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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.
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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.
miR503 promotes tumour growth and invasion by directly targeting PDCD4.
A novel mechanism of Pdcd4 action as a translation inhibitor and tumor suppressor has been proposed.
Taken together, this study highlights an important role for miR (Montrer MLXIP Protéines)-23a/b as oncomiRs in gastric cancer through the inhibition of PDCD4 translation. These findings may shed new light on the molecular mechanism of gastric carcinogenesis and provide a new avenue for gastric cancer treatment.
lncRNA CASC9 functions as an oncogene (Montrer RAB1A Protéines) by negatively regulating PDCD4 expression through recruiting EZH2 (Montrer EZH2 Protéines) and subsequently altering H3K27me3 level. Our study implicates lncRNA CASC9 as a valuable biomarker for ESCC diagnosis and prognosis.
Exosomes derived from cisplatin-resistant OSCC cells transferred miR (Montrer MLXIP Protéines)-21 to oral squamous cell carcinoma (OSCC) parental cells and induced cisplatin resistance by targeting phosphatase and tensin homolog (PTEN) and programmed cell death 4 (PDCD4).
These results indicate that the ROS (Montrer ROS1 Protéines)-STAT3 (Montrer STAT3 Protéines)-miR (Montrer MLXIP Protéines)-21-PDCD4 signaling axis plays an important role in arsenic -induced carcinogenesis.
PDCD4 is expressed in the cytoplasm of glandular epithelium of control endometrium and varied during the cycle changes of endometrium. Compared with the proliferative phase of control endometrium, PDCD4 expression was down-regulated in proliferative phase of eutopic or ectopic endometrium. There was no cyclic variation of PDCD4 expression in eutopic endometrium of adenomyosis patients due to progesterone resistance.
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.
PDCD4 serves as an important regulator of keratinocytes proliferation and contact inhibition in vitro.
In conclusion, miR (Montrer MLXIP Protéines)-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 (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