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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. De plus, nous expédions PDCD4 Anticorps (254) et PDCD4 Kits (19) et beaucoup plus de produits pour cette protéine.
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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 (Montrer MLXIP Protéines)-21.
Various studies support evidence that PDCD4, is a novel tumor suppressor gene, and is downregulated or even absent in colorectal cancer (CRC (Montrer CALR Protéines)) and suppresses CRC (Montrer CALR Protéines) deterioration. [review]
In the high malignant group the PDCD4 mRNA and PDCD5 (Montrer PDCD5 Protéines) mRNA expressions were significantly decreased compared with the low malignant group and the control group. PDCD4 mRNA and PDCD5 (Montrer PDCD5 Protéines) mRNA expressions are promising targets for the diagnosis and treatment of glioma.
miR (Montrer MLXIP Protéines)-21 may promote salivary adenoid cystic carcinoma progression via PDCD4 and PTEN down-regulation and Bcl-2 (Montrer BCL2 Protéines) up-regulation.
The expression of PDCD4 is decreased in cervical cancer tissues, compared to miR (Montrer MLXIP Protéines)-150 which is increased.
Our study demonstrated that lncRNA-XIST, which acts as a miRNA sponge, impedes miR (Montrer MLXIP Protéines)-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 (Montrer MLXIP Protéines)-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 (Montrer MLXIP Protéines)-93 and miR (Montrer MLXIP Protéines)-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 (Montrer FAM126A Protéines)) cell invasion and migration induced by miR (Montrer MLXIP Protéines)-93, while the knockdown of PDCD4 would promote HCC (Montrer FAM126A Protéines) cell migration and invasion via the EMT (Montrer ITK Protéines) 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 (Montrer MLXIP Protéines)-21 deficiency through miR (Montrer MLXIP Protéines)-21 targeting programmed cell death 4 (PDCD4), despite the existence of RANKL (Montrer TNFSF11 Protéines). 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 (Montrer MLXIP Protéines)-21, which mediates ischemic neuronal death.
In colorectal cancer tissues, the Sin1 (Montrer MAPKAP1 Protéines) protein but not mRNA was significantly upregulated while Pdcd4 protein was downregulated, suggesting that loss of Pdcd4 might correlate with Sin1 (Montrer MAPKAP1 Protéines) protein level but not mRNA level in colorectal cancer.
-induced expression of PDCD4 is associated with increased beta cell death.
miR (Montrer MLXIP Protéines)-155 not only directly inhibited SOCS1 (Montrer SOCS1 Protéines) expression, but also increased the expression of p-STAT (Montrer STAT1 Protéines) and PDCD4, as well as the production of proinflammation mediators IL-6 (Montrer IL6 Protéines) and TNF-alpha (Montrer TNF Protéines) in atherogenesis
our data suggest that Pdcd4 as a crucial regulator in SGs (Montrer SKI Protéines) 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 (Montrer IL10 Protéines).
PDCD4 Deficiency Aggravated Colitis and Colitis-associated Colorectal Cancer Via Promoting IL-6 (Montrer IL6 Protéines)/STAT3 (Montrer STAT3 Protéines) Pathway.
Study found that miR-16 (Montrer GDE1 Protéines) was the direct regulatory element of PDCD4 and played a vital role in atherosclerosis by regulating PDCD4 and the downstream NF-kappaB (Montrer NFKB1 Protéines) and MAPK (Montrer MAPK1 Protéines) 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 (Montrer MYLIP Protéines)-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 (Montrer NFKB1 Protéines)/ TNF-alpha (Montrer TNF Protéines) 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