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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 (248) and PDCD4 Kits (16) and many more products for this protein.
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We demonstrated that miR (show MLXIP Proteins)-208a-3p suppressed apoptosis in gastric cancer cells by targeting PDCD4.
PDCD4 is involved in negative control of stromal fibroblasts conversion into cancer associated fibroblast
Results identify PDCD4 as a novel RSK (show RPS6KA1 Proteins) substrate. Authors demonstrate that RSK (show RPS6KA1 Proteins)-mediated phosphorylation of PDCD4 at S76 promotes PDCD4 degradation.
evaluate the relative expression levels of miR (show MLXIP Proteins)-196a2 and three of its selected apoptosis-related targets; ANXA1 (show ANXA1 Proteins), DFFA (show DFFA Proteins) and PDCD4 in a sample of GI cancer patients
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.
miRNA-96 is significantly overexpressed in glioma tissues. Moreover, miRNA-96 plays a critical role in apoptosis by inhibiting the expression of PDCD4 in glioma.
Supporting the clinical relevance of our results, we found an inverse correlation between ErbB-2 (show ERBB2 Proteins)/Stat3 (show STAT3 Proteins) nuclear co-expression and PDCD4 expression in ErbB-2 (show ERBB2 Proteins)-positive primary invasive breast cancer
this study highlights an oncomiR role for miR (show MLXIP Proteins)-181b in regulating PDCD4 in colorectal cancer and suggests that miR (show MLXIP Proteins)-181b may be a novel molecular therapeutic target for colorectal cancer.
Higher PDCD4 expression plays a role in polycystic ovary syndrome by affecting obesity, insulin (show INS Proteins) resistance, lipid metabolism disorders, and granulosa cell apoptosis.
results revealed that microRNA 200a inhibits erythroid differentiation by targeting PDCD4 and THRB (show THRB Proteins)
-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.
PDCD4 serves as an important regulator of keratinocytes proliferation and contact inhibition in vitro.
In conclusion, miR (show MLXIP Proteins)-21 is sensitive to high-concentration glucose treatment in macrophages, and appears to have a protective effect in macrophage apoptosis induced by high concentrations of glucose via PDCD4.
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
, programmed cell death 4
, protein I11/6
, programmed cell death 4 (neoplastic transformation inhibitor)
, programmed cell death protein 4-like