalling in several disorders, including erectile dysfunction, pulmonary hypertension, acute refractory cardiac failure, intermittent claudication and chronic obstructive pulmonary disease.
A switch in the expression of embryonic EMT-inducers drives the development of malignant melanoma.
Tulchinsky et al., Lyon, France. In Cancer Cell, 2013
In response to NRAS/BRAF activation, EMT-TF network undergoes a profound reorganization in favor of TWIST1 and ZEB1.
Activation of the Notch1/STAT3/Twist signaling axis promotes gastric cancer progression.
Yeh et al., Taipei, Taiwan. In Carcinogenesis, 2012
results suggest that Notch1/STAT3/Twist signaling axis is involved in progression of human gastric cancer and modulation of this cascade has potential for the targeted combination therapy
Twist1 regulates Ifng expression in Th1 cells by interfering with Runx3 function.
Kaplan et al., Indianapolis, United States. In J Immunol, 2012
Twist1 negatively regulates the T helper (Th)1 cell transcription factor network as it inhibits interferon-gamma production.
Twist1 causes the transcriptional repression of claudin-4 with prognostic significance in esophageal cancer.
Kim et al., South Korea. In Biochem Biophys Res Commun, 2012
these results indicate that Twist1 induces the repression of claudin-4 expression during the epithelial-mesenchymal transition in esophageal carcinoma.
Bmps and id2a act upstream of Twist1 to restrict ectomesenchyme potential of the cranial neural crest.
Crump et al., Los Angeles, United States. In Plos Genet, 2011
the ventral migration of Cranial neural crest cells (CNCCs) away from a source of Bmps in the dorsal ectoderm promotes ectomesenchyme development by relieving Id2a-dependent repression of Twist1 function.
Twist1 suppresses senescence programs and thereby accelerates and maintains mutant Kras-induced lung tumorigenesis.
Felsher et al., Baltimore, United States. In Plos Genet, 2011
the suppression of Twist1 to physiological levels is sufficient to cause Kras mutant lung tumors to undergo senescence and lose their neoplastic features
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