Mouse Anti Human Synaptobrevin-3 VAMP3
- Known as:
- Mouse Anti Human Synaptobrevin-3 VAMP3
- Catalog number:
- ant-352
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Mouse Anti Human Synaptobrevin-3 VAMP3
Related genes to: Mouse Anti Human Synaptobrevin-3 VAMP3
- Gene:
- VAMP3 NIH gene
- Name:
- vesicle associated membrane protein 3
- Previous symbol:
- -
- Synonyms:
- CEB
- Chromosome:
- 1p36.23
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-22
- Date modifiied:
- 2015-11-05
Related products to: Mouse Anti Human Synaptobrevin-3 VAMP3
Related articles to: Mouse Anti Human Synaptobrevin-3 VAMP3
- Severe COVID-19 involves hyperinflammation and multiorgan pathology, but consistent gene signatures remain elusive. We aimed to identify consensus transcriptomic signatures and molecular mechanisms in severe COVID-19. We performed an integrative analysis of 39 studies spanning 11 tissue types, 1551 bulk RNA-seq samples, and over 2 million single cells. A vote-counting strategy combined with a systems-biology approach was applied to detect consensus differentially expressed genes (DEGs). Pathways related to interferon/TNF-α signaling, hypoxia response, and platelet activation were consistently enriched across data sets. Among consensus DEGs-such as IFITM3, BCL2A1, CAMK2D, and CCR1-RAB8B was prioritized for functional validation based on its recurrence in ~45% of tissues and its known role in vesicle trafficking, a process intimately linked to viral life cycles. Molecular dynamics simulations and in vitro assays in SARS-CoV-2-infected CaCo-2 cells demonstrated that RAB8B modulates VAMP-3 clustering and intracellular trafficking. Silencing of Rab8b-1 and Rab8b-2 reduced viral infection by 30% (p = 0.0302) and 76% (p < 0.001), respectively. This study defines robust consensus signatures and positions RAB8B as a critical host factor and potential therapeutic target in severe COVID-19. Further exploration of RAB8B inhibitors is warranted to explore therapeutic utility. An interactive database at https://covidatlas.sysbio.tools/. - Source: PubMed
Avila Jonathan PeñaPark PeterSingh YouvikaAmaral Paulo PCastro ÍcaroTen-Caten FelipeSchuch VivianeGonçalves André N AGiddaluru JeevanMorais Mauro César CafundóOgava Rodrigo L TLubiana Thiagode Castro Gabriel AmorosoAquino RodrigoDurão LuizMartins Júlia RaspanteJimenez LeandroCosta-Martins André GGonzalez-Dias PatríciaHirata Thiago Dominguez CrespoDias Thomaz LüscherPeixe Débora GuerraSimizo AdrianaE Silva Juan Carlo SantosVasconcelos Amanda PereiraRodrigues Marcelo BerçotCastelucci Bianca GVirgillio-da-Silva João VictorMenezes LarissaMoraes-Vieira Pedro MCabral-Marques OtavioNakaya Helder I - Vascular smooth muscle cell (VSMC)-derived foam cells critically drive atherosclerotic plaque progression, yet their regulatory mechanisms remain incompletely understood. This study aimed to elucidate the pathophysiological role of the VSMC-enriched factor axin interactor, dorsalization-associated (AIDA) in this process and evaluate its therapeutic potential. We utilized VSMC-specific AIDA knockout in male ApoE mice and adenoviral shRNA silencing in oxLDL-stimulated murine aortic vascular smooth muscle cells (MOVAS), combined with co-immunoprecipitation (Co-IP), cholesterol flux assays, and ubiquitination profiling, which revealed that AIDA is selectively upregulated in VSMCs within human and murine atherosclerotic plaques. AIDA knockout attenuated aortic plaque burden, fibrosis, and elastic fiber fragmentation in vivo, and suppressed oxidized low-density lipoprotein (oxLDL) uptake and foam cell formation in vitro by specifically impairing CD36 membrane trafficking without affecting cholesterol efflux. Mechanistically, AIDA scaffolds HMG-CoA reductase degradation protein 1 (HRD1)-mediated K63-linked ubiquitination of vesicle-associated membrane protein 3 (VAMP3), resulting in the VAMP3-CD36 interaction and subsequent CD36 membrane translocation. These results demonstrate that AIDA promotes VSMC-derived foam cell formation by facilitating CD36 trafficking through the HRD1-VAMP3 ubiquitination axis, identifying the AIDA-HRD1-VAMP3-CD36 pathway as a potential novel strategy for the treatment of atherosclerosis. - Source: PubMed
Publication date: 2026/04/20
Lyu RuolinHe ZiyiLi NaZhang ZixuanWang Dao WenZhou NingLin LiShu Hongyang - Skeletal muscle is a central regulator of metabolic health, serving as the primary site of postprandial glucose uptake and playing a critical role in whole-body insulin sensitivity. Despite its importance, the molecular mechanisms governing muscle differentiation (myogenesis) and their modulation by metabolic interventions remain poorly defined. This study identifies the clathrin adaptor protein Picalm (phosphatidylinositol-binding clathrin assembly protein) as a novel regulator of myogenesis and investigates its regulation in response to exercise training and intermittent fasting. - Source: PubMed
Publication date: 2026/03/13
Gaugel JasminHaacke NeeleKuropka BennoJähnert MarkusRominger JuliaJonas WenkeSpeckmann ThiloRausch NiclasKleinert MaximilianWeigert CoraGarcia-Carrizo FranciscoSchulz Tim JEbner MichaelFreund ChristianSchürmann AnnetteVogel Heike - Although liver fibrosis presents a substantial global health challenge, therapeutic options that directly target liver fibrosis remain limited. Hepatic stellate cells (HSCs) are key contributors to fibrosis through extracellular matrix production. This study uncovers a previously unrecognized function of HSCs: ATP secretion. We found that HSCs express the vesicular nucleotide transporter (VNUT) on secretory vesicles and actively release ATP. In mouse HSCs, VNUT is localized to the cytosol and around lipid droplets. In a thioacetamide-induced liver fibrosis model, VNUT inhibition with clodronate suppressed HSC proliferation and fibrosis progression, while restoring AMPK phosphorylation. In human hepatic stellate LX-2 cells, VNUT colocalized with v-SNARE proteins VAMP3 and VAMP7 and the vesicular proton pump V-ATPase. ATP secretion from LX-2 cells was observed upon stimulation with the Ca ionophore ionomycin and was inhibited by Ca chelation or low temperature, supporting an exocytotic mechanism. Clodronate and VNUT-targeting siRNA significantly reduced ATP release. Thapsigargin, an inducer of endoplasmic reticulum Ca release, upregulated VNUT expression, suggesting a transcriptional regulation of VNUT-dependent ATP release by Ca signaling. TGF-β1 stimulation also upregulated VNUT expression, suggesting its involvement in TGF-β1-induced fibrogenesis pathway. Additionally, serotonin was identified as an ATP secretion stimulator in LX-2 cells, and this effect was blocked by clodronate. Platelets-a major peripheral serotonin source-were increased in TAA-treated liver and found adjacent to serotonin receptor 5-HT2B-positive HSCs. Clodronate treatment reduced CD41-positive platelets in liver tissue. These findings highlight VNUT-mediated ATP secretion as a key regulator of HSC function and a potential therapeutic target for liver fibrosis. - Source: PubMed
Publication date: 2026/02/04
Kabashima MasaharuHasuzawa NaoWang LixiangRikitake JunjiroNomura SeijiNiimoto TomohiroTokubuchi RieMoriyama SawakoGobaru MizukiInoguchi YukihiroNagayama AyakoAshida KenjiOhta KeisukeMoriyama YoshinoriNomura Masatoshi - Neurodevelopmental disorders (NDDs) arise from disruptions in brain development, yet the underlying pathways remain incompletely understood. Here we demonstrate that genome-wide CRISPR knockout screens in mouse embryonic stem cells differentiating into neural lineages identify hundreds of essential genes, only a minority of which are currently implicated in NDDs. Dominant NDD genes were enriched for transcriptional regulators, whereas recessive NDD genes were predominantly involved in metabolic processes. Mouse models for eight genes (Eml1, Dusp26, Dynlrb2, Mta3, Peds1, Sgms1, Slitrk4 and Vamp3) revealed marked neuroanatomical abnormalities, including microcephaly in half of the cases. Focusing on PEDS1, a key enzyme in plasmalogen biosynthesis, we identified a bi-allelic variant in individuals with microcephaly, global developmental delay and congenital cataracts. In mice, Peds1 deficiency led to accelerated cell-cycle exit and impaired neuronal differentiation and migration. These pathways required for neural differentiation provide a genetic framework for discovering additional NDD genes. - Source: PubMed
Publication date: 2026/01/05
Amelan AlanaCollins Stephan CDamseh Nadirah SHamada NanakoSalim AhdDvir EladMonderer-Rothkoff GalyaHarel TamarNagata Koh-IchiYalcin BinnazShifman Sagiv