We are analyzing https://link.springer.com/article/10.1007/s11033-008-9419-9.

Title:
Gadd45-α and Gadd45-γ utilize p38 and JNK signaling pathways to induce cell cycle G2/M arrest in Hep-G2 hepatoma cells | Molecular Biology Reports
Description:
The Gadd45 family of proteins, which includes α, β, and γ isoforms, has recently been shown to play a role in the G2/M cell cycle checkpoint in response to DNA damage; however, the mechanisms by which Gadd45 proteins inhibit cell cycle control are not fully understood. Using immunohistochemical analysis, we found that protein expression of Gadd45γ, but not Gadd45α, was down-regulated in hepatocellular carcinoma. We thus investigated possible mechanisms by which Gadd45α and Gadd45γ might differentially induce G2/M arrest in the human hepatoma Hep-G2 cell line. Flow cytometric analysis revealed significant G2/M arrest in cells transfected with either Gadd45α or Gadd45γ. Importantly, we found that expression of either Gadd45α or Gadd45γ activated the P38 and JNK kinase pathways to induce G2/M arrest. Taken together, these findings suggest that the induction of G2/M arrest by Gadd45α or Gadd45γ involves activation of two distinct signaling pathways in Hep-G2 hepatoma cell lines.
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Keywords {🔍}

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Topics {✒️}

dna-damage-inducible proteins 45alpha nf-kappa b-mediated repression stress-responsive mtk1/mekk4/mapkkk month download article/chapter hep-g2 hepatoma cells insulin-stimulated glucose uptake p53-responsive stress protein cdc2/cyclinb1 kinase inhibitors gadd45-mediated growth suppression jnk/sapk-dependent apoptosis cell cycle checkpoint gadd45-γ utilize p38 p53-regulated protein gadd45 cr6-interacting factor1 interacts proteins mediate activation full article pdf stress-inducible gadd45 inhibits cell growth molecular biology privacy choices/manage cookies p38 kinase activity dna damage modifies dna assessibility gadd45 family proteins jnk kinase pathways luhong sun hyo kyun chung cdc2 kinase correlates cancer cell survival myd genes define hypertonic stress phenotype p53-regulated inhibitor differentially induce g2/ gadd45 regulates g2/ cell cycle jnk signaling pathways smad-dependent expression human hepatocellular carcinoma european economic area aryl hydrocarbon receptor altered subcellular distribution anderson cancer center electronic supplementary material sustain g2 arrest distinct signaling pathways gadd45 isoforms contribute conditions privacy policy nuclear protein murine kidney cells fornace aj jr

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         description:The Gadd45 family of proteins, which includes α, β, and γ isoforms, has recently been shown to play a role in the G2/M cell cycle checkpoint in response to DNA damage; however, the mechanisms by which Gadd45 proteins inhibit cell cycle control are not fully understood. Using immunohistochemical analysis, we found that protein expression of Gadd45γ, but not Gadd45α, was down-regulated in hepatocellular carcinoma. We thus investigated possible mechanisms by which Gadd45α and Gadd45γ might differentially induce G2/M arrest in the human hepatoma Hep-G2 cell line. Flow cytometric analysis revealed significant G2/M arrest in cells transfected with either Gadd45α or Gadd45γ. Importantly, we found that expression of either Gadd45α or Gadd45γ activated the P38 and JNK kinase pathways to induce G2/M arrest. Taken together, these findings suggest that the induction of G2/M arrest by Gadd45α or Gadd45γ involves activation of two distinct signaling pathways in Hep-G2 hepatoma cell lines.
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      description:The Gadd45 family of proteins, which includes α, β, and γ isoforms, has recently been shown to play a role in the G2/M cell cycle checkpoint in response to DNA damage; however, the mechanisms by which Gadd45 proteins inhibit cell cycle control are not fully understood. Using immunohistochemical analysis, we found that protein expression of Gadd45γ, but not Gadd45α, was down-regulated in hepatocellular carcinoma. We thus investigated possible mechanisms by which Gadd45α and Gadd45γ might differentially induce G2/M arrest in the human hepatoma Hep-G2 cell line. Flow cytometric analysis revealed significant G2/M arrest in cells transfected with either Gadd45α or Gadd45γ. Importantly, we found that expression of either Gadd45α or Gadd45γ activated the P38 and JNK kinase pathways to induce G2/M arrest. Taken together, these findings suggest that the induction of G2/M arrest by Gadd45α or Gadd45γ involves activation of two distinct signaling pathways in Hep-G2 hepatoma cell lines.
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