Buffer Drain Caps 5_pk
- Known as:
- Buffer Drain Caps 5_pk
- Catalog number:
- 1298130
- Category:
- -
- Supplier:
- Ato
- Gene target:
- Buffer Drain Caps 5_pk
Related genes to: Buffer Drain Caps 5_pk
- Gene:
- CAPS NIH gene
- Name:
- calcyphosine
- Previous symbol:
- -
- Synonyms:
- CAPS1, MGC126562
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-05-31
- Date modifiied:
- 2016-07-18
Related products to: Buffer Drain Caps 5_pk
Related articles to: Buffer Drain Caps 5_pk
- Alzheimers disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of β-amyloid (Aβ) plaques and neurofibrillary tangles, leading to cognitive decline. The enzyme γ-secretase (γS) plays a central role in Aβ production and is therefore an important therapeutic target. In this study, interaction energies were evaluated using the Molecular Fragmentation with Conjugated Caps (MFCC) method combined with Density Functional Theory (DFT) calculations to investigate the interactions between γS and the inhibitors Semagacestat (SEM) and Avagacestat (AVA). The SEM-γS complex exhibited a more favorable total interaction energy, primarily driven by interactions with residues such as Ala431, Lys380, and Leu425. In contrast, the AVA-γS complex showed prominent interactions involving key residues, including Leu381, Leu425, and Leu432, which participate in substrate recognition and stabilization within the enzymes binding pocket. Overall, both ligands highlight the combined importance of hydrophobic and hydrophilic interactions in stabilizing the complexes. This study provides molecular-level insights into the interaction mechanisms of γ-secretase inhibitors, contributing to a better understanding of structure-energy relationships that are essential for the rational design of more selective and effective therapeutic agents for Alzheimers disease. - Source: PubMed
Publication date: 2026/08/27
Junior W S ClementeBezerra K SMatias E G COliveira J I NFulco U L - Fracture healing depends on coordinated osteogenesis and restoration of the vascular microenvironment. Endothelial cells support skeletal repair through angiogenesis, tissue perfusion and angiocrine signaling that regulates osteoprogenitor recruitment and differentiation. This narrative review examines endothelial dysfunction (ED) as a potential systemic contributor to impaired fracture healing by integrating evidence from vascular biology, experimental models and clinical studies. ED is characterized by reduced nitric oxide (NO) bioavailability, oxidative stress, inflammation and impaired vascular repair. These changes may disrupt angiogenic-osteogenic coupling through altered hypoxia-inducible factor 1-alpha subunit (HIF-1α)/vascular endothelial growth factor (VEGF) signaling, endothelial Notch activity, platelet-derived growth factor (PDGF)-mediated vascular remodeling and endothelial progenitor cell (EPC) mobilization. Conditions associated with endothelial dysfunction, including diabetes, aging, chronic kidney disease (CKD), smoking, obesity and chronic inflammatory disease, are also linked to delayed union, nonunion and poorer orthopedic outcomes. Cardiovascular disease and perioperative cardiovascular instability may further impair perfusion and physiological reserve during repair. However, the available evidence is predominantly experimental or observational, and direct causal evidence in fracture patients remains limited. Prospective studies combining standardized endothelial assessments with fracture-healing outcomes are needed to clarify clinical relevance and identify potential therapeutic targets. - Source: PubMed
Publication date: 2026/08/14
Michalczak JakubZnamierowski JacobBondarowicz JustinZgoda Wiktoria MałgorzataMichalczak MateuszPrigent-Tessier AnneBasset ChristelleTokarek Tomasz - The spectrum of syndromes associated with chronic urticaria (CU) is broad, ranging from monogenic autoinflammatory diseases (a single gene defect drives disease through dysregulated innate immunity) to multifactorial and acquired conditions (urticaria arises as part of a broader, polygenic or immune-mediated systemic process). Monogenic autoinflammatory conditions presenting with urticaria include cryopyrin-associated periodic syndromes (CAPS)-encompassing familial cold autoinflammatory syndrome (FCAS), Muckle-Wells syndrome (MWS), and neonatal-onset multisystem inflammatory disease (NOMID/CINCA) and the broader group of familial cold urticarias. Monogenic conditions with well-characterized gain-of-function NLR family pyrin domain containing 3 () variants present with recurrent hives, a cardinal feature associated with recurrent fevers. Multifactorial and acquired autoinflammatory or immune-mediated conditions include Schnitzler syndrome, adult-onset Still's disease, hypereosinophilic syndrome, Gleich syndrome, Wells syndrome, and Sjögren syndrome. Multifactorial conditions, including Schnitzler syndrome and Still's disease, manifest similarly, with CU as an initial sign and a shared pathogenic mechanism of innate immune dysregulation, with interleukin-1β playing a central, pro-inflammatory role as a major pyrogen. Here, we also present a female patient with clinically established Andersen-Tawil syndrome (ATS) who developed recurrent hives on her extremities within minutes after vigorous exercise. To our knowledge, this is the first report of a co-occurrence of CU and ATS. The hives were successfully attenuated by oral intake of effervescent potassium chloride during physical activity. This observation raises the possibility that chronic inducible urticaria may represent a previously unrecognized cutaneous ATS manifestation and suggests a potential pathophysiological link between potassium-channel dysfunction and mast cell activation. Distinguishing whether hives are an isolated symptom or part of a broader syndrome is critically important, as it might be crucial for the patient outcome. - Source: PubMed
Publication date: 2026/08/19
Bulat VedranaZanze LucijaPeček MirtaSmoljan-Filipović DajanaDragun KatarinaLugović-Mihić Liborija - Technology-critical elements are increasingly used in electronics, renewable-energy systems, high-performance alloys and other strategic technologies, yet their occurrence in wild fungi remains poorly characterised. This study evaluated gallium (Ga), germanium (Ge), niobium (Nb), tantalum (Ta) and tungsten (W) in wild mushrooms collected from Leicester and Leicestershire, UK. The dataset was reconstructed at fruiting-body level to avoid pseudo-replication from paired cap and stem records, yielding 121 analytical units. Results were corrected using digestion-date acid blanks, interpreted against analytical-portion-specific working limits of detection and classified as fully quantified (FQ), partially censored (PC) or fully censored (FC). Ga was FQ in 106/121 units and was the only element with sufficient quantitative coverage for continuous distributional estimation; its regression-on-order-statistics median was 475.48 ng g dw (IQR: 278.70-941.63). The corresponding FQ counts were 16 for Ge, 33 for Nb, 10 for Ta and 24 for W, with 7, 4 and 4 additional PC observations for Nb, Ta and W, respectively. In 22 paired fruiting bodies, Ga concentrations were higher in stems than caps (Wilcoxon = 5.25 × 10; BH-FDR = 1.05 × 10). Composite topsoils from 26 monitored sites provided park-scale geochemical context only and were not used to infer bioaccumulation or direct soil-to-fungus transfer. These findings establish a blank-corrected and censoring-aware occurrence baseline and suggest exploratory, site-specific potential for wild mushrooms as complementary biomonitoring matrices for selected technology-critical elements, while demonstrating that their usefulness is element-, taxon- and design-dependent. - Source: PubMed
Publication date: 2026/08/14
Peña-Fernández AntonioCámara-Pastor TomásDurán Guillermo TorradoLobo-Bedmar M Carmen - Diadenosine tetraphosphate (ApA) and related dinucleoside tetraphosphates (ApNs) are important stress-signalling molecules that coordinate bacterial adaptation to changing environmental conditions. Although the enzymes for turnover of ApA are known in several bacteria, the structural basis for substrate recognition and the cellular consequences of impaired ApA turnover remain poorly understood. Here, we characterize the Histidine-Aspartate (HD)-domain hydrolase YqeK from Bacillus subtilis. Deletion of yqeK impaired growth in stationary-phase, sporulation, and biofilm formation demonstrating a general role upon nutrient limitation. YqeK forms a homodimer and functions as a manganese-dependent phosphohydrolase symmetrically cleaving ApA into two ADP molecules and removing ApA caps from RNA. The enzyme was active not only toward ApA but also toward the mixed dinucleotides ApG, ApC, and ApU in both in vitro and in vivo assays, hence acting as a broad-spectrum regulator of ApN homeostasis. To understand this promiscuity, we determined crystal structures of YqeK in its apo- and ADP-bound state and in complex with a non-hydrolysable ApA analogue. The structures revealed an asymmetric recognition mechanism in which one nucleoside moiety and the proximal phosphate groups are tightly coordinated, whereas the distal nucleoside is accommodated largely through nonspecific interactions, explaining the ability of YqeK to process diverse substrates. Together, our findings establish YqeK as a central regulator of dinucleotide homeostasis and RNA metabolism and provide the structural framework for ApN recognition by HD-domain phosphohydrolases. - Source: PubMed
Publication date: 2026/08/25
Shivakumar Renuka DharaniHappel NatalieBurchert FabianaBrück MichelRandau LennartPané-Farré JanLinne UweFreitag JohannesHinrichs RebeccaKiontke StephanBange GertBedrunka-Meinert Patricia