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

Phospholipase D family, member 3

PLD3, SAM-9, HindIII K4L, phospholipase D3, Hu-K4
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Top mentioned proteins: APP, TREM2, ACID, CAN, Bin1
Papers on PLD3
Rare Variants in PLD3 Do Not Affect Risk for Early-Onset Alzheimer Disease in a European Consortium Cohort.
Belgium Neurology (BELNEU) Consortium and the European Early-Onset Dementia (EU EOD) Consortium et al., Antwerp, Belgium. In Hum Mutat, Dec 2015
Rare variants in the phospholipase D3 gene (PLD3) were associated with increased risk for late-onset Alzheimer disease (LOAD).
Next Generation Sequencing in Alzheimer's Disease.
Bertram, Lübeck, Germany. In Methods Mol Biol, Dec 2015
Notable recent discoveries using NGS include the identification of rare susceptibility modifying alleles in APP, TREM2, and PLD3.
Impact of Common Variations in PLD3 on Neuroimaging Phenotypes in Non-demented Elders.
Alzheimer’s Disease Neuroimaging Initiative et al., Qingdao, China. In Mol Neurobiol, Sep 2015
UNASSIGNED: Rare variants of phospholipase D3 (PLD3) have been identified as Alzheimer's disease (AD) susceptibility loci, whereas little is known about the potential role of common variants in the progression of AD.
Alzheimer's disease: rare variants with large effect sizes.
Cruchaga et al., Saint Louis, United States. In Curr Opin Genet Dev, Aug 2015
Recent advances in sequencing technology and novel genotyping arrays (focused on low-frequency and coding variants) have made it possible to identify novel coding variants with large effect sizes and also novel genes (TREM2, PLD3, UNC5C, and AKAP9) associated with Alzheimer's disease (AD) risk.
PLD3 in Alzheimer's Disease: a Modest Effect as Revealed by Updated Association and Expression Analyses.
Yao et al., Kunming, China. In Mol Neurobiol, Aug 2015
Recent next-generation sequencing studies of large AD pedigrees had identified phospholipase D3 (PLD3) p.V232M as the potentially functional rare variant with causal effect.
PLD3 in Alzheimer's disease.
Tan et al., Qingdao, China. In Mol Neurobiol, Apr 2015
Rare coding variants in the phospholipase D3 (PLD3) gene, also known as HU-K4, have recently been identified to increase the risk for late-onset Alzheimer's disease (LOAD) by the whole exome sequencing (WES) in 14 large LOAD families and follow-up analyses of the candidate variants in several large independent LOAD case-control data series.
Microarray analysis of differentially expressed genes regulating lipid metabolism during melanoma progression.
Sudhakar et al., In Indian J Biochem Biophys, Apr 2015
Melanoma also upregulated genes which prevented lipotoxicity (CPT2 and ACOT7) and regulated lipid second messengers, such as phosphatidic acid (AGPAT-4, PLD3) and inositol triphosphate (ITPKB, ITPR3).
Hypoxia induces a lipogenic cancer cell phenotype via HIF1α-dependent and -independent pathways.
Kessler et al., Reus, Spain. In Oncotarget, Mar 2015
Palmitate, stearate, PLD3 and PAFC16 were regulated in a HIF-independent manner.
Alzheimer's disease risk genes and mechanisms of disease pathogenesis.
Goate et al., Saint Louis, United States. In Biol Psychiatry, 2015
Emerging technologies to analyze the entire genome in large data sets have also revealed coding variants that increase AD risk: PLD3 and TREM2.
Common Variants in PLD3 and Correlation to Amyloid-Related Phenotypes in Alzheimer's Disease.
Alzheimer's Disease Neuroimaging Initiative et al., Qingdao, China. In J Alzheimers Dis, 2014
The phospholipase D3 (PLD3) gene has shown association with Alzheimer's disease (AD).
Acinetobacter baumannii Virulence Is Mediated by the Concerted Action of Three Phospholipases D.
Averhoff et al., Frankfurt am Main, Germany. In Plos One, 2014
The third candidate, PLD3, is found in bacteria as well as in eukaryotes and harbours only one PLDc_2 PFAM domain and one conserved HKD motif, which however do not overlap.
Rare coding variants in the phospholipase D3 gene confer risk for Alzheimer's disease.
Goate et al., Saint Louis, United States. In Nature, 2014
A rare variant in PLD3 (phospholipase D3; Val232Met) segregated with disease status in two independent families and doubled risk for Alzheimer's disease in seven independent case-control series with a total of more than 11,000 cases and controls of European descent.
PLD3 is accumulated on neuritic plaques in Alzheimer's disease brains.
Arima et al., Tokyo, Japan. In Alzheimers Res Ther, 2013
INTRODUCTION: Recently, a whole-exome sequencing (WES) study showed that a rare variant rs145999145 composed of p.Val232Met located in exon 7 of the phospholipase D3 (PLD3) gene confers a doubled risk for late-onset Alzheimer's disease (AD).
Genetics of Alzheimer's disease.
Seshadri et al., Boston, United States. In Adv Genet, 2013
This effort has identified two novel genes, TREM2 and PLD3, and shown a role for APP in LOAD.
Late-Onset Alzheimer's Disease Genes and the Potentially Implicated Pathways.
Kamboh et al., Pittsburgh, United States. In Curr Genet Med Rep, 2013
In addition, rare variants associated with LOAD have also been identified in APP, TREM2 and PLD3 genes.
A role for phospholipase D3 in myotube formation.
Frohman et al., Stony Brook, United States. In Plos One, 2011
PLD3 plays a role in myogenesis during myotube formation, potentially in the events surrounding ER reorganization.
[Over-expression of phospholipase D3 inhibits Akt phosphorylation in C2C12 myoblasts].
Wang et al., China. In Sheng Wu Gong Cheng Xue Bao, 2009
PLD3 overexpression may inhibit Akt phosphorylation and further block the transduction of insulin signaling in C2C12 cells.
Sustained receptor stimulation leads to sequestration of recycling endosomes in a classical protein kinase C- and phospholipase D-dependent manner.
Hannun et al., Charleston, United States. In J Biol Chem, 2009
receptor stimulation leads to sequestration of recycling endosomes in a classical protein kinase C- and phospholipase D-dependent manner
Prospective isolation and molecular characterization of hematopoietic stem cells with durable self-renewal potential.
Eaves et al., Vancouver, Canada. In Blood, 2009
Pld3 expression is associated with hematopoietic stem cells that have durable self-renewal potential.
HindIII(+/-) polymorphism of the Y chromosome, blood pressure, and serum lipids: no evidence of association in three white populations.
Siani et al., Avellino, Italy. In Am J Hypertens, 2006
Our data do not support the hypothesis that the HindIII(+/-) site of the Y chromosome is a marker of cardiovascular risk in white men, highlighting the need for replication in genetic association studies.
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