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Growth arrest and DNA-damage-inducible, alpha

GADD45, Gadd45a, GADD45alpha
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] (from NCBI)
Top mentioned proteins: p53, p21, CAN, PCNA, Bax
Papers on GADD45
Benzyl isothiocyanate alters the gene expression with cell cycle regulation and cell death in human brain glioblastoma GBM 8401 cells.
Chung et al., Laizhou, China. In Oncol Rep, Feb 2016
The results show that expression of 317 genes was upregulated, and two genes were associated with DNA damage, the DNA-damage-inducible transcript 3 (DDIT3) was increased 3.66-fold and the growth arrest and DNA-damage-inducible α (GADD45A) was increased 2.34-fold.
The DNA-damage response gene GADD45A induces differentiation in hematopoietic stem cells without inhibiting cell cycle or survival.
Rieger et al., Frankfurt am Main, Germany. In Stem Cells, Feb 2016
Growth arrest and DNA-damage-inducible 45 alpha (GADD45A) is induced by genotoxic stress in HSCs.
The dual nature of Nek9 in adenovirus replication.
Pelka et al., Canada. In J Virol, Jan 2016
Here we show that Nek9 is a transcriptional repressor that functions together with E1A to silence the expression of p53-inducible GADD45A gene in the infected cell.
Selective inhibition of the p38 alternative activation pathway in infiltrating T cells inhibits pancreatic cancer progression.
Ashwell et al., Bethesda, United States. In Nat Med, Nov 2015
Notably, a plasma membrane-permeable peptide derived from GADD45-α, the naturally occurring inhibitor of p38 pY323(+) (ref.
Fucoxanthin and Its Metabolite Fucoxanthinol in Cancer Prevention and Treatment.
Martin, Moncton, Canada. In Mar Drugs, Aug 2015
Anti-proliferative and cancer preventing influences of fucoxanthin and fucoxanthinol are mediated through different signalling pathways, including the caspases, Bcl-2 proteins, MAPK, PI3K/Akt, JAK/STAT, AP-1, GADD45, and several other molecules that are involved in cell cycle arrest, apoptosis, anti-angiogenesis or inhibition of metastasis.
Akbu-LAAO exhibits potent anti-tumor activity to HepG2 cells partially through produced H2O2 via TGF-β signal pathway.
Sun et al., Dalian, China. In Sci Rep, 2014
TGF-β pathway related molecules CYR61, p53, GDF15, TOB1, BTG2, BMP2, BMP6, SMAD9, JUN, JUNB, LOX, CCND1, CDK6, GADD45A, CDKN1A were deregulated in HepG2 following Akbu-LAAO stimulation.
Transcriptome profiling of bovine inner cell mass and trophectoderm derived from in vivo generated blastocysts.
Sirard et al., Eşfahān, Iran. In Bmc Dev Biol, 2014
Moreover, a great majority of genes that were found to be misregulated following in vitro culture of bovine embryos were known genes involved in epigenetic regulation of pluripotency and cell differentiation including DNMT1, GADD45, CARM1, ELF5 HDAC8, CCNB1, KDM6A, PRDM9, CDX2, ARID3A, IL6, GADD45A, FGFR2, PPP2R2B, and SMARCA2.
Whipping NF-κB to Submission via GADD45 and MKK7.
Karin, San Diego, United States. In Cancer Cell, 2014
In this issue of Cancer Cell, Tornatore and colleagues solve this problem by targeting the GADD45:MKK7 module mediating NF-κB-induced survival of multiple myelomas.
Fucoxanthin: a marine carotenoid exerting anti-cancer effects by affecting multiple mechanisms.
Miyashita et al., Hakodate, Japan. In Mar Drugs, 2013
In view of its potent anti-carcinogenic activity, the need to understand the underlying mechanisms has gained prominence. Towards achieving this goal, several researchers have carried out studies in various cell lines and in vivo and have deciphered that fucoxanthin exerts its anti-proliferative and cancer preventing influence via different molecules and pathways including the Bcl-2 proteins, MAPK, NFκB, Caspases, GADD45, and several other molecules that are involved in either cell cycle arrest, apoptosis, or metastasis.
The molecular mechanisms of zinc neurotoxicity and the pathogenesis of vascular type senile dementia.
Kawahara et al., Musashino, Japan. In Int J Mol Sci, 2012
A DNA microarray analysis revealed that the expression of several genes, including metal-related genes (metallothionein and Zn transporter 1), endoplasmic reticulum (ER)-stress related genes (GADD34, GADD45, and p8), and the calcium (Ca)-related gene Arc (activity-related cytoskeleton protein), were affected after Zn exposure.
Gadd45 in modulation of solid tumors and leukemia.
Liebermann et al., Philadelphia, United States. In Adv Exp Med Biol, 2012
The stress response gadd45 gene family participates in cell cycle control, cell survival, apoptosis, maintenance of genomic stability, DNA repair, and active DNA demethylation, in response to environmental and physiological stress including oncogenic stress.
Immunoregulatory molecules are master regulators of inflammation during the immune response.
Sánchez-Madrid et al., Madrid, Spain. In Febs Lett, 2012
In addition, other molecules as CD69, AhR (Aryl hydrocarbon Receptor), and GADD45 (Growth Arrest and DNA Damage-inducible 45) family members, have emerged as potential targets for the regulation of the activation/suppression balance of immune cells.
Stress-induced skeletal muscle Gadd45a expression reprograms myonuclei and causes muscle atrophy.
Adams et al., Iowa City, United States. In J Biol Chem, 2012
Gadd45a reduces multiple barriers to muscle atrophy (including PGC-1alpha, Akt activity, and protein synthesis) and stimulates pro-atrophy mechanisms (including autophagy and caspase-mediated proteolysis).
Gadd45a transcriptional induction elicited by the Aurora kinase inhibitor MK-0457 in Bcr-Abl-expressing cells is driven by Oct-1 transcription factor.
Santucci et al., Bologna, Italy. In Leuk Res, 2012
AK inhibitor MK-0457 induces the growth arrest DNA damage-inducible (Gadd) 45a through recruitment of octamer-binding (Oct)-1 transcription factor at a critical promoter region for gene transcription and covalent modifications of histone H3.
NAMPT pathway is involved in the FOXO3a-mediated regulation of GADD45A expression.
Welte et al., Hannover, Germany. In Biochem Biophys Res Commun, 2012
the increased expression of GADD45A under the above experimental conditions, NAMPT inhibition by FK866, involves acetylation of FOXO3a, a member of the important family of forkhead (FOXO) proteins.
Kinetics of GADD45α, TP53 and CASP3 gene expression in the rat lens in vivo in response to exposure to double threshold dose of UV-B radiation.
Söderberg et al., Stockholm, Sweden. In Exp Eye Res, 2012
A transient upregulation of the stress sensor GADD45alpha, a concurrent downregulation of TP53 and CASP3, followed by a constant upregulation of TP53 that precedes a constant upregulation of CASP3.
Overexpression of DNA damage-induced 45 α gene contributes to esophageal squamous cell cancer by promoter hypomethylation.
Yin et al., Changsha, China. In J Exp Clin Cancer Res, 2011
Overexpression of DNA damage-induced 45 alpha gene contributes to esophageal squamous cell cancer by promoter hypomethylation
Thymine DNA glycosylase is essential for active DNA demethylation by linked deamination-base excision repair.
Bellacosa et al., Philadelphia, United States. In Cell, 2011
TDG interacts with the deaminase AID and the damage response protein GADD45a.
DNMT1 maintains progenitor function in self-renewing somatic tissue.
Khavari et al., Stanford, United States. In Nature, 2010
In contrast, Gadd45A and B, which promote active DNA demethylation, are required for full epidermal differentiation gene induction.
DNA demethylation in zebrafish involves the coupling of a deaminase, a glycosylase, and gadd45.
Cairns et al., Salt Lake City, United States. In Cell, 2009
The injection of methylated DNA into embryos induced a potent DNA demethylation activity, which was attenuated by depletion of AID or the non enzymatic factor Gadd45.
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