Ask about this productRelated genes to: ATG5 antibody
- Gene:
- ATG5 NIH gene
- Name:
- autophagy related 5
- Previous symbol:
- APG5L
- Synonyms:
- ASP, APG5, hAPG5
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-16
- Date modifiied:
- 2014-11-19
Related products to: ATG5 antibody
Related articles to: ATG5 antibody
- Autophagy functions as a context-dependent stress adaptation pathway in T cells; however, its role in sustaining chimeric antigen receptor (CAR)-T cell function within solid tumor environments remains insufficiently defined. In this study, we investigated whether ATG5-mediated autophagy regulation contributes to CAR-T cell functional durability under tumor-associated stress conditions. ATG5 overexpression (OE) CAR-T cells did not increase basal autophagy activity but instead selectively enhanced autophagy flux in response to inducible stimuli. Under tumor-mimicking immunosuppressive conditions, ATG5 OE CAR-T cells maintained cytotoxic activity during prolonged antigen exposure and exhibited preserved effector cytokine production together with reduced oxidative stress. Consistent with these findings, ATG5 OE CAR-T cells exhibited enhanced antitumor efficacy under IR-preconditioned settings, characterized by improved tumor control and survival, which was associated with sustained effector function of tumor-infiltrating CAR-T cells. Collectively, these findings demonstrate that reinforcing inducible autophagy capacity through ATG5 promotes the maintenance of CAR-T cell function under tumor-associated challenges, highlighting a targeted strategy to enhance CAR-T cell persistence in solid tumor immunotherapy. - Source: PubMed
Publication date: 2026/04/22
Jung Sang-EunLim MinjiJeong HyungwooMoon YoungchaeSeo Hyungseok - Midbrain dopamine (mDA) neurons play a wide range of brain functions, but the molecular mechanisms driving the formation of mDA circuits remain largely unknown. Here, we show that autophagy, the main cellular recycling pathway, is present in the growth cones of developing mDA neurons, and its level changes dynamically in response to guidance cues. To characterize the role of autophagy in mDA axon growth and guidance, we knocked out essential autophagy genes (Atg12, Atg5) specifically in mDA neurons in mice of either sex. Autophagy-deficient mDA axons exhibit axonal swellings and reduced branching both and in vivo. Strikingly, deletion of autophagy-related genes completely blunted the response of mDA neurons to both chemorepulsive and chemoattractive guidance cues. Our data demonstrate that autophagy plays a central role in regulating mDA neuron development by orchestrating axonal growth and guidance. Midbrain dopaminergic neurons form circuits essential for movement, motivation, and cognition, yet the intracellular mechanisms controlling their axon growth and guidance remain poorly understood. Here we show that autophagy, a major cellular recycling pathway, operates locally in dopaminergic growth cones and is dynamically regulated by guidance cues. Using neuron-specific deletion of core autophagy genes, we demonstrate that autophagy is required for proper axonal morphology, branching, and responsiveness to both chemoattractive and chemorepulsive signals. These findings identify autophagy as a key regulator of dopaminergic circuit formation and reveal a previously unrecognized mechanism linking intracellular degradation pathways to axon guidance during brain development. - Source: PubMed
Publication date: 2026/05/07
Schaan Profes MarcosGora CharlesLavoie-Cardinal FlavieSaghatelyan ArmenLévesque Martin - Root hairs are tubular tip-growing extensions of root epidermal cells that enhance root surface area for water and nutrient acquisition. While the mechanisms governing root hair fate, polarity and tip growth are well understood, the regulation of root hair longevity remains largely unknown. Here we show that root hair cells employ high levels of autophagy to maximize their lifespan in Arabidopsis thaliana. Loss-of-function mutations in the genes encoding the autophagy regulators ATG2, ATG5 or ATG7 induce a premature, cell-autonomous cell death program. This cell death is activated via a gene regulatory network promoted by the NAC transcription factors ANAC046 and ANAC087. Our findings uncover an antagonistic relationship between autophagy and senescence-controlled programmed cell death in root hair lifespan regulation, with potential implications for optimizing plant nutrient and water uptake in crop breeding. - Source: PubMed
Publication date: 2026/05/06
Feng QiangnanZhu ShihaoWang XinchaoLiu YujieZhao JieruiDagdas YasinNowack Moritz K - Intervertebral disc degeneration (IDD) is the primary cause of lower back pain. Transient receptor potential canonical 3 (TRPC3) is a nonselective cation channel permeable to Ca2+. - Source: PubMed
Publication date: 2026/05/05
Gao YingchaoZhang NingZhang Jun-FeiFei Zhengqi - Hepatocellular carcinoma (HCC) remains a therapeutic challenge due to late-stage diagnosis and suboptimal response to standard therapies. Resveratrol, a plant-derived polyphenol, suppresses proliferation of HCC cells by inducing apoptosis and autophagy. However, the regulatory mechanism that integrates these two processes is poorly understood. This study aimed to elucidate how resveratrol coordinately regulates apoptosis and autophagy in HCC cells. Using integrated network pharmacology and QIAGEN Ingenuity Pathway Analysis (IPA), was predicted as the central hub target gene of resveratrol in HCC, where it coordinated both apoptosis and autophagy. Molecular docking and molecular dynamics simulation confirmed direct and stable binding of resveratrol to p53 protein. Functional validation revealed that resveratrol significantly ( < 0.01) inhibited the viability of p53-wild-type HepG2 cells, accompanied by mRNA upregulation of pro-apoptotic and autophagy-related genes (, , , 5), with concordant changes at the protein level (upregulated Bax and ATG5 proteins, increased ratios of Bax/Bcl-2, cleaved-Caspase 9/Caspase 9, cleaved-Caspase 3/Caspase 3, and LC3B-II/I, decreased p62 protein). These effects were strictly p53-dependent, as they were absent in p53-null Hep3B cells and significantly ( < 0.05) attenuated upon pharmacological inhibition of p53 in HepG2 cells. Mechanistically, resveratrol activated p53 not by increasing its protein level but by enhancing its acetylation at Lysine 382. This study established p53 acetylation as a critical switch through which resveratrol coordinately induced apoptosis and autophagy. These findings provide a mechanistic framework for anti-HCC effect of resveratrol and underscore the therapeutic relevance of p53 activation pathways in HCC. - Source: PubMed
Publication date: 2026/04/30
Zhang HuiZhang HuidongLi WeiZhang HongXu YangLiu WenBao LiyaZhou SiyuZhang XiaoyuLi Jiao