Ask about this productRelated genes to: UVRAG antibody
- Gene:
- UVRAG NIH gene
- Name:
- UV radiation resistance associated
- Previous symbol:
- -
- Synonyms:
- VPS38
- Chromosome:
- 11q13.5
- Locus Type:
- gene with protein product
- Date approved:
- 1997-01-10
- Date modifiied:
- 2016-10-05
Related products to: UVRAG antibody
Related articles to: UVRAG antibody
- Natural products are biologically active compounds used for therapeutic interventions for various diseases, particularly infections. Autophagy is an intracellular catabolic pathway involving lysosomal degradation and is closely associated with immunological pathways, effectively combating bacterial, viral, fungal, and parasitic infections. Accumulating evidence suggests that autophagy activation or inhibition by natural products promotes antimicrobial responses against various pathogens. Numerous natural products can modulate autophagy through diverse signaling pathways, suggesting their potential as a host-directed therapeutic strategy that may complement conventional drug regimens or help mitigate drug resistance in various infectious diseases. However, it remains largely unclear whether these effects are mediated by direct modulation of autophagy or indirectly through associated mechanisms, including enhanced immune defense, attenuation of pathological inflammation, or crosstalk with other organelle functions. Additionally, multiple pathogens can evade host responses; thus, autophagy activation may inadvertently create favorable conditions for certain pathogens. This review discusses the current knowledge of natural products in terms of their antimicrobial actions through autophagy regulation, particularly the roles of distinct natural product classes, such as polyphenols, alkaloids, terpenoids, quinones, peptides, and macrolides in modulating autophagy for potentially contributing to control various infectious diseases. Exploring the intricate molecular interplay between natural products and autophagy in limiting infections may provide valuable insights that could inform the development of innovative host-directed antimicrobial treatments based on autophagy regulation. 3-MA: 3-methyladenine; AM: alveolar macrophages; AMP: antimicrobial peptides; AMPK: 5' adenosine monophosphate-activated protein kinase; ARDS: acute respiratory distress syndrome; ART: artemisinin; ASFV: African swine fever virus; ATG: autophagy related; AZM: azithromycin; BafA1: bafilomycin A; BECN1: beclin 1; BMDM: bone marrow-derived macrophage; BNIP3: BCL2 interacting protein 3; BNIP3L: BCL2 interacting protein 3 like; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CAMKK2: calcium/calmodulin-dependent protein kinase kinase 2; CBD: cannabidiol; CF: cystic fibrosis; CGA: chlorogenic acid; CGAS: cyclic GMP-AMP synthase; CHUK/IKKα: component of inhibitor of nuclear factor kappa B kinase complex; CLP: cecal ligation and puncture; CLR: clarithromycin; CMA: chaperone-mediated autophagy; CoV: coronavirus; DHT: dihydrotanshinone I; EGCG: epigallocatechin-3-gallate; EIF2A: eukaryotic translation initiation factor 2A; EIF2AK2: eukaryotic translation initiation factor 2 alpha kinase 2; ESKAPE: , and spp.; ESRRA: estrogen related receptor alpha; FOXO1: forkhead box O1; FUNDC1: FUN14 domain containing 1; HBV: hepatitis B virus; HCV: hepatitis C virus; HDT: host-directed therapy; HIV: human immunodeficiency virus; HMGB1: high mobility group box 1; HSV: herpes simplex virus; IAV: influenza A virus; ICT: isocryptotanshinone; IFN: interferon; IKBKB/IKKβ: inhibitor of nuclear factor kappa B kinase subunit beta; IL: interleukin; INH: isoniazid; IRF3: IFN regulatory factor 3; KEAP1: kelch like ECH associated protein 1; LAMP: lysosomal associated membrane protein; LAP: LC3-associated phagocytosis; LPS: lipopolysaccharide; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPK: mitogen-activated protein kinase; MDM: monocyte-derived macrophage; MDR: multidrug-resistant; MON: monotropein; Mtb: ; MTOR: mechanistic target of rapamycin kinase; mtROS: mitochondrial ROS; NET: neutrophil extracellular trap; NFE2L2/Nrf2: NFE2 like bZIP transcription factor 2; NFKB/NF-κB: nuclear factor kappa B; NLRP3: NLR family pyrin domain containing 3; NLRX1: NLR family member X1; NOTCH1: notch receptor 1; NTM: nontuberculous mycobacteria; OMS: ohmyungsamycin; PAK1: p21 (RAC1) activated kinase 1; PINK1: PTEN induced kinase 1; PKM/PKM2: pyruvate kinase M1/2; PLD: phospholipase D; PM: peritoneal macrophage; PPM1A: protein phosphatase, Mg2+/Mn2+ dependent 1A; PRKN/parkin: parkin RBR E3 ubiquitin protein ligase; PtdIns3K: phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; PTEN: phosphatase and tensin homolog; RB1CC1/FIP200: RB1 inducible coiled-coil 1; RELA/p65: RELA proto-oncogene, NF-kB subunit; RIF: rifampicin; ROS: reactive oxygen species; RSV: resveratrol; RUBCN/rubicon: rubicon autophagy regulator; SAR: selective autophagy receptor; SIRT: sirtuin; STING1: stimulator of interferon response cGAMP interactor 1; STX17: syntaxin 17; Tat: trans-activator of transcription; TB: tuberculosis; TBK1: TANK binding kinase 1; TFEB: transcription factor EB; TLR: toll like receptor; TNA: tanshinone IIA; TNF: tumor necrosis factor; UA: ursolic acid; ULK1/Atg1: unc-51 like autophagy activating kinase 1; UPR: unfolded protein response; UVRAG: UV radiation resistance associated; VAMP8: vesicle associated membrane protein 8; VDR: vitamin D receptor; WIPI2: WD repeat domain, phosphoinositide interacting 2; ZFYVE1/DFCP1: zinc finger FYVE-type containing 1; ZIKV: Zika virus. - Source: PubMed
Publication date: 2026/04/28
Paik SeungwhaUm SoohyunKim In SooPark Eun-JinKim Kyung TaeBasu JoyotiOh Dong-ChanJo Eun-Kyeong - - Source: PubMed
Publication date: 2026/03/19
Li YuanbinZhou JinhaoWang DanYan XuOuyang YiguoWang WeiZhu ChenyaoChen Zhuang - Intravenous immunoglobulin (IVIG), a therapeutic preparation of pooled normal IgG is extensively used as a first-line immunotherapy for many autoimmune and inflammatory diseases, including Kawasaki disease (KD). IVIG provides therapeutic benefits through several non-exclusive mechanisms. Our recent data demonstrate that IVIG induces autophagy in inflammatory innate immune cells, a finding further supported by observations in IVIG-treated myopathy patients. However, whether IVIG selectively activates specific autophagy pathways across distinct innate immune cell subsets remains unclear. - Source: PubMed
Publication date: 2026/02/25
Singh Suraj ChandrabhanRetnakumar Sruthi VijayaDas MrinmoyKaveri Srini VMathew Mano JosephBayry Jagadeesh - Class III phosphatidylinositol 3-kinase (PtdIns3K) occupies the nexus of autophagy and endomembrane trafficking. Within its core complex, the VPS34 catalytic subunit partners with VPS15, Beclin-1, and ATG14L or UVRAG to convert phosphatidylinositol into PtdIns3P-the lipid cue that seeds phagophore nucleation and endosome-lysosome maturation. By tuning this single signaling node, cells safeguard proteostasis and orchestrate rapid stress responses; when this regulatory network is disrupted, PtdIns3K dysregulation fuels neurodegeneration, tumor progression, immune imbalance, and metabolic disease. This review fuses cutting-edge structural and biochemical insights into PtdIns3K, dissects its multilayered regulation-spanning post-translational modifications, adaptor engagement, and higher-order assembly-and appraises next-generation small-molecule inhibitors designed for precision autophagy control. Decoding and therapeutically exploiting this pathway will open a new chapter in the discovery of innovative therapeutic approaches. - Source: PubMed
Liu QiaoYe JingChen CanZhu YanghuiHe GuWu Fengbo - Deprivation of nutrients in the tumor microenvironment drives malignant progression, yet the molecular mechanisms linking metabolic stress to metastasis in bladder cancer remain incompletely understood. Here, we report that nutrient-deprivation stress promotes metastasis by orchestrating a post-translational modification cascade centered on Beclin-1. Clinical analysis revealed that acetylation of Beclin-1 at lysine residues K430 and K437 was significantly reduced in muscle-invasive bladder cancer (MIBC) compared with non-muscle-invasive bladder cancer (NMIBC), a molecular signature inversely correlated with elevated phospho-eIF2α, a marker of cellular starvation. Mechanistically, nutrient deprivation dynamically regulates the expression of the deacetylase SIRT1 and acetyltransferase p300, shifting the balance toward Beclin-1 deacetylation. This deacetylation event serves a dual function: it enhances Beclin-1 protein stability by shielding it from TRIM21-mediated K48-linked ubiquitination and proteasomal degradation, and it promotes autophagosome formation by strengthening its interaction with pro-autophagic partners VPS34, ATG14, and UVRAG while weakening its binding to the inhibitor Rubicon. Consequently, this leads to sustained autophagy activation and epithelial-mesenchymal transition. Genetic and pharmacological interventions further confirmed the central role of this axis, demonstrating that SIRT1 activation by resveratrol promoted metastasis, whereas p300 activation by CTB suppressed it. Crucially, these effects were abrogated in cells expressing deacetylation-mimetic Beclin-1 mutants, suggesting a direct causal link. Our study unveils the SIRT1/p300-Beclin-1-TRIM21 axis as a key nutrient-sensing pathway that promotes bladder cancer metastasis through crosstalk between acetylation and ubiquitination. These findings identify new therapeutic vulnerabilities in advanced bladder cancer. - Source: PubMed
Publication date: 2026/02/16
Sun YanTong HangZhao GuozhiWu LinfengZhang XiaoyuLi TinghaoZhu JunlongZhu KunyaoYin HubinLi XinyuanHe Weiyang