WIPI1 Polyclonal Antibody [AT130]
- Known as:
- WIPI1 Polyclonal Antibody [AT130]
- Catalog number:
- A-0508-100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- EpigenTek
- Gene target:
- WIPI1 Polyclonal Antibody [AT130]
Related genes to: WIPI1 Polyclonal Antibody [AT130]
- Gene:
- WIPI1 NIH gene
- Name:
- WD repeat domain, phosphoinositide interacting 1
- Previous symbol:
- -
- Synonyms:
- FLJ10055, WIPI49, ATG18, ATG18A
- Chromosome:
- 17q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-15
- Date modifiied:
- 2016-03-01
Related products to: WIPI1 Polyclonal Antibody [AT130]
Related articles to: WIPI1 Polyclonal Antibody [AT130]
- l-Phenylalanine and l-glutamine were conjugated with maslinic acid and 3- maslinic acid to generate 16 derivatives. Most of them exhibited higher cytotoxic activity than maslinic acid towards various tumour cell lines. Based on the results from the human apoptosis array and western blotting assays, derivative 7, a 2α,3β-dipropionylated maslinic acid-l-phenylalanine conjugate, could promote autophagy and intrinsic and extrinsic apoptosis in the T24 cell line in a dose-dependent manner. Furthermore, 7 could decrease the mitochondrial membrane potential and overload mitochondrial Ca and ROS. These effects can lead to significant apoptosis induction and activate apoptotic signaling caspase-8 and caspase-9. In addition, 7 could decline proliferation activity by inhibiting the expression of the PI3K, AKT and EGFR proteins. RNA-seq analysis suggested that 7 can induce the formation of autophagosomes by upregulating WIPI1, p62, LC3B-I/II, and Beclin-1. Meanwhile, western blotting analysis revealed that 7 could simultaneously upregulate the pro-apoptotic factors (Bax and Bak) and autophagy proteins (Beclin-1, LC3B II/I, PI3-kinase class III, mTOR and p62). This implies that 7 could synergistically promote apoptosis and autophagy to induce cell death. - Source: PubMed
Publication date: 2026/09/16
Liu Jing-JingSun LiGuo Dan-TingLiang Yu-JieZhang Li-QiongChen Jun-JiWang Quan-deCheng Ke-Guang - Endosomes generate tubulo-vesicular carriers to redistribute proteins between plasma membrane, Golgi, and lysosomes. These transport routes employ distinct combinations of sorting nexins with complexes such as Retromer or Retriever. We now show that, while Retromer associates with the PROPPIN WIPI1 to form the previously described CROP complex, Retriever associates with WIPI2, forming CROP2. WIPI2 integrates into Retriever-dependent coat complexes since it interacts both with the Commander subunit CCDC93 and its cognate sorting nexin SNX17. CROP and CROP2 are exclusive in their physical associations and pathway selective. Whereas CROP2 is required for endosomal exit of Integrin β1, it does not affect CROP-dependent cargos such as EGFR or GLUT1. Vice versa, CROP is not required for Integrin β1 trafficking. WIPI1 and WIPI2 rely on similar molecular features. Their activity depends on the same FSSS motif to integrate into Retromer and Retriever complexes, respectively, and on an amphipathic membrane-inserting α-helix, which conveys membrane fission activity to PROPPINs. This suggests that Retromer and Retriever coats integrate distinct PROPPIN isoforms to promote fission of the respective endosomal carriers formed by them. - Source: PubMed
Publication date: 2026/07/24
De Leo Maria GiovannaMayer Andreas - Alopecia areata (AA) is a common autoimmune alopecia disease. Evidence suggests that autophagy-related genes (ARGs) may contribute to its pathophysiology. This study aims to explore and identify potential autophagy-related biomarkers and molecular subtypes in AA. In this study, autophagy-related differential expression genes (ARDEGs) in AA were identified by comparing the differentially expressed genes (DEGs) in the GSE68801 dataset with the ARGs. Then, we applied three different machine learning methods to identify key hub genes and further verified them on independent datasets. We used the receiver operating characteristic (ROC) curve to evaluate the diagnostic potential of these hub genes and constructed a predictive nomogram. In addition, this study also used the consensus clustering method to define two AA subtypes and explored their immune characteristics and functional pathways through ssGSEA, MCPcounter and enrichment analysis. Experimental validation included qRT-PCR for four hub genes and Western blotting for critical autophagy markers. Our analysis detected 10 ARDEGs in AA. Applying three machine learning algorithms, we identified four candidate hub genes, , , and , and verified their expression patterns in independent cohorts. The combined four-gene model and nomogram showed potential diagnostic performance. Consensus cluster analysis divided AA cases into two subtypes, each associated with different immune infiltration and functional pathways. Downregulation of and and upregulation of were verified by qRT-PCR. Western blotting further suggested altered autophagy-related protein expression in AA lesions, characterized by a reduced LC3B-II/I ratio and Beclin-1 expression and increased SQSTM1 expression. This study identified four candidate autophagy-related genes and two exploratory molecular subtypes in AA and may provide clues for understanding autophagy-related immune dysregulation and support further validation of candidate diagnostic markers. - Source: PubMed
Publication date: 2026/05/23
Li YufenZhang XiaolinWang JiatingJiang Yiqun - Environmental pollutants are increasingly recognized as disease modifiers, reshaping host homeostasis and shifting host-pathogen dynamics toward higher infection risk in aquatic ecosystems. Here, we show that the widely used strobilurin fungicide trifloxystrobin (TFS) persistently erodes antiviral competence in fish and increases susceptibility to spring viremia of carp virus (SVCV) by driving dynamin-related protein 1 (Drp1)-mediated excessive mitophagy and sustained mitochondrial dysfunction. Using epithelioma papulosum cyprini (EPC) cells and zebrafish as complementary models, we find that environmentally plausible TFS exposures (2.5-25 μg/L) elevate SVCV permissiveness; notably, this phenotype resolves incompletely after chemical withdrawal. Transcriptomics revealed a dose-concordant shift toward stress/innate immune signaling and mitophagy programs, alongside broad repression of proliferative and DNA-repair pathways. Consistently, TFS induces persistent mitochondrial membrane depolarization, promotes fragmentation and ultrastructural deterioration, and increases mitochondria-lysosome coupling. Mechanistically, TFS elevates Drp1 abundance and Ser616 phosphorylation, promotes Drp1 recruitment to mitochondria, and sustains microtubule-associated protein 1 light chain 3B (LC3B)/lysosomal-associated membrane protein 2 (LAMP2) engagement, accompanied by persistent induction of core autophagy regulators (, , , and ) across extended recovery windows. , prolonged TFS exposure similarly yields durable enhancement of SVCV susceptibility even after long recovery periods, indicating incomplete restoration of host resistance. Together, these findings link a major agricultural fungicide to persistent Drp1-driven mitophagy overactivation and identify long-term antiviral resistance as an ecologically relevant endpoint for pesticide risk assessment and aquatic disease forecasting.IMPORTANCEViral diseases pose a significant challenge to sustainable aquaculture, and effective antiviral interventions remain limited. In this study, we reveal that trifloxystrobin, a widely used fungicide, induces mitochondrial dysfunction and Drp1-mediated excessive mitophagy, leading to long-term suppression of antiviral immune responses in fish. Importantly, this work identifies mitochondrial dynamics as a key determinant of viral susceptibility and demonstrates how environmental pollutants can reshape host-pathogen interactions. By linking mitophagy and Drp1 activation to increased spring viremia of carp virus susceptibility, our findings provide a novel perspective on how pollutants may exacerbate viral infections in aquaculture species. This work underscores the urgent need for ecosystem-based antiviral strategies and offers a mechanistic framework for assessing ecological risks posed by common agricultural chemicals, thereby informing environmental and disease management in aquaculture. - Source: PubMed
Publication date: 2026/06/01
Wang HuanHu YangLiu LeiChen Jiong - Autophagosome formation depends on PtdIns3P, its presence is deciphered by PROPPINs, a family of β-propellers, which in yeast consists of Atg18, Atg21 and Hsv2 and in mammals of WIPI1, WIPI2, WDR45B/WIPI3 and WDR45/WIPI4. While Atg18 is required for scaffolding the Atg2-Atg9 complex, which mediates non-vesicular membrane transport to the phagophore, Atg21 organizes the Atg8 lipidation machinery. Atg18 further acts as part of a retromer complex in vacuole fragmentation. So far, the function of Hsv2 remained elusive. Here we show that Hsv2 is required for autophagy of large cargos such as the fatty acid synthase complex (FAS) and ribosomes. We further found that Hsv2 interacts with the key retromer component Vps35 and mediates vacuole fission cooperatively with Atg18. Interestingly, the residues for interaction of Hsv2 with Atg2 and Vps35 are distinct from those of Atg18. Hsv2 is known to affect the biogenesis of the spore wall, which prompted us to include diploid cells in our analyses. We found that Hsv2 interacts with the SNARE Pep12, and that Pep12 mislocalized to the vacuole in diploid but not haploid cells. This suggests a role of Hsv2 in protein sorting in diploid cells. The loop 6C/D of PROPPINs partially inserts into membranes causing their bending. We found that the membrane bending activity of Hsv2 is required for vacuole fragmentation and sorting in diploids but not for its autophagic function. Mutations in WDR45/WIPI4, the presumed mammalian homolog of Hsv2 cause the neurodegenerative disease BPAN, our study thus also helps to understand its underlying principles. CSC: cargo specific complex, FAS: fatty acid synthase, PAS: phagophore assembly site; PROPPIN: beta-propeller that binds phosphoinositides. - Source: PubMed
Publication date: 2026/05/14
Taylor Matthew FFoerster JanKramer FlorianStrubel NoreenThumm Michael