CAMK2B Mouse Monoclonal Antibody
- Known as:
- CAMK2B Mouse Monoclonal Antibody
- Catalog number:
- APO-000816-M04
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CAMK2B Mouse Monoclonal Antibody
Related genes to: CAMK2B Mouse Monoclonal Antibody
- Gene:
- CAMK2B NIH gene
- Name:
- calcium/calmodulin dependent protein kinase II beta
- Previous symbol:
- CAMKB
- Synonyms:
- CAM2, CAMK2
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-24
- Date modifiied:
- 2016-10-05
Related products to: CAMK2B Mouse Monoclonal Antibody
Related articles to: CAMK2B Mouse Monoclonal Antibody
- Pathogenic variants in the calcium/calmodulin-dependent protein kinase II B gene (CAMK2B) have been associated with neurodevelopmental disorders, including epilepsy, yet the mechanisms underlying cortical dysfunction remain largely unclear. Building on our previous clinical report of a patient carrying the CaMKIIβ P213L variant and our prior characterization of the corresponding mouse models, we investigated how P213L-associated CaMKIIβ insufficiency alters cortical network dynamics and susceptibility to pentylenetetrazol (PTZ)-induced seizures in vivo. - Source: PubMed
Publication date: 2026/04/15
Mutoh HirokiAoto KazushiFukuda AtsuoSaitsu Hirotomo - Thyroid hormones (THs) and estrogen (E2) play essential roles in neuronal differentiation and plasticity during brain development. S-equol, a plant-derived isoflavone metabolite, is a selective E2 receptor (ER) ligand that exhibits neurotrophic effects; however, its interaction with TH receptor (TR) signaling remains unclear. In this study, we investigated the effects of S-equol on TR-associated transcriptional activity and neuronal morphogenesis in mouse neuroblastoma-derived Neuro-2a cells or rat C6 glioma cells. Luciferase reporter assays demonstrated that S-equol significantly enhanced T3-induced TR transcriptional activity in a concentration- and time-dependent manner. Additionally, exposure to S-equol or T3 alone promoted neurite outgrowth and wound closure, whereas co-exposure to both compounds resulted in a more significant enhancement of these processes. Furthermore, mRNA expression levels of synapse-related genes (, , , , and ) were significantly increased by S-equol co-exposure in the presence of T3. In silico docking analysis revealed that S-equol exhibited moderate to high binding affinity for TR (-8.7 kcal/mol), ER, and ER, suggesting a structural basis for TR-ER crosstalk. Collectively, these findings indicate that S-equol functions as a dual-acting modulator that may modulate T3 signaling involving TR-ER interaction. Although S-equol may exert beneficial effects on neurodevelopment, it may also act as an endogenous endocrine modulator that alters the fine regulation of TH action during development, warranting careful evaluation from physiological and toxicological perspectives. - Source: PubMed
Publication date: 2026/04/03
Fujiwara YukiAriyani WindaNinomiya AyaneMiyazaki WataruOta RirikaAmano IzukiKoibuchi Noriyuki - Prolonged occupational exposure to oil mist particulate matter (OMPM) poses health risks, yet its neurotoxic effects and underlying mechanisms remain poorly understood. Here, OMPM generated from turbine oil commonly used in occupational labor environments was used to expose rats. The rats were divided into the control and OMPM groups. Following 42 days of exposure, a multidimensional assessment was performed using untargeted metabolomics, phosphoproteomics, behavioral testing, hematoxylin-eosin (HE) staining, transmission electron microscopy (TEM), colorimetric assays, enzyme-linked immunosorbent assay, and Western blotting (WB) to evaluate metabolic alterations, protein phosphorylation, and tissue integrity in the striatum. Integrated omics analyses revealed that differentially phosphorylated proteins and metabolites were remarkably enriched in dopaminergic synapse, Parkinson's disease, and amphetamine addiction pathways (FDR < 0.05), with a regulatory axis involving L-tyrosine, tyrosine hydroxylase (TH), and dopamine (DA) identified. OMPM-exposed rats exhibited depression- and anxiety-like behaviors, alongside striatal pathological and ultrastructural damage. Biochemical analyses showed elevated malondialdehyde and reactive oxygen species levels; reduced superoxide dismutase, glutathione, and glutathione peroxidase activities and total antioxidant capacity; increased glutathione disulfide and inducible nitric oxide synthase expression; and decreased DA and L-tyrosine levels. Additionally, proinflammatory mediators (IL-1β, IL-6, TNF-α, MCP-1, and PGD) were significantly upregulated in the striatum. WB analysis further confirmed significant reductions in the relative phosphorylation levels of key regulators in dopaminergic and calcium signaling pathways, including CALM3, CaMK2b, GSK-3β, PRKCG, and TH. Collectively, these findings reveal critical molecular and biochemical alterations in the rat striatum following OMPM exposure and provide a mechanistic basis for understanding depression-like behaviors associated with prolonged OMPM exposure in occupational workers. - Source: PubMed
Publication date: 2026/03/12
Nie HuipengLiu XuanShi YueLiu HuanliangLai WenqingLi KangTian LeiXi ZhugeLin Bencheng - Ca/calmodulin-dependent protein kinase II (CaMKII) plays a critical role in calcium signaling. Several studies have shown that mice with single or gene knockouts are viable, yet exhibit distinct phenotypes, whereas the double knockout of both genes is lethal. These findings indicate that each gene can have distinct roles and that they also partially compensate for each other in yet unknown essential brain functions. In order to provide insight into potential novel CaMKII functions, we performed parallel phosphoproteomic analyses on nonstimulated cortex tissues from inducible and double knockout () mice and from wild type mice. A total of 5622 phosphorylated peptides derived from 2080 proteins were identified. Phosphorylation at serine/threonine residues in 130 proteins was downregulated in the double knockout mice, including residues in 113 proteins that have not previously been identified as potential CaMKII substrates. Comparison of amino acid sequences surrounding the downregulated phosphorylation residues provided new insights into the CaMKII-substrate consensus sequences in vivo. This data set provides an important resource for future studies examining novel roles for CaMKII in the brain. - Source: PubMed
Publication date: 2026/02/25
Rigter Pomme M FBezstarosti KarelKoc Oguz CanPerfitt Tyler LDemmers Jeroen A AColbran Roger JStratton Margaret MElgersma Ypevan Woerden Geeske M - Glioblastoma (GBM) is a lethal brain cancer demanding novel therapeutic targets. This study integrated bioinformatics to identify hub genes and dysregulated pathways in GBM. - Source: PubMed
Publication date: 2025/12/30
Beygi Haniyeh SoheilShahraki AliSheervalilou Roghayeh