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Human Monoclonal GADD45A Primary Antibody for PLA, ELISA - ABIN560584
Al-Romaih, Sadikovic, Yoshimoto, Wang, Zielenska, Squire: Decitabine-induced demethylation of 5' CpG island in GADD45A leads to apoptosis in osteosarcoma cells. in Neoplasia (New York, N.Y.) 2008
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Human Polyclonal GADD45A Primary Antibody for FACS, WB - ABIN650724
Li, Morales, Hwang, Wagner, Boothman: DNA mismatch repair-dependent activation of c-Abl/p73alpha/GADD45alpha-mediated apoptosis. in The Journal of biological chemistry 2008
Show all 5 Pubmed References
Human Polyclonal GADD45A Primary Antibody for IF (p), IHC (p) - ABIN685432
Yuan, Han, Cong, Ge, Ma, Dai, Li, Bi: Docetaxel-loaded solid lipid nanoparticles suppress breast cancer cells growth with reduced myelosuppression toxicity. in International journal of nanomedicine 2014
Gadd45a and Gadd45g regulate neural development and exit from pluripotency in Xenopus.
Results provide evidence for a coupled mechanism of 5-methylcytosine (5-meC) demethylation, whereby 5-meC deaminase (AID) deaminates 5-meC, followed by thymine base excision by G:T mismatch-specific thymine glycosylase (Mbd4), promoted by Gadd45.
GADD45A gene variants are associated with meat quality in pigs.
Gadd45a relaxes the promoter regions of miR-295 and promotes the expression of miR-295 during reprogramming, implying a concise mechanism of Gadd45a and miR-290 cluster cooperation in cell-fate determination.
Retinoic acid inhibits white adipogenesis by inducing retinoic acid receptor and ING1 interaction and inhibiting Gadd45a expression, which prevents GADD45A-mediated DNA demethylation.
identifed Gadd45a as a chromatin relaxer in embryonic fibroblasts, which also enhances somatic cell reprogramming efficiency; showed that residue glycine 39 in Gadd45a is essential for interacting with core histones, opening chromatin and enhancing reprogramming. demonstrateed that Gadd45a destabilizes histone-DNA interactions and facilitates binding of Yamanaka factors to their targets for activation
Data show that loss of growth arrest and DNA-damage-inducible 45 alpha protein (Gadd45a) accelerates the onset of BCR-ABL driven leukemia in bone marrow recipient mice.
by forming a complex with MEKK4 in skeletal muscle fibers, Gadd45a increases MEKK4 protein kinase activity, which is both sufficient to induce skeletal muscle fiber atrophy and required for Gadd45a-mediated skeletal muscle fiber atrophy.
Gadd45a may counteract hepatic fi brosis by regulating the activation of hepatic stellate cells via the inhibition of TGF-beta/Smad signaling.
These data indicate that genotoxic stress-induced GADD45A expression in HSCs prevents their fatal transformation by directing them into differentiation and thereby clearing them from the system
provide the novel evidence that GADD45A inhibits autophagy via impairing the BECN1-PIK3C3 complex formation
Results suggest the possibility that differential Gadd45a, Gadd45b and Gadd45g expression during development affects neurons, contributing cortical evolution and diversity
GADD45a promoter regulation by a functional genetic variant is associated with acute mechanical lung injury.
In SOD1 and Neurotomized mice the results of this studysuggest LC3, Fn14, Bcl3 and Gadd45a as candidate genes involved in the maintenance of the severe atrophic state.
results for the first time demonstrate that nucleolin-SUMO at K294R plays a critical role in its nucleus sequestration and gadd45alpha mRNA binding activity.
Dendrin is dispensable for the function of the normal glomerular filtration barrier, and it interacts with Wtip and Gadd45a.
Loss of Gadd45a leads to more DNA damage accumulation and increased sensitivity to ionizing radiation.
Signalling pathway analyses indicate that Gadd45a overexpression suppresses Akt, P38 and JNK phosphorylation.
results suggest Gadd45g is involved in the regulation of epithelial cell proliferation through induction of p21 via the p38 MAPK pathway during tooth germ development.
these results identify HDAC4 as an important regulator of Gadd45a in denervation-induced muscle atrophy and elucidate Gadd45a as a convergence point for distinct upstream regulators during muscle denervation and fasting.
Gadd45a inhibits tumor angiogenesis via blocking of the mTOR/STAT3 pathway.
The expression of Gadd45a in normal, developing brain is tightly regulated.
To examine the functions of Gadd45a in cell invasion and metastasis, we performed the adhesion, wound-healing and transwell assays in Gadd45a (+/+) and Gadd45a (-/-) MEF cell lines.
GADD45A is an epigenetic R-loop reader that recruits the demethylation machinery to promoter CGIs.
Over-expression of Gadd45a and activation of the p38 MAPK signaling pathway are associated with oxidative stress (OS) in preeclampsia (PE). Furthermore, Gadd45a knockdown promotes cell migration and invasion, and the tube formation, thus alleviating OS in PE.
GADD45A protein protects different GBM cell lines, which express different level of chemo-sensitivity and TP53 status, from TMZ induced genotoxicity.
data in the current study have revealed a novel role for IKKbeta in negatively regulating GADD45alpha protein stability and the contribution of p53-dependent IKKbeta reduction to mediating cancer cell apoptosis.
Our results suggested that p53 could alternatively upregulate GADD45A in human NSCLC cells through a post-transcriptional pathway in which miR-138 is involved.
Microarray analysis revealed differential expression of three vitamin D associated genes in the aortic adventitia in rheumatoid arthritis (RA) and non-RA patients with coronary artery disease: while the expression of GADD45A and NCOR1 was higher, the expression of PON2 was lower in RA patients.
Human miR-374 induces apoptosis and inhibits proliferation, migration, and invasion of human squamous carcinoma cells through P53 signaling pathway by down-regulating Gadd45a.
Findings demonstrated that miR-148a promotes glioma cell invasion and tumorigenesis by downregulating GADD45A. Findings provide novel insights into how GADD45A is downregulated by miR-148a in IDH1R132H glioma
A mechanism in which GADD45a is required for demethylation of the MMP-9 promoter and the induction of diabetic wound healing. The inhibition of GADD45a might be a therapeutic strategy for diabetic foot ulcers.
present study provides evidence that variations in GADD45B rs2024144T, MAPK14 rs3804451A and GADD45A rs581000C may predict platinum-based chemotherapy toxicity outcomes in patients with advanced non-small cell lung cancer
Our findings indicate that GADD45 essentially suppresses the MKK7-JNK pathway and suggest that differentially expressed GADD45 family members fine-tune stress-inducible JNK activity.
Stimulation of ribosomal RNA gene promoter by transcription factor Sp1 involves active DNA demethylation by Gadd45-NER pathway.
The findings indicate that p38alpha and GADD45alpha are involved in an enhanced vitamin D signaling on TRPV6 expression.
the enhancement of GADD45A-mediated base excision repair modulated by ATF2 might be a potential protective mechanism of visible red light.
Data show that growth arrest and DNA-damage-inducible 45 alpha protein (Gadd45a) expression is up-regulated in chronic phase myelocytic leukemia, chronic (CML) patient samples but down-regulated in accelerated and blast crisis phase samples.
These data revealed that Riboflavin plus ultraviolet (UV) pathogen reduction technology effectively inhibited proliferation and induced apoptosis of lymphocytes by promoting GADD45alpha expression, which subsequently activates p38 and JNK signaling pathways.
data suggest GADD45 proteins play a role in controlling HIV-1 transcription and in regulating HIV-1 latency
Taken together, our results suggest that ROS generation might be a predisposing event in berberine-induced mitochondrial apoptosis in EBV-transformed B cells through the upregulation of XAF1 and GADD45alpha expression by MAPK and functional p53.
Collective results lead us to conclude that GADD45alpha modulates curcumin sensitivity through activation of c-Abl > JNK signaling in a mismatch repair-dependent manner
BRCA1 may act as an important negative regulator in cell cycle progression and tumorigenesis through regulating the stability of Smad4; this defines a novel link that connects BRCA1 to TGF-beta1/Smad pathway.
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.
growth arrest and DNA-damage-inducible, alpha
, growth arrest and DNA damage-inducible protein GADD45 alpha
, growth arrest and DNA-damage-inducible protein 45 alpha
, growth arrest and DNA-damage-inducible protein alpha
, growth arrest and DNA damage-inducible protein 45
, Growth arrest and DNA-damage-inducible protein GADD45 alpha
, DNA damage-inducible transcript 1 protein
, DNA-damage inducible transcript 1
, DNA-damage-inducible transcript 1
, growth arrest and DNA-damage-inducible protein GADD45 alpha
, DNA damage-inducible transcript-1
, growth arrest and DNA-damage-inducible 45 alpha