Subtractive hybridization of mRNA from early passage and senescent endothelial cells.
about
SNEV is an evolutionarily conserved splicing factor whose oligomerization is necessary for spliceosome assemblyInteraction of U-box E3 ligase SNEV with PSMB4, the beta7 subunit of the 20 S proteasomeEarly embryonic lethality of mice lacking the essential protein SNEVThe Prp19/Pso4 core complex undergoes ubiquitylation and structural alterations in response to DNA damageThe fate of chemoresistance in triple negative breast cancer (TNBC)EGF-mediated regulation of IGFBP-3 determines esophageal epithelial cellular response to IGF-IInhibition of pre-mRNA splicing by a synthetic Blom7α-interacting small RNAThe senescence-associated secretory phenotype: the dark side of tumor suppressionA mathematical model for suppression subtractive hybridization.Senescent cells as a source of inflammatory factors for tumor progression.Epidermal growth factor receptor regulates aberrant expression of insulin-like growth factor-binding protein 3IGFBP-3 regulates esophageal tumor growth through IGF-dependent and independent mechanisms.Endothelial p53 deletion improves angiogenesis and prevents cardiac fibrosis and heart failure induced by pressure overload in mice.Induction of cellular senescence by insulin-like growth factor binding protein-5 through a p53-dependent mechanism.Proteome profiling in IL-1β and VEGF-activated human umbilical vein endothelial cells delineates the interlink between inflammation and angiogenesis.Contributions of DNA interstrand cross-links to aging of cells and organisms.Senescent peritoneal mesothelial cells promote ovarian cancer cell adhesion: the role of oxidative stress-induced fibronectinVascular endothelial senescence: from mechanisms to pathophysiology.Blom7alpha is a novel heterogeneous nuclear ribonucleoprotein K homology domain protein involved in pre-mRNA splicing that interacts with SNEVPrp19-Pso4.Effects of long-term serial cell passaging on cell spreading, migration, and cell-surface ultrastructures of cultured vascular endothelial cellsBiogerontology in Austria.The function of the NineTeen Complex (NTC) in regulating spliceosome conformations and fidelity during pre-mRNA splicing.Senescence-associated secretory phenotype and its possible role in chronic obstructive pulmonary disease.Enhancement of mitochondrial biogenesis with polyphenols: combined effects of resveratrol and equol in human endothelial cells.The cell senescence inducing gene product MORF4 is regulated by degradation via the ubiquitin/proteasome pathway.ATM-dependent phosphorylation of SNEVhPrp19/hPso4 is involved in extending cellular life span and suppression of apoptosis.Endothelial cells maintain a reduced redox environment even as mitochondrial function declines.Quantitative proteomic analysis reveals induction of premature senescence in human umbilical vein endothelial cells exposed to chronic low-dose rate gamma radiation.The Dual Role of Cellular Senescence in Developing Tumors and Their Response to Cancer Therapy.
P2860
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P2860
Subtractive hybridization of mRNA from early passage and senescent endothelial cells.
description
2000 nî lūn-bûn
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2000 թուականի Մարտին հրատարակուած գիտական յօդուած
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2000 թվականի մարտին հրատարակված գիտական հոդված
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2000年の論文
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2000年論文
@yue
2000年論文
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2000年論文
@zh-hk
2000年論文
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2000年論文
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2000年论文
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name
Subtractive hybridization of mRNA from early passage and senescent endothelial cells.
@ast
Subtractive hybridization of mRNA from early passage and senescent endothelial cells.
@en
type
label
Subtractive hybridization of mRNA from early passage and senescent endothelial cells.
@ast
Subtractive hybridization of mRNA from early passage and senescent endothelial cells.
@en
prefLabel
Subtractive hybridization of mRNA from early passage and senescent endothelial cells.
@ast
Subtractive hybridization of mRNA from early passage and senescent endothelial cells.
@en
P2093
P1476
Subtractive hybridization of mRNA from early passage and senescent endothelial cells.
@en
P2093
Grabherr RM
Grillari J
Hohenwarter O
Katinger H
P304
P356
10.1016/S0531-5565(00)00080-2
P577
2000-03-01T00:00:00Z