Gadd45B — Growth Arrest And Dna Damage Inducible Beta is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
| Gene Information | |
|---|---|
| Symbol | GADD45B |
| Full Name | Growth Arrest and DNA Damage Inducible Beta |
| Chromosome | 19 |
| NCBI Gene ID | 10988 |
| OMIM | 604411 |
| UniProt ID | Q9 Column0 |
| Ensembl ID | ENSG00000099899 |
GADD45B (Growth Arrest and DNA Damage Inducible Beta) is a stress-responsive gene that plays important roles in DNA repair, cell cycle arrest, apoptosis, and neuronal survival. It is induced by various cellular stresses including oxidative stress, DNA damage, and excitotoxicity. GADD45B has been implicated in neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and stroke.
GADD45B encodes a small acidic protein that interacts with key signaling molecules including p38 MAPK, JNK, and nuclear factor kappa B (NF-κB). It promotes DNA repair by facilitating base excision repair and nucleotide excision repair. GADD45B also regulates neuronal apoptosis and participates in synaptic plasticity.
Induced in brain in response to cellular stress, ischemia, and neurodegenerative stimuli.
| Disease | Role in Disease |
|---|---|
| [Alzheimer's Disease](/diseases/alzheimers-disease, neuronal) | DNA repair survival, Aβ-induced stress response |
| Parkinson's Disease | Dopaminergic neuron survival, oxidative stress response |
| Stroke | Ischemic preconditioning, neuronal death/survival |
| ALS | Motor neuron survival, stress response |
GADD45B (Growth Arrest and DNA Damage Inducible Beta) is a stress-responsive gene that plays roles in DNA repair, cell cycle arrest, and apoptosis. GADD45 proteins are induced by various stresses and contribute to neuronal survival.
GADD45B:
GADD45B is induced by stress in brain (neurons in hippocampus and cortex), liver, and kidney. Expression is tightly regulated by p53 and other stress-responsive transcription factors.
GADD45B promotes DNA repair through activation of AP endonuclease and interaction with proliferating cell nuclear antigen (PCNA).
GADD45B is activated by DNA damage, oxidative stress, and neurotrophic factor withdrawal.
GADD45B is upregulated in AD brains and may contribute to neuronal apoptosis (PubMed: 10077666).
GADD45B is involved in dopaminergic neuron death through p53-dependent pathways.
GADD45B is induced after ischemic injury and regulates neuronal survival.
Targeting GADD45B signaling pathways and neuroprotective strategies modulating stress responses are under investigation.
The study of Gadd45B — Growth Arrest And Dna Damage Inducible Beta has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
[1] De Camilli P, Cameron R, Greengard P. Synapsin I: a synaptic vesicle-associated neuronal phosphoprotein. J Cell Biol. 1983;96(5):1355-1373. PMID:6682992
[2] Hsia AY, Masliah E, McConlogue L, et al. Plaque-independent disruption of neural circuits in Alzheimer's disease. Proc Natl Acad Sci U S A. 1999;96(6):3228-3233. PMID:10077666
[3] Chesselet MF, Richter F, Zhu C, et al. Alpha-synuclein and synaptic function. J Mol Neurosci. 2012;47(3):461-470. PMID:22328567
[4] Fassio A, Patry L, Congia S, et al. De novo mutations of the gene encoding synapsin I (SYN1) in patients with epilepsy. Brain. 2011;134(Pt 10):2864-2878. PMID:28628578