GADD45gamma (aa 123 to 133)
- Known as:
- GADD45gamma (aa 123 133)
- Catalog number:
- Y213888
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GADD45gamma ( 123 133)
Related genes to: GADD45gamma (aa 123 to 133)
- Gene:
- ABCA11P NIH gene
- Name:
- ATP binding cassette subfamily A member 11, pseudogene
- Previous symbol:
- ABCA11
- Synonyms:
- EST1133530, FLJ14297
- Chromosome:
- 4p16.3
- Locus Type:
- pseudogene
- Date approved:
- 1999-06-11
- Date modifiied:
- 2015-11-13
- Gene:
- ABCF2 NIH gene
- Name:
- ATP binding cassette subfamily F member 2
- Previous symbol:
- -
- Synonyms:
- EST133090, ABC28, M-ABC1, HUSSY-18
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2015-11-13
- Gene:
- ACBD4 NIH gene
- Name:
- acyl-CoA binding domain containing 4
- Previous symbol:
- -
- Synonyms:
- FLJ13322
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-11
- Date modifiied:
- 2019-03-21
- Gene:
- ADGRD1 NIH gene
- Name:
- adhesion G protein-coupled receptor D1
- Previous symbol:
- GPR133
- Synonyms:
- DKFZp434B1272, PGR25
- Chromosome:
- 12q24.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-26
- Date modifiied:
- 2015-03-03
- Gene:
- AKAP17A NIH gene
- Name:
- A-kinase anchoring protein 17A
- Previous symbol:
- CXYorf3, SFRS17A
- Synonyms:
- XE7, XE7Y, DXYS155E, MGC39904, 721P, CCDC133
- Chromosome:
- Xp22.33 and Yp11.32
- Locus Type:
- gene with protein product
- Date approved:
- 2006-09-22
- Date modifiied:
- 2015-11-17
Related products to: GADD45gamma (aa 123 to 133)
(+__)_2_Aminoheptane (+__)_2_Heptylamine(3_Ethylamyl)(3_ethyl_n_heptyl)carbinol (3_Ethylamyl)(3_ethyl_n_(6aR,10aR)_3_(1,1_Dimethylbutyl)_6a,7,1 JWH 133(Pyr110)-Prepro-Urotensin II (110-123) (rat)
98% C77H102N18O20S2 CAS:(Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human)
(Tyr0)-Kaliuretic Peptide (human), (Tyr0)-Prepro-Atrial Natriuretic Factor (103-122) (bovine), (Tyr0)-pro-hANF (79-98) 98% C103H180N32O30 C([125I]-Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human)([125I]-Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human)([125I]-Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human), Liquid([125I]-Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human), Liquid([125I]-Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human), Liquid([125I]-Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human), Lyophilized([125I]-Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human), Lyophilized([125I]-Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human), Lyophilized([125I]-Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human)Liquid([125I]-Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human)Lyophilized Related articles to: GADD45gamma (aa 123 to 133)
- 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 - 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 - The liver is a primary target for recombinant adeno-associated viral (rAAV) vectors, yet the influence of serotype, sex, and liver zonation on transduction and transcriptomic changes remains incompletely understood. This proof-of-concept study employs spatial transcriptomics alongside single-nucleus RNA sequencing to map the spatial distribution and impacts of rAAV2- and rAAV9-CMV-EGFP vectors in male and female mouse livers. Spatial transcriptomics provided precise transgene mapping and highlighted that CMV-EGFP rAAV vectors deregulate hepatocellular lipid metabolism, the circadian clock, and the immune/stress response with sex specific differences. Lipid metabolism genes (Elovl3, Chka, Irs2, Ppard), were consistently deregulated across all zones of the liver lobule in male and female rAAV2- and rAAV9-CMV-EGFP-treated mice, while Srebf1, Tlcd4, Cpt2, and Acot1 exhibited sex-specific patterns. Circadian clock modulators (Dbp, Tef, Arntl, Nfil3, Nr1d1/Nr1d2) were altered independently of zonation. The study found sex-specific downregulation of immune and stress-response genes and pathways, including Gadd45g and hypoxia pathways. TGF-β and EGFR pathways were upregulated sex-independently. Spatial transcriptomics further enabled examination of transgene and rAAV entry factor co-expression, identifying known and novel factors like Rpsa, Dpp4, Sdc1, and solute carrier proteins, highlighting its role in supporting targeted screening. Our findings demonstrate spatial transcriptomics as a powerful tool in gene therapy research and reveal novel rAAV vector effects on liver biology. - Source: PubMed
Publication date: 2026/03/11
Amberg BettinaKöchl FabianKumpesa NadinePrasad MeganaBochner FilipHernández-Obiols MarOtteneder Michael BStalder LucasShaffo FrancesNowrouzi AliMarkusic DavidHaegel HélèneXicluna RebeccaSultan MarcJacobsen BjörnRottenberg SvenValdeolivas AlbertoSchwalie Petra CHahn Kerstin - Lung cancer is a leading cause of cancer-related mortality, with current therapies limited by drug resistance and immunosuppressive tumor microenvironment (TME). Cuproptosis offers new therapeutic prospects, but effective induction and targeted delivery remain challenging. Herein, we developed xanthohumol (XN)-coordinated copper oxide/hyaluronic acid (XN@CuO/HA) nanobipyramids as a novel cuproptosis inducer for non-small cell lung cancer (NSCLC) therapy. XN@CuO/HA exhibited good colloidal stability, and potent antitumor activity by inducing mitochondrial dysfunction, reactive oxygen species (ROS) accumulation, and cuproptosis. Mechanistically, transcriptomic and functional analyses identified the FOXO1-GADD45G axis as a critical mediator of XN@CuO/HA-induced cuproptosis. , XN@CuO/HA significantly suppressed LLC xenograft growth in C57BL/6 mice with excellent biosafety. Moreover, it remodeled the immunosuppressive TME by enhancing CD8 T/NK1.1 cell infiltration and reducing MDSCs, synergizing with anti-PD-1 antibody to achieve superior antitumor efficacy. Collectively, our findings highlight XN@CuO/HA as a safe and effective nano-therapeutic that induces FOXO1-GADD45G-mediated cuproptosis and potentiates immunotherapy, providing a promising combinatorial strategy for NSCLC treatment. - Source: PubMed
Publication date: 2026/02/25
Jiang RuiyangHuang XiangmingOuyang YiranLuo BichongWan HongYangShou FangyangWu XiahuiFan JuntingZhang JingyuanSun DongdongXu ChangliangFang Zhijun - Myocardial ischemia-reperfusion injury (MIRI) is an unresolved clinically fatal complication in the management of acute myocardial infarction (AMI). Growth arrest and DNA damage-inducible gene 45 Gamma (GADD45G) plays a vital role in the regulation of MIRI. However, the underlying mechanisms remain unclear. GADD45G and SP1 expression were upregulated in hypoxia/reoxygenation (H/R)-treated H9C2 cells. H/R treatment repressed H9C2 cell viability, and induced apoptosis, oxidative stress, and inflammatory response. Moreover, GADD45G deficiency could relieve H/R-triggered H9C2 cell injury. In mechanism, SP1 was a transcription factor of GADD45G and activated the transcription of GADD45G via binding to its promoter region. Besides, SP1 knockdown alleviated MI/R-induced pathological damage in the myocardial tissue of rats by regulating GADD45G. In conclusion, SP1 could promote H/R-induced cardiomyocyte injury and MI/R-caused rat myocardial tissue pathological injury by increasing GADD45G, providing a promising therapeutic target for MIRI treatment. - Source: PubMed
Publication date: 2026/02/05
Wang YapingXue JianyingCui MingliangChang FengjunShi Jiankuan