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Growth arrest and DNA-damage-inducible, beta

GADD45B, GADD45beta, MyD118
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 genes in this group respond to environmental stresses by mediating activation of the p38/JNK pathway. This activation is mediated via their proteins binding and activating MTK1/MEKK4 kinase, which is an upstream activator of both p38 and JNK MAPKs. The function of these genes or their protein products is involved in the regulation of growth and apoptosis. These genes are regulated by different mechanisms, but they are often coordinately expressed and can function cooperatively in inhibiting cell growth. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: GADD45, Cr6, p53, JNK, CAN
Papers using GADD45B antibodies
Cytoplasmic accumulation of the nuclear receptor CAR by a tetratricopeptide repeat protein in HepG2 cells.
Supplier
Zanger Ulrich, In PLoS ONE, 2002
... serum from Atlanta biological; anti-phospho-SAPK/JNK (Thr183/Thy185) antibody and anti-SAPK/JNK (56G8) antibody from Cell Signaling Technology; GADD45B (N-19) antibody from Santa Cruz Biotechnology; CytoTox 96 kit from ...
Papers on GADD45B
Cancer cell-selective killing polymer/copper combination.
New
Xu et al., Columbia, United States. In Biomater Sci, Jan 2016
In addition, RNA microarray analysis revealed that the treatment can reverse cancer cells' upregulated oncogenes (CIRBP and STMN1) and downregulated tumor suppressor genes (CDKN1C and GADD45B) to further enhance the selectivity for cancer cells.
Microarray Analysis of Human Blood During Electroconvulsive Therapy.
New
Yoneda et al., Suita, Japan. In J Ect, Dec 2015
RESULTS: Of 4 genes examined (AKT3, TCF7, PPP3R1, and GADD45B), only TCF7 was increased during the mECT procedure (P = 0.0025).
Simultaneous Host-Pathogen Transcriptome Analysis during Granulibacter bethesdensis Infection of Neutrophils from Healthy Subjects and Patients with Chronic Granulomatous Disease.
New
Zarember et al., Dallas, United States. In Infect Immun, Nov 2015
We detected upregulation of antiapoptotic genes (e.g., XIAP and GADD45B) and downregulation of proapoptotic genes (e.g., CASP8 and APAF1) in infected PMN.
Mineralocorticoid receptors are present in skeletal muscle and represent a potential therapeutic target.
New
Rafael-Fortney et al., Columbus, United States. In Faseb J, Nov 2015
Genes down-regulated more than 2-fold by MR antagonism included FOS, ANKRD1, and GADD45B, with known roles in skeletal muscle, in addition to NPR3 and SERPINA3, bona fide targets of MR in other tissues.
Effects of a Neonatal Experience Involving Reward Through Maternal Contact on the Noradrenergic System of the Rat Prefrontal Cortex.
New
Stamatakis et al., Athens, Greece. In Cereb Cortex, Sep 2015
The RER experience resulted in adulthood in increased levels of the active demethylase GADD45b, hypomethylation of the β1 adrenergic receptor (ADRB1) gene promoter, and consequent enhanced expression of its mRNA in the PFC.
Global Transcriptional Changes Following Statin Treatment in Breast Cancer.
New
Borgquist et al., Lund, Sweden. In Clin Cancer Res, Sep 2015
Significantly upregulated genes included DUSP1, RHOB1, GADD45B, and RGS1.
T-cell activation and early gene response in dogs.
Williamson et al., Sydney, Australia. In Plos One, 2014
These included, prostaglandin-endoperoxide synthase 2 (PTGS2/COX2), early growth response 1 (EGR1), growth arrest and DNA damage-inducible gene (GADD45B), phorbol-12-myristate-13-acetate-induced protein 1 (PMAIP1), V-FOS FBJ murine osteosarcoma viral oncogene homolog (FOS), early growth response 2 (EGR2), hemogen (HEMGN), polo-like kinase 2 (PLK2) and polo-like kinase 3 (PLK3).
Inhibition of microRNA-1 attenuates hypoxia/re-oxygenation-induced apoptosis of cardiomyocytes by directly targeting Bcl-2 but not GADD45Beta.
Zhang et al., Jinan, China. In Am J Transl Res, 2014
MicroRNAs are small non-coding RNAs that are able to regulate gene expression and play important roles in some biological and pathological processes, including the myocardial ischemia/reperfusion (I/R) injury.
Genetic and epigenetic mutations of tumor suppressive genes in sporadic pituitary adenoma.
Review
Klibanski et al., Boston, United States. In Mol Cell Endocrinol, 2014
The RB group includes CDKN2A, CDKN2B, CDKN2C, RB1, BMP4, CDH1, CDH13, GADD45B and GADD45G; AIP and MEN1 genes also belong to this group.
Comparison of immunological characteristics of peripheral, splenic and tonsilar naïve B cells by differential gene expression meta-analyses.
Review
Ruxrungtham et al., Bangkok, Thailand. In Asian Pac J Allergy Immunol, 2012
These included enhanced expressions of CD27, CR2, EGR1, GADD45B, ICAM1, ICOSLG, IGHA, IL6, MMP9, SAMSN1, SMAD7, TNFAIP3, but reduced HLA-DOB expression.
Gadd45a and Gadd45b modulate innate immune functions of granulocytes and macrophages by differential regulation of p38 and JNK signaling.
GeneRIF
Liebermann et al., Philadelphia, United States. In J Cell Physiol, 2012
these data highlight a novel role for both Gadd45a and Gadd45b in myeloid innate immune functions by differential modulation of p38 and JNK signaling in granulocytes compared to macrophages.
Growth arrest and DNA-damage-inducible, beta (GADD45b)-mediated DNA demethylation in major psychosis.
GeneRIF
Guidotti et al., Chicago, United States. In Neuropsychopharmacology, 2012
finding show there is an increased expression and decreased promoter binding of GADD45b in psychotic subjects.
Gadd45a, Gadd45b and Gadd45g expression during mouse embryonic development.
GeneRIF
Niehrs et al., Heidelberg, Germany. In Gene Expr Patterns, 2011
Gadd45a, Gadd45b and Gadd45g expression during mouse embryonic development.
Gadd45β is an inducible coactivator of transcription that facilitates rapid liver growth in mice.
GeneRIF
Locker et al., New York City, United States. In J Clin Invest, 2011
defined separate Gadd45beta domains that mediated binding to CAR and transcriptional activation
[The effects of the cadmium chloride on the DNA damage and the expression level of gadd gene in HepG2 cell line].
GeneRIF
Fan et al., Shijiazhuang, China. In Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi, 2011
Cadmium chloride can induce DNA damage and increase expression levels of the gadd153 and gadd45beta promoters in HepG2 cells.
Redox regulation of tumor necrosis factor signaling.
Review
Kaplowitz et al., Los Angeles, United States. In Antioxid Redox Signal, 2009
In liver and other tissues, TNF treatment results in the simultaneous activation of an apoptotic pathway (i.e., TRADD, RIP, JNK) and a survival pathway mediated by NF-kappaB transcription of survival genes (i.e., GADD45beta, Mn-SOD, cFLIP).
Gadd45 modulation of intrinsic and extrinsic stress responses in myeloid cells.
Review
Liebermann et al., Philadelphia, United States. In J Cell Physiol, 2009
Induction of gadd45 genes at the onset of myeloid differentiation suggested that Gadd45 protein(s) play a role in hematopoiesis, yet no apparent abnormalities were observed in either the bone marrow (BM) or peripheral blood compartments of mice deficient for either gadd45a or gadd45b.
Role of gadd45 in myeloid cells in response to hematopoietic stress.
Review
Liebermann et al., Philadelphia, United States. In Blood Cells Mol Dis, 2007
Induction of gadd45 genes at the onset of myeloid differentiation suggested that Gadd45 protein(s) play a role in hematopoiesis, yet no apparent abnormalities were observed in either the bone marrow or peripheral blood compartments of mice deficient for either gadd45a or gadd45b.
Induction of gadd45beta by NF-kappaB downregulates pro-apoptotic JNK signalling.
Impact
Franzoso et al., Chicago, United States. In Nature, 2001
This link involves the transcriptional upregulation of gadd45beta/myd118 (ref.
A family of stress-inducible GADD45-like proteins mediate activation of the stress-responsive MTK1/MEKK4 MAPKKK.
Impact
Saito et al., Boston, United States. In Cell, 1998
Using a yeast two-hybrid method, three related proteins, GADD45alpha (= GADD45), GADD45, (= MyD118), and GADD45gamma, were identified that bound to an N-terminal domain of MTK1.
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