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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 18 Nov 2014.

Programmed cell death 4

T is, PDCD4, programmed cell death 4
This gene is a tumor suppressor and encodes a protein that binds to the eukaryotic translation initiation factor 4A1 and inhibits its function by preventing RNA binding. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Dec 2010] (from NCBI)
Top mentioned proteins: miR, V1a, PTEN, CAN, HAD
Papers on T is
Inhibiting CARD11 translation during BCR activation by targeting the eIF4A RNA helicase.
New
Gartenhaus et al., Baltimore, United States. In Blood, 15 Nov 2014
PDCD4 inhibits eIF4A and PDCD4 knockout mice have a high penetrance for B-cell lymphomas.
miR-21 in Ischemia/Reperfusion Injury: A Double-edged Sword?
Review
New
Ding et al., Shanghai, China. In Physiol Genomics, Sep 2014
Preconditioning-induced upregulation of miR-21 contributes to the protection against subsequent renal I/R injury through the targeting of genes such as the pro-apoptotic gene programmed cell death 4 and interactions between miR-21 and hypoxia-inducible factor.
[Gleevec induces apoptosis in K562 cells through activating caspase-3].
New
Wang et al., In Yao Xue Xue Bao, Aug 2014
Moreover, Gleevec significantly increased the protein expression of programmed cell death 4 (PDCD4).
The role of microRNAs in the control and mechanism of action of IL-10.
Review
New
O'Neill et al., Dublin, Ireland. In Curr Top Microbiol Immunol, Dec 2013
Another miRNA, miR-21, has been shown to indirectly regulate IL-10 via downregulation of the IL-10 inhibitor PDCD4.
The C2238/αANP Variant Is a Negative Modulator of Both Viability and Function of Coronary Artery Smooth Muscle Cells.
New
Volpe et al., Isernia, Italy. In Plos One, Dec 2013
CC2238/αANP reduced cell vitality, increased apoptosis and necrosis, increased oxidative stress levels, suppressed miR21 expression along with consistent changes of its molecular targets (PDCD4, PTEN, Bcl2) and of phosphorylated Akt levels.
MicroRNA-21 Promotes Cell Growth and Migration by Targeting Programmed Cell Death 4 Gene in Kazakh's Esophageal Squamous Cell Carcinoma.
New
Lu et al., Ürümqi, China. In Dis Markers, Dec 2013
It has been reported that miR-21 was upregulated in most malignant cancers, the proposed mechanism of which was through suppressing expression of programmed cell death 4 (PDCD4).
MicroRNA-183 inhibits apoptosis and promotes proliferation and invasion of gastric cancer cells by targeting PDCD4.
New
Hu et al., Shanghai, China. In Int J Clin Exp Med, Dec 2013
Mechanistically, we demonstrated that overexpression of miR-183 decreased, and inhibition of miR-183 increased the expression of PDCD4, a tumor suppressor, at both mRNA and protein levels.
MicroRNA-21 Attenuates Renal Ischemia Reperfusion Injury via Targeting Caspase Signaling in Mice.
New
Ye et al., Nanchang, China. In Am J Nephrol, Dec 2013
RESULTS: Mice upregulated miR-21 had lower plasma levels of blood urea nitrogen (BUN) and creatinine, lower histopathological scores and a decrease in programmed cell death 4 (PDCD4) mRNA and active caspase-3, caspase-8 proteins expressions.
Pdcd4 knockdown up-regulates MAP4K1 expression and activation of AP-1 dependent transcription through c-Myc.
GeneRIF
Yang et al., Lexington, United States. In Biochim Biophys Acta, 2012
Pdcd4 knockdown up-regulates MAP kinase kinase kinase kinase 1 (MAP4K1) expression and increases phosphorylation of c-Jun.
Role of microRNA-21 and programmed cell death 4 in the pathogenesis of human uterine leiomyomas.
GeneRIF
Christenson et al., Kansas City, United States. In Fertil Steril, 2012
Elevated leiomyoma miR-21 levels are predicted to decrease PDCD-4 levels, thus leiomyomas differ from other tumors where loss of PDCD-4 is associated with tumor progression.
Regulatory effects of programmed cell death 4 (PDCD4) protein in interferon (IFN)-stimulated gene expression and generation of type I IFN responses.
GeneRIF
Platanias et al., Chicago, United States. In Mol Cell Biol, 2012
IFN-dependent phosphorylation of PDCD4 results in downregulation of PDCD4 protein levels as the phosphorylated form of PDCD4 interacts with the ubiquitin ligase beta-TRCP (beta-transducin repeat-containing protein) and undergoes degradation.
PTEN and PDCD4 are bona fide targets of microRNA-21 in human cholangiocarcinoma.
GeneRIF
Chen et al., Beijing, China. In Chin Med Sci J, 2012
microRNA-21 expression is up-regulated in human cholangiocarcinoma and PTEN, PDCD4 are direct effectors of microRNA-21.
Protein kinase GSK3β regulates tumor suppressor Pdcd4 expression in lung cancer cells.
GeneRIF
Korobko et al., Moscow, Russia. In Dokl Biochem Biophys, 2012
role of GSK3beta in Pdcd4 expression lung cancer cells
The role of microRNA in modulating myocardial ischemia-reperfusion injury.
Review
Birnbaum et al., Galveston, United States. In Physiol Genomics, 2011
By altering the expression of various key elements in cell survival and apoptosis [such as phosphoinositide 3-kinase (PI3K), phosphatase and tensin homolog deleted on chromosome 10 (PTEN), Bcl-2, Mcl-1, heat shock protein (HSP)60, HSP70, HSP20, programmed cell death 4 (Pdcd4), LRRFIP1, Fas ligand (FasL), Sirt-1, etc.], miRNAs alter the response to ischemia-reperfusion injury.
Resistance may not be futile: microRNA biomarkers for chemoresistance and potential therapeutics.
Review
Weiss et al., Phoenix, United States. In Mol Cancer Ther, 2010
microRNAs have recently been identified as playing a role in the regulation of key genes implicated as cancer therapeutic targets or in mechanisms of chemoresistance including EGFR, MDR1, PTEN, Bak1, and PDCD4 among others.
MicroRNA-21 in cardiovascular disease.
Review
Zhang et al., Newark, United States. In J Cardiovasc Transl Res, 2010
Programmed cell death 4 (PDCD4), phosphatase and tensin homology deleted from chromosome 10 (PTEN), sprouty1 (SPRY1), and sprouty2 (SPRY2) are the current identified target genes of miR-21 that are involved in miR-21-mediated cardiovascular effects.
Negative regulation of TLR4 via targeting of the proinflammatory tumor suppressor PDCD4 by the microRNA miR-21.
Impact
GeneRIF
O'Neill et al., Dublin, Ireland. In Nat Immunol, 2010
miR-21 regulates PDCD4 expression after LPS stimulation.
A network model of a cooperative genetic landscape in brain tumors.
Impact
Sikic et al., Chicago, United States. In Jama, 2009
A multigene risk scoring model based on 7 landscape genes (POLD2, CYCS, MYC, AKR1C3, YME1L1, ANXA7, and PDCD4) is associated with the duration of overall survival in 189 glioblastoma samples from TCGA (global log-rank P = .02
SMAD proteins control DROSHA-mediated microRNA maturation.
Impact
Hata et al., Boston, United States. In Nature, 2008
miR-21 downregulates PDCD4 (programmed cell death 4), which in turn acts as a negative regulator of smooth muscle contractile genes.
S6K1- and betaTRCP-mediated degradation of PDCD4 promotes protein translation and cell growth.
Impact
GeneRIF
Pagano et al., New York City, United States. In Science, 2006
in response to mitogens, PDCD4 was rapidly phosphorylated by protein kinase S6K1 & then degraded by ubiquitin ligase SCF(betaTRCP); it is proposed that regulated degradation of PDCD4 in response to mitogens allows efficient protein synthesis & cell growth
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