| ID | Sequence | Length | GC content |
|---|---|---|---|
| AGUGGCUGGUAGGCAGUGGCUGGGAGGCAGCGGCCCAAUUAGUGUCGUG… | 1250 nt | 0.5000 | |
| AGUGGCUGGUAGGCAGUGGCUGGGAGGCAGCGGCCCAAUUAGUGUCGUG… | 1114 nt | 0.4722 | |
| AGUGGCUGGUAGGCAGUGGCUGGGAGGCAGCGGCCCAAUUAGUGUCGUG… | 1352 nt | 0.5074 |
This gene 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. The DNA damage-induced transcription of this gene is mediated by both p53-dependent and -independent mechanisms. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene.[provided by RefSeq, Dec 2010] CIViC Summary for GADD45A Gene
A study in human primary lung microvascular endothelial cells demonstrated that acute X-ray irradiation (10 Gy) induced significant transcriptional changes, including the upregulation of the GADD45A gene, which showed a 3.4-fold increase in mRNA expression at 24 hours post-irradiation as part of the DNA damage response [Bouten et al. DOI:10.1038/s41598-021-03636-7]. A study in human keratinocytes and mouse skin demonstrated that X-ray irradiation induced the expression of the GADD45A mRNA, which was identified as a proapoptotic gene induced by UVB irradiation [Koike et al. DOI:10.1269/jrr.46.173]. In a separate mouse model of myotonic dystrophy, Ingenuity Pathway Analysis indicated that downregulation of epidermal growth factor activated the GADD45A as part of a stress response network in cardiomyocytes [Lee et al. DOI:10.1093/hmg/ddac108].