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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
Dissimilar microRNA-21 functions and targets in trophoblastic cell lines of different origin.
Morales-Prieto et al., Jena, Germany. In Int J Biochem Cell Biol, 27 Sep 2015
Expression of the potential miR-21 targets phosphatase and tensin homolog (PTEN) and programmed cell death 4 (PDCD4) were analyzed by Western blotting.
Antisense-miR-21 enhances differentiation/apoptosis and reduces cancer stemness state on anaplastic thyroid cancer.
Larijani et al., Tehrān, Iran. In Tumour Biol, 20 Sep 2015
Apoptosis was assessed by PDCD4 and Mcl-1 gene expression and flow cytometry.
Effects of exercise training together with tamoxifen in reducing mammary tumor burden in mice: Possible underlying pathway of miR-21.
Fayad et al., Gorgān, Iran. In Eur J Pharmacol, 20 Sep 2015
Exercise training and tamoxifen reduced tumor IL-6 levels, NF-kB and STAT3 expressions, and up-regulated TPM1 and PDCD4 expressions (P <0.05).
Targeting strategies on miRNA-21 and PDCD4 for glioblastoma.
To et al., Shanghai, China. In Arch Biochem Biophys, 15 Sep 2015
Programmed cell death 4 (PDCD4) is critical in mediating apoptosis in GBM, and is downregulated by miR-21, which may mediate the resistance of glioblastoma cells against chemotherapy or radiation via its target genes PDCD4.
miR-155, identified as anti-metastatic by global miRNA profiling of a metastasis model, inhibits cancer cell extravasation and colonization in vivo and causes significant signaling alterations.
Ditzel et al., Odense, Denmark. In Oncotarget, 10 Sep 2015
Downregulation of the three metastasis-associated proteins ALDH1A1, PIR and PDCD4 in miR-155-overexpressing tumors was validated by immunohistochemistry. Our results demonstrate that miR-155 inhibits the ability of cancer cells to extravasate and/or colonize at distant organs and brings additional insight into the complexity of miR-155 regulation in metastatic seeding.
4-protein signature predicting tamoxifen treatment outcome in recurrent breast cancer.
Umar et al., Rotterdam, Netherlands. In Mol Oncol, 07 Sep 2015
Immunohistochemical (IHC) staining of PDCD4, one of the signature proteins, on an independent set of formalin-fixed paraffin-embedded tumor tissues provided and independent technical validation (HR = 0.72; 95% CI = 0.57 to 0.92; multivariate Cox regression p value = 0.009).
Integrated molecular analysis to investigate the role of microRNAs in pancreatic tumour growth and progression.
Jiao et al., Roma, Italy. In Lancet, Mar 2015
FINDINGS: We identified three miRNAs (miR-21, miR-23a, and miR-27a) that acted as cooperative repressors of a network of tumour suppressor genes that included PDCD4, BTG2, and NEDD4L.
miR-21 in ischemia/reperfusion injury: a double-edged sword?
Ding et al., Shanghai, China. In Physiol Genomics, Dec 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 proapoptotic gene programmed cell death 4 and interactions between miR-21 and hypoxia-inducible factor.
The role of microRNAs in the control and mechanism of action of IL-10.
O'Neill et al., Dublin, Ireland. In Curr Top Microbiol Immunol, 2013
Another miRNA, miR-21, has been shown to indirectly regulate IL-10 via downregulation of the IL-10 inhibitor PDCD4.
Pdcd4 knockdown up-regulates MAP4K1 expression and activation of AP-1 dependent transcription through c-Myc.
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.
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.
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.
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.
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.
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.
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.
Negative regulation of TLR4 via targeting of the proinflammatory tumor suppressor PDCD4 by the microRNA miR-21.
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.
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.
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.
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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