GADD45G (1-159) antigen

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443.56 €

Known as:: GADD45G (1-159) antigenic
Catalog number:: 'AR09109PU-N
Product Quantity:: 0.1 mg
Category:: -
Supplier:: ACR
Gene target:: GADD45G (1-159) antigen

Related genes to: GADD45G (1-159) antigen

Gene:: GADD45G ^{NIH gene}
Name:: growth arrest and DNA damage inducible gamma
Previous symbol:: -
Synonyms:: DDIT2, GADD45gamma, GRP17, CR6
Chromosome:: 9q22.2
Locus Type:: gene with protein product
Date approved:: 1999-09-06
Date modifiied:: 2016-10-05

Gene:: MAP9 ^{NIH gene}
Name:: microtubule associated protein 9
Previous symbol:: -
Synonyms:: ASAP, FLJ21159
Chromosome:: 4q32.1
Locus Type:: gene with protein product
Date approved:: 2006-06-15
Date modifiied:: 2015-11-16

Gene:: MOB1A ^{NIH gene}
Name:: MOB kinase activator 1A
Previous symbol:: C2orf6, MOBK1B, MOBKL1B
Synonyms:: FLJ10788, MOB1, FLJ11595, Mob4B, Mats1
Chromosome:: 2p13.1
Locus Type:: gene with protein product
Date approved:: 2001-06-29
Date modifiied:: 2014-11-18

Gene:: RIOK2 ^{NIH gene}
Name:: RIO kinase 2
Previous symbol:: -
Synonyms:: FLJ11159
Chromosome:: 5q15
Locus Type:: gene with protein product
Date approved:: 2003-06-25
Date modifiied:: 2016-10-05

Gene:: SEMA6D ^{NIH gene}
Name:: semaphorin 6D
Previous symbol:: -
Synonyms:: KIAA1479, FLJ11598
Chromosome:: 15q21.1
Locus Type:: gene with protein product
Date approved:: 2004-09-17
Date modifiied:: 2016-01-14

Related products to: GADD45G (1-159) antigen

Related articles to: GADD45G (1-159) antigen

Therapeutic target exploration of Shugan Jianpi formula in liver fibrosis: an integrated lncRNA-mRNA co-expression network analysis.
Shugan Jianpi Formula (SGJPF), a traditional Chinese herbal formulation, has been clinically used for decades in the management of various chronic liver diseases, including liver fibrosis (LF). Previous studies have demonstrated the efficacy of SGJPF in ameliorating pathological manifestations in murine models of LF. However, the precise molecular mechanisms underlying its therapeutic effects remains unclear. In the present study, we aimed to explore the therapeutic mechanisms of SGJPF through comprehensive analysis of LncRNA-mRNA co-expression network.The therapeutic efficacy of SGJPF in a CCL-induced LF murine model was assessed by histopathological alterations, α-smooth muscle actin (α-SMA) and collagen Ⅰ expression. To elucidate the molecular mechanisms underlying the efficacy of SGJPF, whole transcriptome RNA sequencing technology was conducted to identify the LncRNAs and mRNAs expression profiles across control, model, and SGJPF-treated groups. GO function and KEGG pathway enrichment analysis was performed to identify the biological functions and signaling pathways associated with the differentially expressed genes (DEGs). Subsequently, the hub LncRNAs and mRNAs were identified based on fold change and correlation analysis. Finally, biological relevance of these core genes were further validated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in mouse liver tissue, revealing the regulatory interactions between LncRNAs and their target mRNAs. Compared with the control group, 401 differentially expressed (DE) LncRNAs and 1224 DE mRNAs were found in the model group. In addition, compared with the model group, 98 DE LncRNAs and 147 DE mRNAs were identified following treatment with SGJPF. Subsequently, 31 DE LncRNAs and 39 DE mRNAs were obtained and served as potential target genes of SGJPF. Functional annotation of the 31 DE LncRNAs revealed predominant involvement in small molecule metabolic processes, with significant associations observed in circadian rhythm regulation, p53 signaling pathway, TGF beta signaling pathway, and Hippo signaling pathway. Correlation analysis indicated significant associations between these 31 DE LncRNAs and 39 DE mRNAs (|PCC|> 0.65, P < 0.05). Additionally, the expression of 2 LncRNAs (Gm28857, D030074P21Rik) and 5 mRNAs (Cdkn1a, Id1, Id4, Wnt9b, Gadd45g) were confirmed by RT-qPCR in mouse liver tissue, which were consistent with RNA sequencing data. This study delineates the comprehensive LncRNA/mRNA expression profiles in LF treated with SGJPF, which may provide valuable insights into the molecular mechanisms underlying LF pathogenesis and identifying potential therapeutic targets for further investigation. - Source: PubMed
Publication date: 2026/06/03
Wan KaiqiangZhou QiongFeng RuiruiFan ChangShi WeibingXu WenbinJiang HuiZhou Qiumei
Integrated bioinformatics analysis and experimental validation of as a potential senescence biomarker in MASLD.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is closely linked to cellular senescence. Identifying senescence-related biomarkers is crucial for discovering potential diagnostic markers and therapeutic strategies for MASLD. - Source: PubMed
Publication date: 2026/04/29
Li MengyueGao ChangShi YuhuiPeng WenyuYin YuanLu BinFu Zhang
EHMT2 aggravates vascular remodeling via epigenetic inhibition of GADD45G.
Euchromatic histone-lysine N-methyltransferase 2 (EHMT2) has been implicated in cardiovascular diseases, yet its role in vascular remodeling remains incompletely understood. Here we investigated the contribution of EHMT2 to vascular smooth muscle cell (VSMC) proliferation, migration and neointima formation following vascular injury using carotid artery injury models and in vitro VSMC studies. Transcriptomic (RNA sequencing) and epigenomic (CUT&Tag) profiling revealed that EHMT2 levels were elevated in injured arteries and growth-stimulated VSMCs, whereas EHMT2 deletion attenuated injury-induced neointima formation. Mechanistically, EHMT2 methyltransferase activity promoted VSMC proliferation and migration, with pathway analyses implicating cell cycle and growth programs as major downstream targets. We further identified GADD45G as a critical EHMT2-regulated gene characterized by H3K9me2 enrichment, and demonstrated that GADD45G enforced G1-phase arrest by suppressing cyclinB1, cyclinD1, CDK2 and CDK4. Importantly, both genetic and pharmacological inhibition of EHMT2, through GADD45G knockdown or administration of the EHMT2 inhibitor BIX-01294, significantly reduced neointimal lesion formation in injury models. These findings collectively establish EHMT2 as a key epigenetic driver of vascular remodeling by repressing GADD45G and facilitating cell cycle progression, highlighting EHMT2 as a potential therapeutic target for vascular proliferative diseases. - Source: PubMed
Publication date: 2026/05/01
Wang ZelanZhao JunyongLuo WenjianSun NingMa XingyuZhong FangyuanWu BojiTang HengNing KeHe JingyuWang XuhongZhang KunZhang JihangLiu ChuanRen JunZhao YanQin Zhexue
Deoxynivalenol drives liver injury progression by dysregulating core molecular networks: integrated multi-omics, network toxicology and molecular docking analysis.
Deoxynivalenol (DON), a prevalent food-borne mycotoxin, increasingly recognized as a potent driver in the progression of chronic liver disease to cirrhosis and hepatocellular carcinoma (HCC); however, its systematic role is unclear. This study aims to decode the pathogenic networks of DON through an integrated multi-omics and toxicological framework. - Source: PubMed
Publication date: 2026/04/08
Fu YunfengYang SichengPan YatingYan RunweiDu FanZhou Xiaodong
Age-Like Methylation Changes of HSCs in GADD45B Knockout Mice Define Methylation Sites Associated With Loss of Function.
Hematopoietic stem cells (HSCs) self-renew and differentiate into all blood cells maintaining the hematopoietic system. Age-related HSC dysfunction impacts all of hematopoiesis, with DNA methylation alterations in aged HSCs contributing to altered function. Growth Arrest and DNA Damage-inducible proteins (Gadd45a, Gadd45b, and Gadd45g) are expressed in HSC activation, and Gadd45b has been reported to induce DNA demethylation. Thus, we explored the relationship between Gadd45b, DNA methylation and age-related HSC changes. WGBS on HSCs from GADD45B knockout mice demonstrated young knockout HSCs have increased DNA methylation, with both unique and overlapping methylation changes compared to aged wild-type HSCs without reflecting aging transcriptional changes. Peripheral blood and bone marrow analysis, competitive transplants, and single-cell culture analyses showed no significant loss of functional potential in the aberrantly methylated GADD45B knockout HSCs. We concluded these altered methylation sites don't alter HSC potential. We generated a searchable HSC DNA methylation database incorporating available datasets and present a truncated list of methylation sites associated with changes in HSC function for prioritization to target for resetting the age-associated loss of HSC potential. - Source: PubMed
Kuribayashi WakakoTanaka-Yano MayuriPark BongsooYanai HagaiTekin-Turhan FerdaBeerman Isabel

GADD45G (1-159) antigen

Related genes to: GADD45G (1-159) antigen

Related products to: GADD45G (1-159) antigen

Related articles to: GADD45G (1-159) antigen

Therapeutic target exploration of Shugan Jianpi formula in liver fibrosis: an integrated lncRNA-mRNA co-expression network analysis.

Integrated bioinformatics analysis and experimental validation of as a potential senescence biomarker in MASLD.

EHMT2 aggravates vascular remodeling via epigenetic inhibition of GADD45G.

Deoxynivalenol drives liver injury progression by dysregulating core molecular networks: integrated multi-omics, network toxicology and molecular docking analysis.

Age-Like Methylation Changes of HSCs in GADD45B Knockout Mice Define Methylation Sites Associated With Loss of Function.