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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 25 Jan 2016.

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
SOX6 and PDCD4 enhance cardiomyocyte apoptosis through LPS-induced miR-499 inhibition.
Zhou et al., Beijing, China. In Apoptosis, 29 Feb 2016
We found that LPS stimulation inhibited microRNA (miR)-499 expression and thereby upregulated the expression of SOX6 and PDCD4 in neonatal rat cardiomyocytes.
MicroRNA-4262 activates the NF-κB and enhances the proliferation of hepatocellular carcinoma cells.
Huang et al., Nanjing, China. In Int J Biol Macromol, 08 Feb 2016
Moreover, the 3'UTR of PDCD4 was complementary to miR-4262 seed region and we confirmed that PDCD4 is the direct target of miR-4262 with 3'UTR luciferase assay.
SRSF3 represses the expression of PDCD4 protein by coordinated regulation of alternative splicing, export and translation.
Jeong et al., South Korea. In Biochem Biophys Res Commun, 07 Feb 2016
Considering diverse roles of SR proteins, we determined whether the tumor-related splicing factor SRSF3 regulates the expression of the tumor-suppressor protein, PDCD4, at multiple steps.
MicroRNA-21 Aggravates Cyst Growth in a Model of Polycystic Kidney Disease.
Patel et al., Kansas City, United States. In J Am Soc Nephrol, 17 Jan 2016
RNA sequencing analysis and additional in vivo assays showed that miR-21 inhibits apoptosis of cyst epithelial cells, likely through direct repression of its target gene programmed cell death 4. Thus, miR-21 functions downstream of the cAMP pathway and promotes disease progression in experimental PKD.
Roles of phosphatidylinositol 3-kinase regulatory subunit alpha, activator protein-1, and programmed cell death 4 in diagnosis of papillary thyroid carcinoma.
Gong et al., Wenzhou, China. In Tumour Biol, 04 Jan 2016
UNASSIGNED: This study evaluated the diagnostic values of phosphatidylinositol 3-kinase regulatory subunit alpha (P85α), activator protein-1 (AP-1), and programmed cell death 4 (PDCD4) in papillary thyroid carcinoma (PTC).
Pdcd4 deficiency enhances macrophage lipoautophagy and attenuates foam cell formation and atherosclerosis in mice.
Zhang et al., Jinan, China. In Cell Death Dis, 31 Dec 2015
Previously, we reported that programmed cell death 4 (PDCD4), a tumor suppressor, negatively regulated autophagy in tumor cells.
The critical roles of miR-21 in anti-cancer effects of curcumin.
Chen et al., Australia. In Ann Transl Med, 31 Dec 2015
Several downstream pathways of miR-21 have been identified including phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), programmed cell death protein 4 (PDCD4) and NF-κB pathways.
Apoptosis-related microRNA changes in the right atrium induced by remote ischemic perconditioning during valve replacement surgery.
Chen et al., Changsha, China. In Sci Rep, 31 Dec 2015
However, the differences in miR-21 and miR-24 expression, together with programmed cell death 4 (PDCD4), which is the target gene of miR-21, were not significant.
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.
Non-Specific Blocking of miR-17-5p Guide Strand in Triple Negative Breast Cancer Cells by Amplifying Passenger Strand Activity.
Wickstrom et al., Philadelphia, United States. In Plos One, 2014
High levels of the oncogenic miRNA (oncomiR) guide strand called miR-17-5p is overexpressed in triple negative breast cancer (TNBC) and can inhibit ribosomal translation of tumor suppressor gene mRNAs, such as programmed cell death 4 (PDCD4) or phosphatase and tensin homolog (PTEN).
Cell Density-Dependent Upregulation of PDCD4 in Keratinocytes and Its Implications for Epidermal Homeostasis and Repair.
Su et al., Chongqing, China. In Int J Mol Sci, 2014
Programmed cell death 4 (PDCD4) is one multi-functional tumor suppressor inhibiting neoplastic transformation and tumor invasion.
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
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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