PF_AOR with cap1
- Known as:
- PF_AOR cap1
- Catalog number:
- 252451
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Herolab
- Gene target:
- PF_AOR with cap1
Related genes to: PF_AOR with cap1
- Gene:
- CAP1 NIH gene
- Name:
- cyclase associated actin cytoskeleton regulatory protein 1
- Previous symbol:
- -
- Synonyms:
- CAP
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-17
- Date modifiied:
- 2017-05-17
Related products to: PF_AOR with cap1
Related articles to: PF_AOR with cap1
- In Pakistan, bovine mastitis has been identified as one of the biggest limitations to dairy production, and Staphylococcus aureus has been identified as one of the most enduring and economically relevant mastitogens. The current study was conducted to examine the capsular genotype and antimicrobial resistance (AMR) of S. aureus isolated from cases of clinical and subclinical mastitis in cows and buffaloes of the Punjab and Sindh provinces. One hundred and fifty S. aureus isolates (109 from cows and 41 from buffaloes) were isolated out of 87 dairy herds and verified using nuc gene-based PCR. Genotyping of capsular polysaccharide (CP) demonstrated that there were only cap5 (56%) and cap8 (44%) loci, but no cap1 and cap2. The cap5 was the most common among clinical (20.66%) and subclinical (35.33%) isolates, whereas cap8 had a frequency of 12.66% and 31.33% in clinical and subclinical isolates, respectively, suggesting that CP5 and CP8 are the common circulating types of capsular pathogens in the study areas. The antimicrobial susceptibility testing involving 13 routine antimicrobial agents revealed that 92% of isolates were resistant to one or more antimicrobials, and 63.3% of the isolates were multidrug-resistant (MDR). The greatest resistance was found with penicillin (72.66%), then amoxicillin (53.33%), and amoxicillin-clavulanic acid (37.33%). Those resistant to methicillin (3.33%) were mecA-positive MRSA, but no isolate was positive for mecC. Molecular screening showed that the prevalence of the blaZ gene (95.33%) was high and in line with the prevalence of resistance mediated by β-lactamase. The tetM (92.10%) and tetK (84.21%) were most common among the tetracycline-resistant isolates. The determinants of macrolide resistance were msrC (87.5%), ermB and ermC, and the aac-aphD aminoglycoside resistance gene was also present in 17.64% of resistant isolates. Resistance to critically important antimicrobials like vancomycin and linezolid was low, and optrA was not identified. Strong genotype-phenotype concordance was shown by correlation analysis to occur in 22 cases where 2 beta-lactam, tetracycline, and macrolide resistance determinants were genotyped and phenotyped, indicating the occurrence of co-selection and possible horizontal gene transfer. This study provides the first comprehensive molecular epidemiological insight in bovine and bubaline S. aureus capsular diversity, as well as AMR determinants of S. aureus, in Punjab and Sindh. The prevalence of CP5/CP8 is in favor of their inclusion in vaccine development, whereas high rate of MDR burden evidences the urgency of antimicrobial stewardship and long term molecular surveillance within one health paradigm. - Source: PubMed
Publication date: 2026/06/15
Ghafoor MSaqib MAshfaq KRehman S U - The conversion of native vegetation to anthropogenic land uses and landscape fragmentation are primary drivers of biodiversity loss and ecosystem services decline in tropical watersheds. Understanding how land use shapes the spatial configuration of forest fragments is essential to inform conservation and restoration strategies. We evaluated the configurational fragility of forest remains in the Lower São Francisco River Watershed, Brazil, combining structural metrics (area, core area and shape index) with land use and land cover (LULC). Fragility levels were defined through hierarchical classification and their relationship with LULC was tested using distance-based redundancy analysis (db-RDA). A principal component analysis (PCA) first summarized LULC variation. The watershed is dominated by anthropogenic matrices, with agriculture and pasture occupying 66.9% of the area, mainly pasture (57.7%). This resulted in 37,022 highly reduced and discontinuous forest fragments, of which 72.2% exhibited high configurational fragility. Savanna formation, the most representative native vegetation, had 96.1% of its patches within intermediate to high fragility levels. The PCA revealed three dominant gradients: herbaceous formations, wooded sandbank vegetation and wetlands (PC1), contrast between savanna formations and pasture (PC2), and heterogeneity of forests, forest plantation and mosaic of uses (PC3). db-RDA confirmed this pattern (adjusted = 0.362), with CAP1 explaining 92.2% of the constrained variation, demonstrating a strong opposition between natural environments and anthropogenic land uses. This study shows that configurational fragility is strongly driven by anthropogenic LULC, revealing that landscapes with the same forest cover may differ in fragility depending on the spatial organization of the remnants. In the area analyzed, sublevels High III and Intermediate I predominated, where small fragments dominated by edges coexist with larger and irregular patches, with occasional occurrences of Low III. As a management guideline, it is recommended to protect strategic remnants, intervene in intermediate areas, and restore zones of high fragility. Future studies should integrate these sublevels with functional indicators and temporal dynamics. - Source: PubMed
Publication date: 2026/06/11
Saraiva-Maia Jessyca Janyny de Oliveirada Silva Milena DutraBeiroz WallaceAlmeida Nadjacleia Vilar - Proprotein convertase subtilisin/kexin type 9 (PCSK9) acts as a pleiotropic modulator of inflammation. This study aimed to investigate the role and underlying mechanism of PCSK9 in Kawasaki disease (KD)-associated vasculitis. A Candida albicans water-soluble fraction (CAWS)-induced murine vasculitis model (n = 5-8 mice per group) and CAWS-stimulated RAW 264.7 macrophages (n = 3-8 independent experiments) were used. PCSK9 was pharmacologically inhibited in vivo with SBC-115076 and in vitro with PF-06446846. Vascular pathology, inflammatory markers, macrophage polarization, and signaling pathways were evaluated using hematoxylin-eosin (H&E) staining, immunofluorescence (IF), Western blot, quantitative real-time polymerase chain reaction (qRT-PCR), and RNA sequencing (RNA-seq). CAP1 overexpression was performed via lentiviral infection in RAW 264.7 cells to further validate its functional role. PCSK9 expression was significantly upregulated (two-fold) in the coronary arteries of CAWS-treated mice, and PCSK9 was predominantly co-localized with macrophages. Pharmacological inhibition of PCSK9 attenuated coronary arteritis, reduced the inflammatory infiltrate fraction by 54%, attenuated systemic inflammation, and decreased cardiac macrophage infiltration by 89%. In vitro, PCSK9 blockade suppressed CAWS-induced M1 macrophage polarization, as shown by reduced expression of the markers CD86 (by 96%) and iNOS (by 60%), and decreased secretion of the pro-inflammatory cytokines TNF-α (by 80%), IL-1β (by 86%), and IL-6 (by 89%). Transcriptomic analysis identified the NF-κB pathway as a key downstream signaling pathway. Mechanistically, PCSK9 inhibition downregulated CAP1 (adenylyl cyclase-associated protein 1) expression by 64% and suppressed NF-κB p65 nuclear translocation by 91% in macrophages. Importantly, CAP1 overexpression reversed the inhibitory effects of PCSK9 blockade on p65 nuclear translocation, M1 polarization, and inflammatory cytokine production. PCSK9 promotes KD-like vasculitis by activating the CAP1-mediated NF-κB pathway in macrophages, thereby driving pro-inflammatory responses. Pharmacological inhibition of PCSK9 attenuates vascular immunopathology, highlighting PCSK9 as a potential therapeutic target for KD. - Source: PubMed
Zhang HaoShuai DujuanRuan MiaohuaWu MaoWang LinlinChu MaopingRong Xing - Cyclase-associated protein 1 (CAP1) is widely expressed in mammalian tissues; however, its physiological role in the lung remains largely unclear. This study aimed to explore the function of CAP1 in alveolar type 2 (AT2) cells and its potential association with pulmonary fibrosis. - Source: PubMed
Publication date: 2026/06/09
Wang BingbingGu YunluZhang JushanTuerhong AmanguliZhu YujieShah Binay KumarWang ChanghuiXie Shuanshuan - Pulmonary capillary endothelial cells (ECs) form a highly specialized vascular interface that sustains gas exchange and organismal survival across species. Recent advances in single-cell transcriptomics and lineage tracing have revealed substantial heterogeneity within the pulmonary endothelium, redefining traditional views of capillary structure and function. In the adult lung, two major capillary populations: general capillary ECs (CAP1) and aerocyte capillary ECs (CAP2), have been identified, with CAP1 cells increasingly recognized as a heterogeneous and functionally diverse compartment that includes EC progenitors and reparative subpopulations. Emerging datasets further demonstrate arterial-venous polarization within the capillary bed and reveal gradients of gene expression that extend from macrovascular arteries and veins into the alveolar microvasculature. Within this polarized CAP1 landscape, several transcriptionally distinct EC subsets exhibit enhanced angiogenic potential and may contribute to EC regeneration during injury. This review synthesizes current knowledge of pulmonary capillary EC heterogeneity, emphasizing arterial-venous polarization of the capillary network, and the identification of reparative EC progenitors within the CAP1 population. We highlight emerging technologies including EC enrichment strategies, and transcriptomics, and epigenomic profiling that are beginning to resolve rare EC states and functional niches within the alveolar microvasculature. A deeper understanding of capillary EC diversity and lineage dynamics will be essential for identifying therapeutic targets aimed at restoring vascular stability, promoting regenerative angiogenesis, and preserving gas exchange in aging lungs and chronic lung diseases. - Source: PubMed
Publication date: 2026/06/02
Majka Susan MNiethamer Terren KCaporarello NunziaThorndyke Hannah FClair GeremyWest James DKarmouty-Quintana HarryAlvira Cristina M