Aven (C-Terminus) Peptide
- Known as:
- Aven (C-Terminus) Peptide
- Catalog number:
- 2413P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- Aven (C-Terminus) Peptide
Related genes to: Aven (C-Terminus) Peptide
- Gene:
- AVEN NIH gene
- Name:
- apoptosis and caspase activation inhibitor
- Previous symbol:
- -
- Synonyms:
- PDCD12
- Chromosome:
- 15q14
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-17
- Date modifiied:
- 2016-10-05
Related products to: Aven (C-Terminus) Peptide
Related articles to: Aven (C-Terminus) Peptide
- This article is the first report highlighting Rhodope avens as a natural source of bioactive compounds with potential pharmaceutical applications. Dry tinctures obtained from herba (HDT) and rhizoma (RDT) from the Balkan Peninsula endemic plant were analyzed and tested for antioxidant activity (DPPH, ABTS, FRAP, CUPRAC assays) and DNA nicking protection potential. The tinctures were characterized by a high total polyphenol content (total the polyphenols in RDT were more than twice that of HDT, i.e., 516.6 mg GAE/g dt; < 0.01). HPLC analysis revealed the presence of 14 phenolics, with the main one being (over 3 mg/g dt) (+)-catechin (28.21 mg/g dt for RDT; 9.67 mg/g dt HDT), followed by protocatechuic acid, salicylic acid, and rutin. Rosmarinic acid content is herein first reported for the genus . GC/MS analysis identified 41 compounds, among which monosaccharides predominated (with the highest fructose content), followed by gluconic acid, glucose-1-phosphate, mannitol, sorbitol, and glycerol in HDT, along with xylitol in RDT. The tinctures exhibited strong antioxidant potential as evaluated by the methods used, with the most pronounced effect found in the CUPRAC assay (5 458.87 μM TE/g dt for HDT; 10 073.99 μM TE/g dt for RDT; < 0.01), as confirmed in comparison to proven antioxidants such as BHT and vitamin C. DNA-protective activity against oxidative damage was established and microscopic identification of the herbal substances was also performed. - Source: PubMed
Publication date: 2026/05/13
Dimitrova-Dyulgerova IvankaMladenova SilviyaApostolova ElenaGeorgiev VasilNaimov SamirMladenova TsvetelinaDincheva IvaylaPavlov AtanasSlavov IliyaMladenov Rumen - The coronavirus disease 2019 (COVID-19) ranges from asymptomatic to very severe infection and death, largely depending on host factors, including genetics. We have investigated clinical and genetic data from 200 COVID-19 patients to search for factors predisposing to increased disease severity. - Source: PubMed
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Lantieri FrancescaCroci StefaniaDecherchi SergioRusmini MartaRecchi GiadaBonacini MartinaFerrigno IlariaRossi AlessandroCastillo De Spelorzi Yeraldin ChiquinquiraHenzen EdoardoRosamilia FrancescaCangelosi DavideLanduzzi FabioAngius AndreaRallo VincenzoMancuso PamelaPezzarossi AnnamariaGiorgi Rossi PaoloCatanoso MariagraziaGattorno MarcoCavalli AndreaMeroni Pier LuigiVozzi DiegoUva PaoloCeccherini IsabellaSalvarani Carlo - Telepathology enables remote diagnostic consultation through digital image transmission and is particularly valuable in settings where subspecialty expertise is not immediately available. This study evaluated the diagnostic accuracy of PathoZoom, a web-based platform that allows real-time remote review of microscope images via mobile devices during intraoperative frozen section examination in a high-complexity academic hospital. - Source: PubMed
Publication date: 2026/05/14
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Publication date: 2026/05/05
Mu WenbiAo JingwenLi YaoZhang JianyongDuan Cancan - Brain arteriovenous malformations (bAVMs) are tangles of abnormal vessels that shunt blood directly from arteries to veins. The reduction of pericytes is linked to hemorrhage in bAVMs. The Pdgfb/Pdgfrβ signaling pathway is crucial for regulating pericyte recruitment during angiogenesis. Here, we show that mice with F7 mutations developed cerebrovascular dysplasia in the brain’s angiogenic region, associated with increased pro-angiogenic and inflammatory signaling. Interestingly, the expression of activin receptor-like kinase 1 (Alk1) is decreased in the brain’s angiogenic region of F7 heterozygous mice. Overexpression of ALK1 in brain endothelial cells (ECs) reduces angiogenic signaling and the severity of vascular dysplasia in F7 heterozygous mice. F7 mutations also increased dysplastic vessels and reduced pericyte coverage in the bAVM in endoglin-deficient mice. Endoglin is an AVM causative gene. Our data indicate that F7 mutations result in cerebrovascular dysplasia and worsen the bAVM phenotype in endoglin mutant mice by enhancing angiogenesis and inflammation. Overexpression of ALK1 in brain ECs reduces the severity of cerebrovascular dysplasia in F7 heterozygous mice through downregulating angiogenic signaling. - Source: PubMed
Publication date: 2026/05/03
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