Cloning of rat <i>GADD45</i> gene and induction analysis following ionizing radiation in vivo

Yoshida, Toru; Okazaki, Takashi; Hughes, Paul E.; Schneider, Edward L.; Mori, Nozomu

doi:10.1016/0014-5793(96)00012-9

Cited by 14 publications

(5 citation statements)

References 26 publications

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“…3A). The northern analysis shows only one transcript of approximately 1.4 kb for Gadd45a, consistent with its predicted molecular size (Yoshida et al. , 1994, 1996; Kojima et al.…”

Section: Resultssupporting

confidence: 73%

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Selective up‐regulation of the growth arrest DNA damage‐inducible gene Gadd45 alpha in sensory and motor neurons after peripheral nerve injury

Befort¹,

Karchewski²,

Lanoue

et al. 2003

Eur J of Neuroscience

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The growth arrest and DNA damage-inducible gene 45 alpha (Gadd45a) was one of 240 genes found previously by high density oligonucleotide microarray analysis to be regulated in the rat L4 and L5 dorsal root ganglia 3 days after transection of the sciatic nerve (>four-fold up-regulation). The Gadd45a mRNA expression profile investigated by northern blot, RNase protection assay and in situ hybridization in the rat shows negligible constitutive mRNA levels in embryonic, neonatal or adult intact dorsal root ganglia. Within 24 h of a sciatic nerve injury, a very large induction is found that persists for as long as regeneration of injured fibres is prevented by peripheral nerve ligation. When axons are allowed to regrow following sciatic nerve crush injury, Gadd45a expression is terminated at later time points, when levels of other markers of injury return towards normal. Colocalization with activating transcription factor 3-LI and c-jun mRNA implies that all peripherally injured primary sensory and motor neurons express Gadd45a mRNA. Injury to the central axons of dorsal root ganglion neurons produces only a minimal induction of Gadd45a while peripheral inflammation is without effect. Gadd45a is a specific marker of the presence of peripheral axonal injury in adult primary sensory and motor neurons.

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“…3A). The northern analysis shows only one transcript of approximately 1.4 kb for Gadd45a, consistent with its predicted molecular size (Yoshida et al. , 1994, 1996; Kojima et al.…”

Section: Resultssupporting

confidence: 73%

“…, 1991) and the mammalian Gadd45 promoter has at least one AP‐1 site (Hollander et al. , 1993; Yoshida et al. , 1996).…”

Section: Discussionmentioning

confidence: 99%

Selective up‐regulation of the growth arrest DNA damage‐inducible gene Gadd45 alpha in sensory and motor neurons after peripheral nerve injury

Befort¹,

Karchewski²,

Lanoue

et al. 2003

Eur J of Neuroscience

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“…Agents that cause DNA ds-breaks, and lesions that are mainly repaired by base excision repair mechanisms are all potent inducers of Gadd45 Hall et al 1995). For example, Gadd45 has been shown to be rapidly induced in vivo in rat brains following DNA damage by γ-ray radiation (Yoshida et al 1996). In Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Specific PCR primers to rat gadd45 and β-actin were designed using published rat gadd45 (GenBank accession number L32591: Yoshida et al 1996Yoshida et al , 1994 and rat β-actin (GenBank accession number J00691: Nudel et al 1983) mRNA sequences. These primers are to gadd45, G1 (5′-CTG GCT GCG GAT GAA GAT GAC GAC-3′), and G2 (5′-TTA TCC ATG TAG CGA CTT TCC CGG-3′), and to β-actin, RA1 (5′-AAC ACC CCA GCC ATG TAC GTA G-3′), and RA2 (5′-GTG TTG GCA TAG AGG TCT TTA CGG-3′).…”

Section: Isolation Of Total Rna and Semiquantitive Reversementioning

confidence: 99%

“…The demonstrated elevation of p53 following transient ischemia may transactivate a battery of downstream effector genes whose products are involved in DNA repair (Li et al 1994b;Tomasevic et al 1996). One of these p53-dependent genes could be gadd45 (growth arrest and DNA damage inducible gene), which was originally found to be induced by DNA-damaging agents and ionizing radiation (Smith and Fornace 1996;Yoshida et al 1996). In addition, Gadd45 binds directly to proliferating cell nuclear antigen (PCNA), an important component of the DNA replication and nucleotide excision-repair machinery (Smith and Fornace 1996), and which has been shown to decrease following cerebral ischemia in hippocampal CA1 neurons sensitive to this insult (Tomasevic et al 1996).…”

Section: Introductionmentioning

confidence: 99%

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Increases in DNA lesions and the DNA damage indicator Gadd45 following transient cerebral ischemia

Hou¹,

MacManus²

1997

Biochem. Cell Biol.

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Transient global or focal ischemia leads to the production of several types of lesions in the DNA backbone including alkali-labile sites, and both single-stranded (ss) and double-stranded (ds) breaks. The ds breaks result in high molecular weight fragments of 10-50 kbp that contain both 3'- and 5'-OH end-groups, suggesting that more than one endonuclease is involved. This lesioning of DNA is followed by the appearance of the damage-response indicator Gadd45 in the ischemic hemisphere following middle cerebral artery occlusion. By 6 h, gadd45 mRNA was shown to increase by semi-quantitative reverse transcriptase - polymerase chain reaction. In situ hybridization histochemistry indicated that these increases in gadd45 mRNA occurred in pyramidal neurons located on the edge of the infarcted cortex. Gadd45 immunostaining yielded similar findings with maximal protein staining detected at 18 h after occlusion. In neurons, in the infarct core with frank DNA fragmentation shown by in situ TdT-mediated dUTP-biotin nick end labeling (TUNEL) at 24 h, the Gadd45 immunostaining was not visible. Taken together, these findings suggest that Gadd45 responds to DNA damage following ischemia as part of a repair response mounted by brain cells attempting to survive the insult.

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The Role of the Gadd45 Family in the Nervous System: A Focus on Neurodevelopment, Neuronal Injury, and Cognitive Neuroepigenetics

Sultan

Sweatt

2013

Advances in Experimental Medicine and Biology

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The growth arrest and DNA damage-inducible (Gadd)45 proteins have been associated with numerous cellular mechanisms including cell-cycle control, DNA damage sensation and repair, genotoxic stress, neoplasia, and molecular epigenetics. The genes were originally identified in in vitro screens of irradiation- and interleukin-induced transcription and have since been implicated in a host of normal and aberrant central nervous system processes. These include early and postnatal development, injury, cancer, memory, aging, and neurodegenerative and psychiatric disease states. The proteins act through a variety of molecular signaling cascades including the MAPK cascade, cell-cycle control mechanisms, histone regulation, and epigenetic DNA demethylation. In this review, we provide a comprehensive discussion of the literature implicating each of the three members of the Gadd45 family in these processes.

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Cloning of rat GADD45 gene and induction analysis following ionizing radiation in vivo

Cited by 14 publications

References 26 publications

Selective up‐regulation of the growth arrest DNA damage‐inducible gene Gadd45 alpha in sensory and motor neurons after peripheral nerve injury

Selective up‐regulation of the growth arrest DNA damage‐inducible gene Gadd45 alpha in sensory and motor neurons after peripheral nerve injury

Increases in DNA lesions and the DNA damage indicator Gadd45 following transient cerebral ischemia

The Role of the Gadd45 Family in the Nervous System: A Focus on Neurodevelopment, Neuronal Injury, and Cognitive Neuroepigenetics

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