DOI . ORG {
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We began analyzing https://link.springer.com/chapter/10.1007/978-1-4614-8289-5_5, but it redirected us to https://link.springer.com/chapter/10.1007/978-1-4614-8289-5_5. The analysis below is for the second page.
Title[redir]:
Gadd45 in the Liver: Signal Transduction and Transcriptional Mechanisms | SpringerLink
Description:
Injury and growth stimulation both remarkably increase the hepatic expression of Gadd45β. In liver cancer, promoter methylation frequently silences Gadd45β, demonstrating due to a suppressive function that is often proapoptotic. This contrasts with normal...
Title[redir]:
Gadd45 in the Liver: Signal Transduction and Transcriptional Mechanisms | SpringerLink
Description:
Injury and growth stimulation both remarkably increase the hepatic expression of Gadd45β. In liver cancer, promoter methylation frequently silences Gadd45β, demonstrating due to a suppressive function that is often proapoptotic. This contrasts with normal...
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Keywords {🔍}
google, scholar, pubmed, article, cas, liver, cell, gadd, growth, expression, jnk, nuclear, receptor, biol, gene, chapter, binding, gaddbeta, transcriptional, gaddβ, regeneration, dna, factor, res, analysis, genes, cancer, proliferation, kinase, arrest, papa, mice, chem, signal, car, hepatocellular, carcinoma, induction, nature, mol, hoffman, beta, privacy, cookies, content, information, publish, stress, mechanisms, tian,
Topics {✒️}
c-jun-dependent cell proliferation month download article/chapter quantitative real-time pcr insulin-regulated gene expression estrogen receptor/coactivator recognition jnk2-foxo3-gadd45 pathway smad4-dependent transcriptional induction mediates nuclear-receptor function gadd45β binds mkk7—downstream cell growth arrest direct dna binding tumor necrosis factor diverse stress conditions sorafenib-induced apoptosis gadd45 beta mediates gadd45 beta forms gadd45a gene expression anti-apoptotic gadd45b ledda-columbano gm decreased dna repair increases cytotoxicity induced early response genes privacy choices/manage cookies gadd45-beta transcription differentially expressed genes constitutive androstane receptor de novo growth device instant download hepatocyte proliferation induced smad-dependent expression rna binding protein modulating jnk signaling von knebel dm gadd45 family proteins editor information editors transcriptional mechanisms chapter mtor signaling pathway hepatocellular carcinoma cells nuclear factor kappa joseph locker stress signaling p38 mapk signal altering bcl-2 proteins targeting mkk7/jnkk2 chapter tian murine liver hyperplasia cyclin-d1 expression gadd45beta-mediated inactivation growth arrest tnf-independent pathway
Schema {🗺️}
ScholarlyArticle:
headline:Gadd45 in the Liver: Signal Transduction and Transcriptional Mechanisms
pageEnd:80
pageStart:69
image:https://media.springernature.com/w153/springer-static/cover/book/978-1-4614-8289-5.jpg
genre:
Biomedical and Life Sciences
Biomedical and Life Sciences (R0)
isPartOf:
name:Gadd45 Stress Sensor Genes
isbn:
978-1-4614-8289-5
978-1-4614-8288-8
type:Book
publisher:
name:Springer New York
logo:
url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
type:ImageObject
type:Organization
author:
name:Jianmin Tian
affiliation:
name:University of Pittsburgh School of Medicine
address:
name:Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, USA
type:PostalAddress
type:Organization
type:Person
name:Joseph Locker
affiliation:
name:University of Pittsburgh School of Medicine
address:
name:Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, USA
type:PostalAddress
type:Organization
email:[email protected]
type:Person
keywords:Liver Regeneration, Partial Hepatectomy, Constitutive Androstane Receptor, Transcriptional Mechanism, Gadd45 Protein
description:Injury and growth stimulation both remarkably increase the hepatic expression of Gadd45β. In liver cancer, promoter methylation frequently silences Gadd45β, demonstrating due to a suppressive function that is often proapoptotic. This contrasts with normal hepatocytes, where Gadd45β facilitates cell survival, growth, and proliferation. Gadd45β binds MKK7—downstream of TNFα and its receptors—to prevent this kinase from activating JNK2. Hence, the Gadd45b−/− genotype increases cell injury and decreases cell proliferation during liver regeneration (i.e., compensatory growth and proliferation). Liver hyperplasia (i.e., de novo growth and proliferation) is an alternate form of growth, caused by drugs that activate the nuclear receptor, CAR. As in regeneration, the Gadd45b−/− genotype considerably slows growth during hyperplasia. However, there is no injury and the slowing occurs because Gadd45β normally binds to CAR and activates its transcriptional stimulation. Thus, Gadd45β protects the liver through two entirely different processes: binding MKK7 to block damaging signal transduction or binding CAR to coactivate anabolic transcription.
datePublished:2013
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name:Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, USA
type:PostalAddress
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name:Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, USA
name:Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, USA
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