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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 (248) et PDCD4 Kits (16) et beaucoup plus de produits pour cette protéine.
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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.
Study confirmed that PDCD4 was downregulated in non-small cell lung cancer (NSCLC). PDCD4 is a functional target for miR (Montrer MLXIP Protéines)-155 at both transcriptional and post-transcriptional levels.
We demonstrated that miR (Montrer MLXIP Protéines)-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 (Montrer RPS6KA1 Protéines) substrate. Authors demonstrate that RSK (Montrer RPS6KA1 Protéines)-mediated phosphorylation of PDCD4 at S76 promotes PDCD4 degradation.
evaluate the relative expression levels of miR (Montrer MLXIP Protéines)-196a2 and three of its selected apoptosis-related targets; ANXA1 (Montrer ANXA1 Protéines), DFFA (Montrer DFFA Protéines) and PDCD4 in a sample of GI cancer patients
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.
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 (Montrer ERBB2 Protéines)/Stat3 (Montrer STAT3 Protéines) nuclear co-expression and PDCD4 expression in ErbB-2 (Montrer ERBB2 Protéines)-positive primary invasive breast cancer
this study highlights an oncomiR role for miR (Montrer MLXIP Protéines)-181b in regulating PDCD4 in colorectal cancer and suggests that miR (Montrer MLXIP Protéines)-181b may be a novel molecular therapeutic target for 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