CAPZb ELISA kit
- Known as:
- CAPZb Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CAPZb-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CAPZb ELISA kit
Related genes to: CAPZb ELISA kit
- Gene:
- CAPZB NIH gene
- Name:
- capping actin protein of muscle Z-line subunit beta
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p36.13
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-26
- Date modifiied:
- 2018-04-23
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- Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease of unknown etiology, characterized by progressive scarring and fibrosis of the lungs, leading to irreversible loss of lung function. Current mechanism studies have found that fibroblasts, as the main effector cells, exhibit abnormal differentiation and proliferation in pulmonary fibrosis, thereby promoting collagen secretion for extracellular matrix (ECM) deposition. Cytoskeletal remodeling is the basis for fibroblast-to-myofibroblast differentiation, however, the key proteins and regulatory mechanisms involved in this process are still unclear. Here, F-actin-capping protein subunit beta (CAPZB) was identified to be desuccinylated at three lysine residues (K57, K95, and K235). Gain- and loss-of-function studies in vitro and in vivo demonstrated that CAPZB regulates cytoskeletal remodeling and differentiation of fibroblasts to myofibroblasts by capping the barbed end of F-actin, and mutation of the modification site confirmed the inhibition of CAPZB function by desuccinylation. Further studies showed that histone deacetylase enzymes 8 (HDAC8) could interacts with CAPZB, and its pro-fibrotic role as a desuccinylase was verified. Our findings suggested that desuccinylation inhibited CAPZB function and promoted cytoskeletal remodeling, targeting the succinylation modification of CAPZB could potentially serve as a novel therapeutic approach for pulmonary fibrosis. - Source: PubMed
Publication date: 2026/04/29
Liu BoKang DiZhang JinjinWang YujieLi RongrongLv ChangjunZhai NailiangSong XiaodongZhang SongziLi Hongbo - Cognitive impairment is a common yet under-recognised complication of ischaemic stroke (IS), with long-term effects on patient quality of life and rehabilitation outcomes. Identifying early biomarkers and protective factors such as cognitive reserve (CR) is essential for improving prognosis and guiding targeted interventions. This study aimed to determine the following: (i) RNA gene expression profiling during acute stroke and (ii) the associations between target genes as well as clinical factors and cognitive impairment during an acute event and at the 3-month follow-up. A three-month prospective cohort study involving 24 adults with mild to moderate IS and 24 age- and sex-matched controls admitted to Hospital Canselor Tuanku Muhriz, Malaysia, was conducted. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) within 48 h of stroke and at 3 months. Peripheral blood samples were collected for RNA extraction, and gene expression was analysed using RT² Profiler PCR arrays. Cognitive reserve was measured using the Cognitive Reserve Index Questionnaire (CRI-q). Statistical analyses included chi-square and independent t tests. At baseline, 83.3% of IS patients exhibited cognitive impairment (mean age 64.6 ± 10.5 years). Increased age (p = 0.006), low education level (p = 0.010), diabetes mellitus (p = 0.010), CRI-Education (p = 0.010) and CRI-Working Activity (p = 0.009) were significantly associated with baseline cognitive impairment. These clinical and CR factors survived False Discovery Rate (FDR) correction at the baseline stage (p < 0.05). However, at the 3-month follow-up, no clinical or CR factors remained statistically significant after FDR correction. Regarding gene expression, while MAPK1 (p = 0.029) and CAPZB (p = 0.042) were nominally upregulated in patients, and RCOR1 (p = 0.043) showed a nominal association with baseline impairment, no genetic markers survived FDR correction at either time point. Age, diabetes, and cognitive reserve are robust determinants of cognitive status during the acute phase of ischaemic stroke. The loss of significance at 3 months suggests these factors are primary drivers of initial functional buffering rather than long-term recovery trajectories in this cohort. CR should be utilised as a prognostic stratification tool during admission to identify high-risk patients rather than as a direct target for acute intervention. Future large-scale studies are required to validate whether the observed nominal gene expression trends can serve as reliable biomarkers for long-term recovery. - Source: PubMed
Publication date: 2026/04/20
Muhamad Nurul NadiahKatijjahbe Md AliAbdul Murad Nor AzianWan Zaidi Wan AsyrafMohamed Saini Suriati - RNA modifications represent a critical layer of post-transcriptional gene regulation, shaping RNA fate and function through modulation of splicing, stability, translation, and immune signaling. Their role in viral infections remains insufficiently explored. We applied direct RNA sequencing to profile three key RNA modifications, 5-methylcytosine (m5C), N6-methyladenosine (m6A), and pseudouridine (psU), in whole blood samples from COVID-19 patients and healthy controls. Using CHEUI and NanoSPA, we identified condition-specific modification sites, their positional distribution, and associated functions. We detected 689 m5C, 738 m6A, and 1,201 psU sites, many uniquely enriched in infected individuals. These modifications localized predominantly to 3' UTRs and final exons. Codon-level and motif analysis revealed distinct enrichment patterns. Functional annotation indicated involvement in immune response, viral defense, inflammation, and stress. Several immune-regulatory genes, including , , and , exhibited co-occurring modifications. Pathway analysis revealed convergence on processes such as endocytosis, Fc receptor-mediated phagocytosis, and phagosome maturation, mechanisms central to viral entry and immune activation. Our findings show that RNA modifications are dynamically regulated during infection and may serve as biomarkers and therapeutic targets in COVID-19. - Source: PubMed
Publication date: 2026/01/26
Maździarz Mateusz AKrawczyk KatarzynaLepiarczyk EwaPaukszto ŁukaszSawicki JakubMajewska Marta - Endothelial dysfunction underlies the pathogenesis of many diseases, including atherosclerosis, diabetes, and kidney failure. The EA.hy926 cell line is one of the most widely used human macrovascular endothelial cell models, and has been shown to enter both dysfunctional- and quiescent-like states. However, there are no validated housekeeping genes (HKGs) for EA.hy926 cells, especially suitable for different growth states and fatty acid treatments. Therefore, we screened transcriptomic data of EA.hy926 cells in their growing and quiescent states and after treatment with or without docosahexaenoic acid (DHA), and identified 18 candidate HKGs. Together with eight other commonly used HKGs and one HKG identified from databases, the stability of the 27 candidate HKGs were analyzed with five algorithms: deltaCt, BestKeeper, geNorm, NormFinder, and RefFinder, using the RT-qPCR results of EA.hy926 cells under 4 different growth conditions. The comprehensive ranking results from RefFinder suggested that the top two most stable genes were CAPZB and FBXO7, whereas the least stable commonly used HKGs were RNA18S and ACTB. The suitability of these genes as HKGs for EA.hy926 cells in different growth states and in response to DHA treatment were validated in relation to the expression of selective endothelial markers. The RT-qPCR validation results confirmed that normalization with CAPZB + FBXO7 provided greater sensitivity than the commonly used HKGs in detecting the expression difference of those endothelial markers under different conditions (growth state × DHA treatment). This novel panel of HKGs is available for future studies of EA.hy926 cell responses to different growth states and/or following DHA treatment. - Source: PubMed
Publication date: 2026/01/20
Huang ShiqiSivakumar Samritha RamanCharney JordanFisher Rachel AkongTaylor Carla GZahradka Peter - Temperature sensitivity has gained considerable attention in the era of precision medicine. This trait has long been used to identify cold-heat patterns (C-HPs), a diagnostic framework in Traditional Korean Medicine that categorizes individuals based on their thermal responses. C-HP helps understand an individual's inherent physical characteristics, which have been shown to be highly heritable and thus shaped by genetic factors. However, genetic markers that are significantly associated with this trait remain scarce. To address this gap, we aimed to identify candidate single-nucleotide polymorphisms (SNPs) based on previous genomewide association studies (GWASs) of related traits. - Source: PubMed
Publication date: 2025/11/21
Jeong SeogyunLee Sanghun