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PDCD4 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. Additionally we are shipping PDCD4 Antibodies (254) and PDCD4 Kits (19) and many more products for this protein.
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the localization of Pdcd4 to the cytoplasm may be responsible for the suppression of the target mRNA translation and apoptosis.
PDCD4 and PTEN were the functional targets of miR (show MLXIP Proteins)-21.
Various studies support evidence that PDCD4, is a novel tumor suppressor gene, and is downregulated or even absent in colorectal cancer (CRC (show CALR Proteins)) and suppresses CRC (show CALR Proteins) deterioration. [review]
In the high malignant group the PDCD4 mRNA and PDCD5 (show PDCD5 Proteins) mRNA expressions were significantly decreased compared with the low malignant group and the control group. PDCD4 mRNA and PDCD5 (show PDCD5 Proteins) mRNA expressions are promising targets for the diagnosis and treatment of glioma.
miR (show MLXIP Proteins)-21 may promote salivary adenoid cystic carcinoma progression via PDCD4 and PTEN down-regulation and Bcl-2 (show BCL2 Proteins) up-regulation.
The expression of PDCD4 is decreased in cervical cancer tissues, compared to miR (show MLXIP Proteins)-150 which is increased.
Our study demonstrated that lncRNA-XIST, which acts as a miRNA sponge, impedes miR (show MLXIP Proteins)-21-5p to maintain the expression of PDCD4, which contributes to the progression of osteosarcoma (OS). Our findings suggest that the newly identified XIST/miR (show MLXIP Proteins)-21-5p/PDCD4 axis could be a potential biomarker or therapeutic target for OS.
miR206 promoted the onset of SANFH by inducing apoptosis and suppressed the proliferation of osteoblasts, which was dependent on the inhibition of PDCD4.
Results found PDCD4 as a target gene of miR (show MLXIP Proteins)-93 and miR (show MLXIP Proteins)-93 could down-regulate the expression of PDCD4 by directly targeting its 3'-UTR. The re-expression of PDCD4 could attenuate the hepatocellular carcinoma (HCC (show FAM126A Proteins)) cell invasion and migration induced by miR (show MLXIP Proteins)-93, while the knockdown of PDCD4 would promote HCC (show FAM126A Proteins) cell migration and invasion via the EMT (show ITK Proteins) pathway.
Reduced expression of PDCD4 was found in decidual and chorionic tissues, and peripheral blood mononuclear cells from patients with missed abortion.
These skeletal effects were attributed to inhibition of bone resorption and osteoclast function by miR (show MLXIP Proteins)-21 deficiency through miR (show MLXIP Proteins)-21 targeting programmed cell death 4 (PDCD4), despite the existence of RANKL (show TNFSF11 Proteins). As far as we know, this is the first in vivo evidence of a pro-osteoclastic microRNA.
MEG3 functions as a competing endogenous RNAs (ceRNAs) and competes with PDCD4 mRNA for directly binding to miR (show MLXIP Proteins)-21, which mediates ischemic neuronal death.
In colorectal cancer tissues, the Sin1 (show MAPKAP1 Proteins) protein but not mRNA was significantly upregulated while Pdcd4 protein was downregulated, suggesting that loss of Pdcd4 might correlate with Sin1 (show MAPKAP1 Proteins) protein level but not mRNA level in colorectal cancer.
-induced expression of PDCD4 is associated with increased beta cell death.
miR (show MLXIP Proteins)-155 not only directly inhibited SOCS1 (show SOCS1 Proteins) expression, but also increased the expression of p-STAT (show STAT1 Proteins) and PDCD4, as well as the production of proinflammation mediators IL-6 (show IL6 Proteins) and TNF-alpha (show TNF Proteins) in atherogenesis
our data suggest that Pdcd4 as a crucial regulator in SGs (show SKI Proteins) induced by ox-LDL or HFD maybe a potential target for mitigating SG-associated stress responses in obesity and related diseases.
Pdcd4 deficiency attenuates atherosclerosis in hyperlipidemic mice in part through the upregulation of the anti-inflammatory cytokine IL-10 (show IL10 Proteins).
PDCD4 Deficiency Aggravated Colitis and Colitis-associated Colorectal Cancer Via Promoting IL-6 (show IL6 Proteins)/STAT3 (show STAT3 Proteins) Pathway.
Study found that miR-16 (show GDE1 Proteins) was the direct regulatory element of PDCD4 and played a vital role in atherosclerosis by regulating PDCD4 and the downstream NF-kappaB (show NFKB1 Proteins) and MAPK (show MAPK1 Proteins) pathways.
Pdcd4 produces unfavorable influences on adipose-derived stem cells(ADSC) stemness, which contribute to adipose dysfunction, obesity and metabolic syndromes, thereby proposing Pdcd4 as a potential intervening target for regulating ADSC cells function.
miR (show MYLIP Proteins)-21 plays a necessary role in cardiac valvulogenesis, in large part due to an obligatory downregulation of PDCD4
TMZ pretreatment effectively reduced the myocardial damage caused by CME via inhibiting the PDCD4/NF-kappaB (show NFKB1 Proteins)/ TNF-alpha (show TNF Proteins) pathway in cardiomyocytes.
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.
neoplastic transformation inhibitor protein
, nuclear antigen H731
, programmed cell death protein 4
, protein 197/15a
, protein MA-3
, topoisomerase-inhibitor suppressed protein
, death up-regulated gene protein
, protein I11/6
, programmed cell death 4 (neoplastic transformation inhibitor)
, programmed cell death protein 4-like