ArticleAdvances in experimental medicine and biology2022
Gadd45 in the Liver: Signal Transduction and Transcriptional Mechanisms.
Article in Advances in experimental medicine and biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Emerging role of FUS in TGFB1 and COL1A1 transcription dependent on GADD45B to induce NASH-fibrosis.Journal of molecular cell biology · 2026Article
- Hepatic Glucocorticoid Receptor Action and Glucose Homeostasis.Endocrine reviews · 2026Review
- Steatotic liver disease induced by TCPOBOP-activated hepatic constitutive androstane receptor: primary and secondary gene responses with links to disease progression.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Transcriptome Sequencing Reveals Autophagy Networks in Rat Livers during the Development of NAFLD and Identifies Autophagy Hub Genes.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Injury and growth stimulation both remarkably increase the hepatic expression of Gadd45β. This contrasts with expression in liver cancer, where promoter methylation frequently silences Gadd45β, due to a suppressive function that is often proapoptotic. In normal hepatocytes, 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 Gadd45β-/- genotype increases cell injury and decreases cell proliferation during liver regeneration (compensatory growth and proliferation). Liver hyperplasia (de novo growth and proliferation) is an alternate form of growth, caused by drugs that activate the nuclear receptor, CAR. As in regeneration, the Gadd45β-/- 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.
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Registered trials
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