ATP6V0C Antibody (C-term) Blocking Peptide
- Known as:
- ATP6V0C Antibody (C-terminus) Blocking Peptide
- Catalog number:
- BP10470b
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ATP6V0C Antibody (C-term) Blocking Peptide
Related genes to: ATP6V0C Antibody (C-term) Blocking Peptide
- Gene:
- ATP6V0C NIH gene
- Name:
- ATPase H+ transporting V0 subunit c
- Previous symbol:
- ATPL, ATP6C, ATP6L
- Synonyms:
- VATL, Vma3
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-12
- Date modifiied:
- 2016-02-11
Related products to: ATP6V0C Antibody (C-term) Blocking Peptide
Related articles to: ATP6V0C Antibody (C-term) Blocking Peptide
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Publication date: 2024/04/01
Feng XiaofangTong LijiaMa LinaMu TongYu BaojunMa RuoshuangLi JiweiWang ChuanchuanZhang JuanGu Yaling - [This corrects the article DOI: 10.3389/fnmol.2022.889534.]. - Source: PubMed
Publication date: 2024/03/01
Tian YangZhai Qiong-XiangLi Xiao-JingShi ZhenCheng Chuan-FangFan Cui-XiaTang BinZhang YingHe Yun-YanLi Wen-BinLuo ShengHou ChiChen Wen-XiongLiao Wei-PingWang Jie - Increasing evidence suggests that autophagy plays a major role during renal fibrosis. Transcription factor EB (TFEB) is a critical regulator of autophagy- and lysosome-related gene transcription. However, the pathophysiological roles of TFEB in renal fibrosis and fine-tuned mechanisms by which TFEB regulates fibrosis remain largely unknown. Here, we found that TFEB was downregulated in unilateral ureteral obstruction (UUO)-induced human and mouse fibrotic kidneys, and kidney-specific TFEB overexpression using recombinant AAV serotype 9 (rAAV9)-TFEB in UUO mice alleviated renal fibrosis pathogenesis. Mechanically, we found that TFEB's prevention of extracellular matrix (ECM) deposition depended on autophagic flux integrity and its subsequent blockade of G2/M arrest in tubular cells, rather than the autophagosome synthesis. In addition, we together RNA-seq with CUT&Tag analysis to determine the TFEB targeted gene ATP6V0C, and revealed that TFEB was directly bound to the ATP6V0C promoter only at specific site to promote its expression through CUT&Run-qPCR and luciferase reporter assay. Interestingly, TFEB induced autophagic flux integrity, mainly dependent on scaffold protein ATP6V0C-mediated autophagosome-lysosome fusion by bridging with STX17 and VAMP8 (major SNARE complex) by co-immunoprecipitation analysis, rather than its mediated lysosomal acidification and degradation function. Moreover, we further investigated the underlying mechanism behind the low expression of TEFB in UUO-induced renal fibrosis, and clearly revealed that TFEB suppression in fibrotic kidney was due to DNMT3a-associated TFEB promoter hypermethylation by utilizing methylation specific PCR (MSP) and bisulfite-sequencing PCR (BSP), which could be effectively recovered by 5-Aza-2'-deoxycytidine (5A-za) to alleviate renal fibrosis pathogenesis. These findings reveal for the first time that impaired TFEB-mediated autophagosome-lysosome fusion disorder, tubular cell G2/M arrest and renal fibrosis appear to be sequentially linked in UUO-induced renal fibrosis and suggest that DNMT3a/TFEB/ATP6V0C may serve as potential therapeutic targets to prevent renal fibrosis. - Source: PubMed
Publication date: 2024/03/03
Ren XiangWang JingWei HuizhiLi XingTian YiqunWang ZhixianYin YishengGuo ZihaoQin ZhenliangWu MinglongZeng Xiaoyong - Kohlschütter-Tönz syndrome (KTS) is a rare autosomal recessive disorder characterized by severe intellectual disability, early-onset epileptic seizures, and amelogenesis imperfecta. Here, we present a novel Rogdi mutant mouse deleting exons 6-11- a mutation found in KTS patients disabling ROGDI function. This Rogdi mutant model recapitulates most KTS symptoms. Mutants displayed pentylenetetrazol-induced seizures, confirming epilepsy susceptibility. Spontaneous locomotion and circadian activity tests demonstrate Rogdi mutant hyperactivity mirroring patient spasticity. Object recognition impairment indicates memory deficits. Rogdi mutant enamel was markedly less mature. Scanning electron microscopy confirmed its hypomineralized/hypomature crystallization, as well as its low mineral content. Transcriptomic RNA sequencing of postnatal day 5 lower incisors showed downregulated enamel matrix proteins Enam, Amelx, and Ambn. Enamel crystallization appears highly pH-dependent, cycling between an acidic and neutral pH during enamel maturation. Rogdi teeth exhibit no signs of cyclic dental acidification. Additionally, expression changes in Wdr72, Slc9a3r2, and Atp6v0c were identified as potential contributors to these tooth acidification abnormalities. These proteins interact through the acidifying V-ATPase complex. Here, we present the Rogdi mutant as a novel model to partially decipher KTS pathophysiology. Rogdi mutant defects in acidification might explain the unusual combination of enamel and rare neurological disease symptoms. - Source: PubMed
Publication date: 2024/01/03
Jimenez-Armijo AlexandraMorkmued SupawichAhumada José TomásKharouf Najide Feraudy YvanGogl GergoRiet FabriceNiederreither KarenLaporte JocelynBirling Marie ChristineSelloum MohammedHerault YannHernandez MagaliBloch-Zupan Agnès - We recently reported that cranberry proanthocyanidins (C-PACs) inhibit esophageal adenocarcinoma (EAC) by 83% through reversing reflux-induced bacterial, inflammatory and immune-implicated proteins and genes as well as reducing esophageal bile acids, which drive EAC progression. This study investigated whether C-PACs' mitigation of bile reflux-induced transporter dysregulation mechanistically contributes to EAC prevention. RNA was isolated from water-, C-PAC- and reflux-exposed rat esophagi with and without C-PAC treatment. Differential gene expression was determined by means of RNA sequencing and RT-PCR, followed by protein assessments. The literature, coupled with the publicly available Gene Expression Omnibus dataset GSE26886, was used to assess transporter expression levels in normal and EAC patient biopsies for translational relevance. Significant changes in ATP-binding cassette (ABC) transporters implicated in therapeutic resistance in humans (i.e., , , , , , and ) and the transport of drugs, xenobiotics, lipids, and bile were altered in the reflux model with C-PACs' mitigating changes. Additionally, C-PACs restored reflux-induced changes in solute carrier (SLC), aquaporin, proton and cation transporters (i.e., , , , and ). This research supports the suggestion that transporters merit investigation not only for their roles in metabolism and therapeutic resistance, but as targets for cancer prevention and targeting preventive agents in combination with chemotherapeutics. - Source: PubMed
Publication date: 2023/12/07
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