Zfyve1 polyclonal antibody
- Known as:
- Zfyve1 pab (anti-)
- Catalog number:
- PAB15787
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- Zfyve1 polyclonal antibody
Ask about this productRelated genes to: Zfyve1 polyclonal antibody
- Gene:
- ZFYVE1 NIH gene
- Name:
- zinc finger FYVE-type containing 1
- Previous symbol:
- ZNFN2A1
- Synonyms:
- DFCP1, KIAA1589, TAFF1, PPP1R172
- Chromosome:
- 14q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-02
- Date modifiied:
- 2016-02-15
Related products to: Zfyve1 polyclonal antibody
Related articles to: Zfyve1 polyclonal 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 - Intestinal ischemia-reperfusion (II/R) injury is a serious condition characterized by high morbidity and mortality rates. Research has shown that II/R injury is closely linked to autophagy and immune dysregulation. This study aims to investigate the potential correlations between autophagy-related genes and infiltrating immune cells in II/R injury. - Source: PubMed
Publication date: 2025/05/26
Hu YichenZou QinghuaSun YanboLi WeimingYin ZhaochuanZhao YuanpeiShi KaiwenLiu HongyuanWang Jiahui - 17-ODYA: 17-octadecynoic acid; 293T: HEK293T; 2-BP: 2-bromopalmitate; 2CS: Cys155Ser and Cys156Ser; ABE: acyl-biotin exchange; AP: adaptor protein; APEX2: ascorbate peroxidase 2; ATG: autophagy related; baf A: bafilomycin A; CRISPR: clustered regularly interspaced short palindromic repeats; CTD: C-terminal domain; Cys: cysteine; DAB: 3,3'-diaminobenzidine; EV: empty vector; HO: hydrogen peroxide; IF: immunofluorescence; IP: immunoprecipitation; KO: knockout; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MTOR: mechanistic target of rapamycin kinase; NTD: N-terminal domain; PAS: phagophore assembly site; PBS: phosphate-buffered saline; PtdIns3K-CI: class III phosphatidylinositol 3-kinase complex I; PM: plasma membrane; PTM: post-translational modifications; Ser: serine; siRNA: small interfering RNA; SQSTM1/p62: sequestosome 1; TEM: transmission electron microscopy; TGN: trans-Golgi network; ULK1: unc-51 like autophagy activating kinase 1; WCL, whole cell lysates; WDR45/WIPI4: WD repeat domain 45; WT: wild-type; ZFYVE1/DFCP1: zinc finger FYVE-type containing 1. - Source: PubMed
Publication date: 2025/05/31
Xia FanLi WeiningWang WenruLiu JiruLi XiaolinCai JingShan HaoCai ZheCui Jun - Zinc finger FYVE-type containing 1 (ZFYVE1), a FYVE-containing protein, exerts a significant function during autophagosome formation and lipid droplet metabolism. Nevertheless, it is currently unclear whether teleost ZFYVE1 influences antiviral innate immunity. In this paper, the black carp (Mylopharyngodon piceus) homolog of ZFYVE1 (bcZFYVE1) was cloned to explore its regulatory function within the interferon (IFN) signaling cascade of teleost fish. The coding region of bcZFYVE1 is composed of 2337 nucleotides and encodes 778 amino acids, including two zinc-binding FYVE domains and a guanylate-binding protein (GBP) domain. bcZFYVE1 transcription in host cells varied upon stimulation with LPS, grass carp reovirus (GCRV) and spring viremia of carp virus (SVCV), respectively. bcZFYVE1 migrated at approximately 86 kDa in immunoblot assay and was primarily detected in the cytoplasm in immunofluorescence staining assay. Upon the co-expression of bcZFYVE1 and bcIRF3/7 in EPC cells, bcZFYVE1 markedly reduced the transcription of the IFN promoter activated by bcIRF3/7. Correspondingly, the mRNA levels of interferon-stimulated genes (ISGs) downstream were reduced. And, overexpressed bcZFYVE1 markedly inhibited the antiviral activity mediated by bcIRF3/7. Additionally, knockdown of bcZFYVE1 attenuated SVCV replication and improved the antiviral capability of host cells. The co-immunoprecipitation assays verified the interaction between bcZFYVE1 and bcIRF3/7. Furthermore, we found that co-expression of bcZFYVE1 with bcIRF3/7 decreased the protein levels of bcIRF3/7 and both MG132 or chloroquine treatment could restore the protein levels. In summary, our data conclude that ZFYVE1 suppresses IRF3/7-mediated antiviral innate immune response in black carp, which expands the understanding of the function of ZFYVE1. - Source: PubMed
Publication date: 2025/04/16
Yi ZewenWang JiaxinTan ShashaLi Zhan'aoWang XinyuYu JiajieYue RuiminXiao JunWu HuiFeng Hao - Chronic HCV infection is a risk factor for end-stage liver disease, leading to a major burden on public health. Mitophagy is a specific form of selective autophagy that eliminates mitochondria to maintain mitochondrial integrity. HCV NS5A is a multifunctional protein that regulates the HCV life cycle and may induce host mitophagy. However, the molecular mechanism by which HCV NS5A activates mitophagy remains largely unknown. Here, for the first time, we delineate the dynamic process of HCV NS5A-activated PINK1/Parkin-dependent mitophagy. By performing live-cell imaging and CLEM analyses of HCV NS5A-expressing cells, we demonstrate the degradation of mitochondria within autophagic vacuoles, a process that is dependent on Parkin and ubiquitin translocation onto mitochondria and PINK1 stabilization. In addition, the cargo receptors of mitophagy, NDP52 and OPTN, are recruited to the mitochondria and required for HCV NS5A-induced mitophagy. Moreover, ATG5 and DFCP1, which function in autophagosome closure and phagophore formation, are translocated near mitochondria for HCV NS5A-induced mitophagy. Furthermore, autophagy-initiating proteins, including ATG14 and ULK1, are recruited near the mitochondria for HCV NS5A-triggered mitophagy. Together, these findings demonstrate that HCV NS5A may induce PINK1/Parkin-dependent mitophagy through the recognition of mitochondria by cargo receptors and the nascent formation of phagophores close to mitochondria. - Source: PubMed
Publication date: 2024/12/23
Hsiao Yuan-ChaoChang Chih-WeiYeh Chau-TingKe Po-Yuan