[9] GADD45G interacts with several other proteins that are involved in DNA repair, cell cycle control, apoptosis, and senescence.

[13] Finally, it also became known as Gadd-related protein 17 during its isolation from a cDNA library by Suzuki due to its homology with Gadd45.

[5] GADD45G is a member of a group of genes whose transcript levels are increased following stressful growth arrest conditions and treatment with DNA-damaging agents.

The protein encoded by this gene responds to environmental stresses by mediating activation of the p38/JNK pathway via MTK1/MEKK4 kinase.

[16] In the male sexual development pathway, GADD45G is essential for activating SRY, leading to proper formation of the gonads and sex-determination.

[6] Deletion of an enhancer close to the GADD45G gene is correlated to increased proliferation of neuronal cells, which could account for part of the difference in neural development between humans and other species.

[7] The deletion of the enhancer reduces the expression of the gene in the forebrain allowing for more brain growth in humans.

The gene modulates p21-mediated epithelial cell proliferation by activating the p38 MAPK pathway during the development of teeth.

GADD45G and GADD45A knockdowns are related to improper gastrulation, defective head growth, and shorter axes.

Within the prelimbic prefrontal cortex, the GADD45G gene is immediately expressed and is required for the consolidation of a type of learning in mice termed associative fear memory.

GADD45G may also be involved in recognition of 5-methylcytosine as an alteration in DNA that needs to be repaired to allow induction of learning-related genes.

Thus GADD45G may guide the rapid demethylation of methylcytosine in the promoter regions of learning-related genes by a DNA repair process[20](see also Epigenetics in learning and memory).

[16] It also interacts with CRIF, which causes the inhibition of Cdc2-cyclin B1 and Cdk-cyclin E.[21] GADD45 also works with the cyclin-dependent kinase inhibitor p21, which can cause growth arrest as well.

[25] Mammalian renal inner medullary (IM) cells routinely face and resist hypertonic stress.

Hypertonicity of various forms (NaCl, KCl, sorbitol, or mannitol) always induces GADD45 transcripts, whereas non-hypertonic hyperosmolality (urea) has no effect.