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LINK . SPRINGER . COM {}

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  2. Matching Content Categories
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  4. Monthly Traffic Estimate
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We are analyzing https://link.springer.com/article/10.1007/s00011-013-0590-7.

Title:
NF-κB RNAi decreases the Bax/Bcl-2 ratio and inhibits TNF-α-induced apoptosis in human alveolar epithelial cells | Inflammation Research
Description:
Objective Apoptosis of alveolar epithelial cells (AECs) plays a key role in acute lung injury (ALI). Understanding the underlying mechanism is conducive to the treatment of ALI. The goal of this study was to determine the possible involvement of nuclear factor-κB (NF-κB)/p65 and Bax/Bcl-2 in tumor necrosis factor-α (TNF-α)-induced apoptosis in AECs. Methods Type II AECs, A549, with or without NF-κB/p65 expression silenced by small interfering RNA (siRNA) were challenged with TNF-α. The levels of NF-κB/p65, Bcl-2 and Bax were detected by reverse transcription-polymerase chain reaction, Western blotting, and immunocytochemical staining. The apoptosis rate was measured by flow cytometry. Results TNF-α challenge significantly increased the transcription and translation of NF-κB/p65 and Bax genes, but significantly decreased the Bcl-2 gene level. siRNA silencing of NF-κB/p65 reversed the effect of TNF-α on NF-κB/p65, Bcl-2 and Bax, and significantly decreased the TNF-α-induced apoptosis rate of AECs, as compared to the non-silenced cells. Conclusions This study indicates that NF-κB plays an important role in the process of TNF-α-induced apoptosis in AECs, via regulation of the expression of Bcl-2 and Bax.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We see no obvious way the site makes money.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

article, google, scholar, pubmed, cas, apoptosis, acute, lung, cells, injury, alveolar, epithelial, regulation, nfkappab, med, research, inflammation, tnfαinduced, nfκbp, bax, access, pulmonary, crit, care, respiratory, privacy, cookies, content, aecs, role, nuclear, type, bcl, transcription, cell, curr, immunol, information, publish, search, nfκb, human, huang, weifeng, respir, neutrophil, distress, syndrome, opin, data,

Topics {✒️}

rel/nf-kappab transcription factors nf-κb rnai decreases tumor necrosis factor-α inhibits tnf-α-induced apoptosis nuclear factor-κb tnf-α-induced apoptosis rate month download article/chapter nuclear factor-kappab1 nf-κb/p65 expression silenced small interfering rna tnf-α-induced apoptosis alveolar epithelial cells nf-κb/p65 reversed lipopolysaccharide-stimulated polymorphonuclear neutrophils alveolar epithelial type ng-nitro-l-arginine fas-induced pulmonary apoptosis nf-kappab pathway inhibition bcl-2 gene level bcl-2-regulated apoptosis switch related subjects small interfering rnas rel/nf-κb acute lung injury acute lung injury nf-κb/p65 epithelial cell apoptosis full article pdf nf-kappab rela nf-kappab inhibitors nf-κb plays privacy choices/manage cookies crit care med ikk nf-kappa nf-κb lung liquid homeostasis tnf family receptors article li major pathway responsible curr med chem curr opin immunol check access instant access bax/bcl-2 ratio nf-kappab induced apoptosis programmed cell death biochem cell biol polymorphonuclear neutrophil apoptosis neutrophil activation

Questions {❓}

  • Epithelial cell apoptosis and neutrophil recruitment in acute lung injury—a unifying hypothesis?

Schema {🗺️}

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         headline:NF-κB RNAi decreases the Bax/Bcl-2 ratio and inhibits TNF-α-induced apoptosis in human alveolar epithelial cells
         description:Apoptosis of alveolar epithelial cells (AECs) plays a key role in acute lung injury (ALI). Understanding the underlying mechanism is conducive to the treatment of ALI. The goal of this study was to determine the possible involvement of nuclear factor-κB (NF-κB)/p65 and Bax/Bcl-2 in tumor necrosis factor-α (TNF-α)-induced apoptosis in AECs. Type II AECs, A549, with or without NF-κB/p65 expression silenced by small interfering RNA (siRNA) were challenged with TNF-α. The levels of NF-κB/p65, Bcl-2 and Bax were detected by reverse transcription-polymerase chain reaction, Western blotting, and immunocytochemical staining. The apoptosis rate was measured by flow cytometry. TNF-α challenge significantly increased the transcription and translation of NF-κB/p65 and Bax genes, but significantly decreased the Bcl-2 gene level. siRNA silencing of NF-κB/p65 reversed the effect of TNF-α on NF-κB/p65, Bcl-2 and Bax, and significantly decreased the TNF-α-induced apoptosis rate of AECs, as compared to the non-silenced cells. This study indicates that NF-κB plays an important role in the process of TNF-α-induced apoptosis in AECs, via regulation of the expression of Bcl-2 and Bax.
         datePublished:2013-01-20T00:00:00Z
         dateModified:2013-01-20T00:00:00Z
         pageStart:387
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            Nuclear factor-κB
            Immunology
            Pharmacology/Toxicology
            Rheumatology
            Allergology
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      headline:NF-κB RNAi decreases the Bax/Bcl-2 ratio and inhibits TNF-α-induced apoptosis in human alveolar epithelial cells
      description:Apoptosis of alveolar epithelial cells (AECs) plays a key role in acute lung injury (ALI). Understanding the underlying mechanism is conducive to the treatment of ALI. The goal of this study was to determine the possible involvement of nuclear factor-κB (NF-κB)/p65 and Bax/Bcl-2 in tumor necrosis factor-α (TNF-α)-induced apoptosis in AECs. Type II AECs, A549, with or without NF-κB/p65 expression silenced by small interfering RNA (siRNA) were challenged with TNF-α. The levels of NF-κB/p65, Bcl-2 and Bax were detected by reverse transcription-polymerase chain reaction, Western blotting, and immunocytochemical staining. The apoptosis rate was measured by flow cytometry. TNF-α challenge significantly increased the transcription and translation of NF-κB/p65 and Bax genes, but significantly decreased the Bcl-2 gene level. siRNA silencing of NF-κB/p65 reversed the effect of TNF-α on NF-κB/p65, Bcl-2 and Bax, and significantly decreased the TNF-α-induced apoptosis rate of AECs, as compared to the non-silenced cells. This study indicates that NF-κB plays an important role in the process of TNF-α-induced apoptosis in AECs, via regulation of the expression of Bcl-2 and Bax.
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         Allergology
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      name:Department of Respiratory Medicine, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou, People’s Republic of China
      name:Department of Respiratory Medicine, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou, People’s Republic of China
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