Disease relevance of Gadd45b

• MATERIALS: Rat insulinoma INS-1E cells and mouse beta-TC3 cells stably expressing Gadd45b were generated [1].

High impact information on Gadd45b

• In T cells, Gadd45b was rapidly induced by T cell receptor (TCR) and inflammatory signals [2].
• We show that Egr-1 contributes to the regulation of the Gadd45a and Gadd45b genes, which are involved in the control of cell cycle, DNA repair and apoptosis, by direct binding to their promoter [3].
• The present study was undertaken to decipher the molecular paths that mediate the survival functions of Gadd45a and Gadd45b against genotoxic stress induced by UV radiation [4].
• It is shown that in hematopoietic cells exposed to UV radiation Gaddd45a and Gadd45b cooperate to promote cell survival via two distinct signaling pathways involving activation of the GADD45a-p38-NF-kappaB-mediated survival pathway and GADD45b-mediated inhibition of the stress response MKK4-JNK pathway [4].
• Furthermore, we also show that TGF-beta can activate p38 and induce apoptosis in mouse primary hepatocytes from wild-type mice, but not from Gadd45b-/- mice [5].

Biological context of Gadd45b

• Hematopoietic cells from Gadd45a- and Gadd45b-deficient mice are sensitized to genotoxic-stress-induced apoptosis [6].

Associations of Gadd45b with chemical compounds

• Acutely elevating NaCl (and/or urea) reduces Gadd45a, but increases Gadd45b and Gadd45g mRNA, depending on the mix of NaCl and urea and the rate of increase of osmolality [7].

Regulatory relationships of Gadd45b

• Although IL-1beta stimulated the time-dependent induction of endogenous Gadd45b in INS-1E cells and rat islets, expression levels were lower in these cells than in IL-1beta-exposed NIH-3T3 and 3DO T cells [1].

Analytical, diagnostic and therapeutic context of Gadd45b

• Expression of endogenous Gadd45b mRNA was measured by RT-PCR [1].

References