ATG7 ELISA kit
- Known as:
- ATG7 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ATG7-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ATG7 ELISA kit
Related genes to: ATG7 ELISA kit
- Gene:
- ATG7 NIH gene
- Name:
- autophagy related 7
- Previous symbol:
- APG7L
- Synonyms:
- GSA7, DKFZp434N0735
- Chromosome:
- 3p25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-20
- Date modifiied:
- 2016-10-05
Related products to: ATG7 ELISA kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit Related articles to: ATG7 ELISA kit
- - Source: PubMed
Publication date: 2026/04/17
Liu JiaWen Chao - Mixed stroke, also known as hemorrhagic infarction or infarction with hemorrhage, presents as a cerebral infarction combined with intracerebral hemorrhage (ICH) on computed tomography (CT) brain scans. ICH is a brain parenchymal hemorrhage caused by the loss of vascular integrity, which can lead to permanent disability or death. The early growth response 2 (EGR2) gene has been studied in a variety of brain diseases. However, effective treatments are still lacking. - Source: PubMed
Publication date: 2026/04/09
Zhang XiujunZhang BensiShi ChunKampan NatnichaTreebupachatsakul WaleephanPantan RungusaNarakornsak SuteeraPhatsara Manussabhorn - Sepsis-induced cardiomyopathy (SICM) is characterized by mitochondrial dysfunction, impaired mitophagic flux, and overwhelming oxidative stress. Spermidine (SPD), a natural polyamine known to enhance autophagy and preserve cardiac function in aging and metabolic disorders, has not been systematically evaluated in the context of septic cardiomyopathy. - Source: PubMed
Publication date: 2026/04/10
Long ShiyunSun JiaxinWu YaguangYi JiaRen ShuangRan XiaopingLi XiaofengSethi GautamLuo ZhenchunDuan Chenyang - Glioblastoma (GBM), a rare, highly aggressive and chemoresistant brain cancer, exhibits profound metabolic plasticity that relies, in part, on aberrant transforming growth factor-β (TGF-β) signaling. Such plasticity was recently associated with TGF-β-regulated apoptosis and autophagy. Here, we questioned whether TGF-β-regulated apoptotic/autophagic phenotypes are recapitulated in a preclinical in vitro 3D spheroid culture model of human U87 GBM-derived cells, and how metabolic alterations affect such phenotypes. - Source: PubMed
Publication date: 2026/03/30
Payet-Desruisseaux MaellisZgheib AlainDanalache Bogdan AlexandruDesjarlais MichelAnnabi Borhane - Myotonic dystrophy type 2 (DM2) is an autosomal dominant, multisystemic disorder caused by the expansion of CCTG repeats in the first intron of the CNBP gene. Repeat-associated non-AUG (RAN) translation of the expanded CCTG RNA generates two tetrapeptide repeat proteins (TPRs), polyQAGR and polyLPAC, whose roles in DM2 pathogenesis remain unclear. To define their individual contributions, we expressed codon-optimized polyQAGR and polyLPAC peptides with an ATG start codon in Drosophila melanogaster. Expression of both TPRs reduced viability and lifespan and induced eye degeneration and locomotor defects. We found that polyQAGR accumulated in the nucleolus, disrupted nucleolar integrity, and impaired rRNA processing. It also interfered with autophagy, promoting Atg5 and Atg7 transcription and accumulation of Atg8a- and Ref(2)P-positive aggregates. Consistently, overexpression of Atg8a or Ref(2)P mitigated polyQAGR-induced eye toxicity, whereas knockdown of autophagy genes worsened it. Conversely, polyLPAC increase the cytoplasmic pool of TIAR in human cells and in DM2 patient-derived myoblasts. Together, these findings show that polyQAGR and polyLPAC exert distinct toxic effects that likely converge to drive DM2 pathogenesis and may represent promising therapeutic targets. - Source: PubMed
Publication date: 2026/04/20
Marzullo MartaDe Simone AssiaTerribili MartaDi Salvio MichelaMengistu Degisew YinurSomma Maria PatriziaD'Amico RodrigoCanettieri GianlucaCestra GianlucaCiapponi Laura