Ask about this productRelated genes to: ZFYVE9 antibody
- Gene:
- ZFYVE9 NIH gene
- Name:
- zinc finger FYVE-type containing 9
- Previous symbol:
- MADHIP
- Synonyms:
- SMADIP, SARA, PPP1R173
- Chromosome:
- 1p32.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-08
- Date modifiied:
- 2016-02-15
Related products to: ZFYVE9 antibody
Related articles to: ZFYVE9 antibody
- Systemic sclerosis (SSc) is an autoimmune condition affecting several organs. It is identified by thickening of the dermis, connective tissue affected by collagen accumulation, and vascular injuries that induce hypoxia. The present study aimed to determine whether extracellular vesicles (EVs) from adipose-derived stem cells (ADSCs) attenuated bleomycin-induced skin fibrosis and oxidative stress in scleroderma. ADSCs and their EVs were separated and a bleomycin-induced SSc mouse model was constructed. High-throughput sequencing was employed to study abnormal expression of circular RNAs in SSc skin tissues with or without ADSC-EV treatment. The regulatory mechanism and targets were studied using bioinformatics analysis, luciferase reporting analysis, angiogenic differentiation experiments, and RT-qPCR detection analysis. EVs from ADSCs were successfully isolated. The exosome treatment prevented dermal thickening and fibrosis in bleomycin-induced scleroderma. In addition, circ-Zfyve9 was demonstrated to have an important function in ADSC-EV-mediated skin tissue protection. GPX4 and miR-135 were shown to be downstream targets of circ-Zfyve9. Overexpressing miR-135 or downregulating GPX4 reversed the promotion effects of circ-Zfyve9 on angiopoiesis by increasing lipidosome ROS in EPCs under hypoxic conditions. Overexpressing miR-135 or downregulating GPX4 reversed the inhibition effect of circ-Zfyve9 on fibrosis in myofibroblasts under hypoxic conditions. Overexpressing circ-Zfyve9 increased the therapeutic effect of ADSC-EVs. EVs from ADSCs attenuated bleomycin-induced skin fibrosis and oxidative stress in scleroderma via circ-Zfyve9 delivery. - Source: PubMed
Li XueZhang WeiguoLiu JiaoZhu ZhidongTang HuiZhu YiqiWang HaoJin MingmingHuang GangHuang Qingqing - Tuberculosis (TB) is a severe respiratory illness that can lead to opportunistic infections in individuals with weakened immune systems. Accurate diagnosis and monitoring of treatment responses are essential. In this study, we analyzed the miRNA and mRNA profiles of 12 patients with active TB (ATB) before and after treatment. - Source: PubMed
Publication date: 2026/06/03
Park HeechulLee Eun JuPark SunyoungPark Sung-BaeKang Yun-JeongLee JiyoungWhang JakeKang Young AeKim SunghyunLee HyejonKim Jungho - Progressive peritoneal fibrosis is a severe complication of peritoneal dialysis (PD) with a complex pathogenesis. Our previous studies demonstrated that parthenolide (PTL) alleviates peritoneal fibrosis by suppressing the transforming growth factor (TGF)-β/Smad pathway. Smad anchor for receptor activation (SARA) acts as an adaptor protein for Smad2 and Smad3; however, its role in PD-associated peritoneal fibrosis and the relationship between PTL and SARA remain to be elucidated. In this study, single-cell sequencing (scRNA-seq) data and long-dwell PD fluid samples were collected. PD mice, a TGF-β1-induced mesothelial-mesenchymal transition (MMT) model, and CRISPR/Cas9-engineered SARA gene (ZFYVE9) knockout MeT-5A cells were established. The results revealed that SARA activates Smad2/3, whereas Smad3 promotes SARA degradation, leading to the downregulation of SARA expression during fibrosis progression in long-term-retained PD fluid samples, PD mice, TGF-β1-treated MeT-5A cells, and HMrSV5 cells. PTL does not regulate SARA protein stability, but luciferin reporter gene experiments revealed that the transcriptional recovery of the effects of PTL on SARA is consistent with its known antifibrotic effects. PTL was further confirmed to inhibit the SARA-Smad3 interaction through both in vitro and in vivo coimmunoprecipitation experiments. Molecular docking and PTL-biotin pulldown assays confirmed that PTL directly binds to the Smad3-binding interface of SARA at the Pro788 and Ser795 residues. In summary, SARA promotes PD-related peritoneal fibrosis through the phosphorylation of Smad2/3. PTL specifically binds to ZFYVE9 (P788/S795), disrupting the interaction between SARA and Smad3, thereby improving MMT and alleviating peritoneal fibrosis, which in turn restores SARA expression. This study provides a theoretical foundation for the clinical diagnosis and treatment of peritoneal fibrosis. - Source: PubMed
Zhang YingWang ZebinLi LiuWang ShulingWei RongDeng CongLong HaiboLiang JianboHuang YingWang ChunPeng XuanDi HuiXiao LongXie Zhiyong - Wound healing is a meticulously coordinated and intricate progression that necessitates precise regulation of fibroblast behavior. Macroautophagy/autophagy is a degradation system for clearing damaged cellular components. SQSTM1/p62 (sequestosome 1), a well-established autophagy receptor, also functions as a signaling hub beyond autophagy. Here, we observed a significant upregulation of autophagy in fibroblasts after wounding. Using mice with fibroblast-specific deletion of (autophagy related 7), we found that fibroblast autophagy governed wound healing. Fibroblast autophagy deficiency delayed proper dermal repair that was mired in insufficient fibroblast proliferation, migration, and myofibroblast transition. experiments further revealed that autophagy deficiency disrupted TGFB1 (transforming growth factor beta 1)-induced fibroblast proliferation, migration, and myofibroblast differentiation. Mechanistically, autophagy deficiency led to SMAD2 (SMAD family member 2) and SMAD3 sequestration within SQSTM1 bodies and attenuated TGFB1-induced receptor-regulated SMAD (R-SMAD) phosphorylation in an SQSTM1-dependent manner. Furthermore, deletion rescued the delayed skin wound healing caused by autophagy deficiency, and autophagy inducers promoted wound healing in an SQSTM1-dependent manner. Our findings highlight the critical role of fibroblast autophagy in wound healing and elucidate the underlying mechanisms by which autophagy regulates fibroblast behavior.: 3-MA: 3-methyladenine; ACTA2/α-SMA: actin alpha 2, smooth muscle; ACTB: actin beta; AMPK: AMP-activated protein kinase; ATG: autophagy related; BiFC: bimolecular fluorescence complementation; COL1A2: collagen type I alpha 2 chain; ECM: extracellular matrix; FGF: fibroblast growth factor; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HDF: human dermal fibroblast; HVGs: highly variable genes; KO: knockout; LMNB1: lamin B1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MKI67/Ki-67: marker of proliferation Ki-67; MTOR/mTOR: mechanistic target of rapamycin kinase; NFE2L2/NRF2: NFE2 like bZIP transcription factor 2; NFKB: nuclear factor kappa B; NLRP3: NLR family pyrin domain containing 3; PCA: principal component analysis; PI3K: phosphoinositide 3-kinase; R-SMAD: receptor-regulated SMAD; SBE: SMAD binding element; shCON: small hairpin negative control; siNC: negative control; siRNA: small interfering RNA; SMAD: SMAD family member; SQSTM1/p62: sequestosome 1; ssGSEA: single-sample gene set enrichment analysis; TGFB/TGF-β: transforming growth factor beta; TGFBR1: transforming growth factor beta receptor 1; TGFBR2: transforming growth factor beta receptor 2; VIM: vimentin; WT: wild-type; ZFYVE9/SARA: zinc finger FYVE-type containing 9. - Source: PubMed
Publication date: 2025/05/31
Xu YujiaoGu XinLi WenshuLin BoyangXu YitingWei QingchengLiu QingyuanZhao YaminLong RongzhuoJiang HulinWu ZhaoqiuLiu YunyaoQiang Lei - The litter trait is one of the most important economic traits, and increasing litter size is of great economic value in the pig industry. However, the molecular mechanisms underlying pig litter traits remain elusive. To identify molecular markers and candidate genes for pig litter traits, a genome-wide association study (GWAS) and selection signature analysis were conducted in a Yorkshire pig population. A total of 518 producing sows were genotyped with Illumina Porcine SNP 50 BeadChip, and 1969 farrowing records for the total number born (TNB), the number born alive (NBA), piglets born dead (PBD), and litter weight born alive (LWB) were collected. Then, a GWAS was performed for the four litter traits using a repeatability model. Based on the estimated breeding values (EBVs) of TNB, 15 high- and 15 low-prolificacy individuals were selected from the 518 sows to implement selection signature analysis. Subsequently, the selection signatures affecting the litter traits of sows were detected by using two methods including the fixation index (FST) and . Combining the results of the GWAS and selection signature analysis, 20 promising candidate genes (, , , , , , , , , , , , , , , , , , , and ) were identified. These findings provide novel insights into the genetic basis of pig litter traits and will be helpful for improving the reproductive performances of sows in pig breeding. - Source: PubMed
Publication date: 2023/11/23
Zhang YuLai JinhuaWang XiaoyiLi MingliZhang YanlinJi ChunlvChen QiangLu Shaoxiong