CAV2 ELISA kit
- Known as:
- CAV2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CAV2-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CAV2 ELISA kit
Ask about this productRelated genes to: CAV2 ELISA kit
- Gene:
- CAV2 NIH gene
- Name:
- caveolin 2
- Previous symbol:
- -
- Synonyms:
- CAV
- Chromosome:
- 7q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-02
- Date modifiied:
- 2016-10-05
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- - Source: PubMed
- Adenoviral vectors are widely used in vaccine development; however, pre-existing immunity to common human adenovirus serotypes can limit their effectiveness. Canine adenovirus type 2 (CAV-2) is a non-human adenovirus with low seroprevalence in humans, making it a suitable alternative vector. Despite its promise, comprehensive preclinical safety data for CAV-2 vector-based vaccine platforms remain limited. In this study, we evaluated the safety profile of a replication-defective CAV-2 vector expressing the Omicron BA.4 SARS-CoV-2 spike immunogen in BALB/c mouse models. The SARS-CoV-2 CAV-2 vector-based vaccine was expressed and propagated in AD293 cells. The mice received intramuscular prime-boost immunisations with low (1 × 10 PFU), moderate (0.5 × 10 PFU), or high (1 × 10 PFU) vaccine doses, alongside empty CAV-2 vector and physiological buffer control groups, and were monitored longitudinally up to Day 72. The mice were clinically assessed at days 0, 7, 21, 42, and 72 for any deviations from normal conditions in comparison to the control groups. Biochemical analyses were performed to evaluate liver and kidney function, as well as any tissue injury due to the vaccine candidate. Hematological parameters were assessed by conducting complete blood counts. Body temperature and weight changes were also monitored as an indicator of systemic toxicity. The biochemical and haematological parameters remained within physiological reference ranges across all dose groups and timepoints, with no dose-related deviations, indicating that the vaccine candidate did not show evidence of hepatotoxicity, nephrotoxicity, tissue or haematological toxicity. Body temperatures remained within normal physiological ranges following both prime and booster immunisations, and body weights increased normally across all groups as the animals grew throughout the study period without any abnormal weight gain or loss. These results suggest that the replication-defective CAV-2-vectored SARS-CoV-2 vaccine candidate was well tolerated and did not demonstrate evidence of systemic toxicity under the conditions tested. These findings demonstrate that the CAV-2 vector exhibits a favourable safety profile in murine models when used as a vaccine delivery platform, supporting its translational potential as an alternative adenoviral vector-based vaccine platform. Further studies incorporating additional safety endpoints, including histopathological, vector persistence and shedding evaluation, are warranted to support continued development of the platform. - Source: PubMed
Publication date: 2026/07/23
Omara DenisNdekezi ChristianMugaba SusanNakyanzi AngellaNatwijuka FortunateKapaata AnneKato FrankByamukama DrakeGgwaabya David EMugulusi OrlaBwanga FreddieKatete David PMatovu EnockOlobo JosephObuku Ekii AndrewSande Obondo JamesSerwanga JenniferCose StephenKaleebu PontianoBalinda Sheila N - Activity-dependent modulation of presynaptic voltage-gated Ca channels (Ca2) regulates Ca influx to control neurotransmitter release and neuronal circuit output. Although Ca2.1 can undergo robust Ca-dependent facilitation (CDF), its contribution to information processing in central neuronal circuits remains unclear. Accurate auditory information processing requires precise and reliable synaptic transmission at high activity rates in the auditory brainstem. To determine if Ca2.1 CDF is a key regulator of high-fidelity synaptic transmission, we expressed Ca2.1 splice variants that are either CDF-capable (Ca2.1 37a) or CDF-incapable (Ca2.1 37b) at the calyx of Held presynaptic terminal. We found no difference in basal Ca2.1 currents or synaptic transmission. However, Ca2.1 37b terminals lacked CDF, synaptic facilitation and had a decreased reliability and precision of postsynaptic action-potential firing. Additionally, loss of CDF decreased the auditory brainstem response wave III amplitude. We propose that Ca2.1 CDF is essential for faithful auditory information transfer. - Source: PubMed
Publication date: 2026/08/22
Al-Yaari MohammedLi JianingKeine ChristianHunger BryceHansen Marlan RYoung Samuel M - Macroautophagy/autophagy is a critical cellular degradation pathway essential for neuronal proteostasis and synaptic function. Its decline with aging is associated with synaptic dysfunction and reduced circuit resilience. NPY (neuropeptide Y), a highly abundant brain neuropeptide, has emerged as an important regulator of autophagy and aging-related processes. In , the NPY-family peptide sNPF modulates age-related changes in presynaptic architecture via non-cell autonomous mechanisms. Here, we examined whether autophagy and NPY interact within hypothalamic NPY AGRP neurons to regulate presynaptic organization in distant brain regions. We show that autophagy in these neurons non-cell autonomously controls hippocampal presynaptic active zone architecture and proteostasis, while maintaining NPY peptide levels. Importantly, dietary supplementation of the natural polyamine spermidine restored NPY expression in the aged hippocampus, highlighting its potential to rejuvenate neuropeptide signaling. Together, these findings reveal a pathway by which hypothalamic autophagy and NPY signaling regulate hippocampal synaptic architecture, linking metabolic state to synaptic resilience.: AGRP: agouti related neuropeptide; ARC: arcuate nucleus; ATG5: autophagy related 5; AZ: active zone; BECN1/beclin1: beclin 1, autophagy related; brp: bruchpilot; BSN: bassoon; CA3-CA1: cornu ammonis 3-cornu ammonis 1; CACNA1A/CaV2.1: calcium channel, voltage-dependent, P/Q type, alpha 1A subunit; cKO: conditional knockout; gSTED: time-gated Stimulated Emission Depletion; HOMER1: homer scaffolding protein 1; KO: knockout; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MB: mushroom body; MF-CA3: mossy fiber-cornus ammonis 3; NPY: neuropeptide Y; NPY1R: neuropeptide Y receptor Y1; NPY2R: neuropeptide Y receptor Y2; NPY5R: neuropeptide Y receptor Y5; PreScale: presynaptic upscaling; RIMBP2: RIMS binding protein 2; SQSTM1/p62: sequestosome 1; sNPF: short neuropeptide F precursor; SLC30A3/ZNT3: solute carrier family 30 (zinc transporter), member 3; Spd: spermidine; Spd-S: spermidine supplementation; WT: wild-type. - Source: PubMed
Publication date: 2026/08/30
Cazzolla GiovannaToppe DavidKrause GinaKochlamazashvili GagaLützkendorf JanineSchedina Ina MStephanowitz HeikeReisenbichler Anna MariaChen XingxiangKerkhoff YannicReifenstein EricErnst Helen Mvon Kleist MaxZimmermann AndreasEisenberg TobiasMadeo FrankLiu FanHerzog HerbertAlbrecht AnneSchmitz DietmarHaucke VolkerSigrist Stephan JMaglione Marta - The purpose of this study was to investigate cellular and molecular mechanisms underlying neovascular age-related macular degeneration (nAMD) and polypoidal choroidal vasculopathy (PCV) via single-cell RNA sequencing (scRNA-seq), then focusing on caveolae-resident proteins based on identified negatively enriched caveolae via Gene Set Enrichment Analysis (GSEA). - Source: PubMed
Yu Richard Ming ChuanOguz GokceFu Nai YangShihabuddeen Waseem AhamedCheung ChristineWang XiaomengWong Tien YinCheung Chui Ming GemmyRamasamy AdaikalavanYanagi Yasuo