CAMK2A
- Known as:
- CAMK2A
- Catalog number:
- NB110-55652
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CAMK2A
Related genes to: CAMK2A
- Gene:
- CAMK2A NIH gene
- Name:
- calcium/calmodulin dependent protein kinase II alpha
- Previous symbol:
- CAMKA
- Synonyms:
- KIAA0968, CaMKIINalpha
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-24
- Date modifiied:
- 2016-04-06
Related products to: CAMK2A
Related articles to: CAMK2A
- Calcium/calmodulin-dependent protein kinase IIα (CAMK2A) is a ubiquitous mediator of Ca²⁺ signal transduction, implicated in the regulation of tumor cell proliferation and differentiation. However, its role and underlying mechanism in glioma remain unclear. In this study, CAMK2A gene expression was analyzed through various glioma-related databases, and confirmed by RT qPCR and Western blotting. Compared with normal brain tissue, CAMK2A expression in glioma tissue was significantly downregulated, with expression levels progressively decreasing as tumor grade increased. Kaplan-Meier survival analysis revealed a significant correlation between low CAMK2A expression and shorter overall survival in glioma patients. The correlation analysis of CAMK2A expression with clinicopathological characteristics revealed that low expression of CAMK2A was significantly associated with tumor recurrence, high pathological grade, TMZ treated, IDH wild-type status, and 1p19q non-codeletion. Enrichment analysis indicated that in the low CAMK2A expression group, biological functions related to calcium signaling pathway, neuroactive ligand-receptor interaction and long-term potentiation were activated. The correlation analysis of CAMK2A expression with the immune microenvironment revealed that the expression level of CAMK2A influenced the immune activity of the TME. CAMK2A expression was negatively correlated with the immune score. Additionally, CAMK2A expression was correlated with multiple immune checkpoint molecules. A significant negative correlation was also observed between CAMK2A expression and TMB. Furthermore, there were associations with Macrophages M0, Plasma cells, T cells regulatory, Dendritic cells activated and T cells gamma delta. All immunobiological functions in the CAMK2A low-expression group were significantly upregulated. Functional CCK-8 assays confirmed that overexpression of CAMK2A inhibited the proliferation of glioma cells, whereas CAMK2A gene knockout produced the opposite effect. Additionally, we discovered that CAMK2A regulates glioma cell proliferation by inhibiting the Ras/Raf/MEK/ERK pathway. In summary, our findings support the notion that CAMK2A is low expressed in gliomas, and this low expression is closely associated with poor prognosis and the immune microenvironment of gliomas. CAMK2A regulates glioma cell proliferation through the Ras/Raf/MEK/ERK signaling pathway. CAMK2A is a potentially important target for glioma therapy. - Source: PubMed
Publication date: 2026/06/25
Sun ZhiminZhang JiaminJin QianxuZhang AoboYao ZhigangZhao ZongmaoMa ZhizhaoHu Jie - Gastric cancer (GC) remains a major global health challenge, characterized by poor outcomes driven by an immunosuppressive tumor microenvironment (TME). Tumor-associated macrophages (TAMs), particularly the M2 subtype, are central mediators of immune evasion and therapeutic resistance. While tumor-derived exosomes are key regulators of intercellular communication, the mechanisms by which they modulate TAM fate remain unclear. - Source: PubMed
Publication date: 2026/05/18
Chen ZetianHuang HongxinShen YikaiYamamoto MasamiTsukamoto TetsuyaNomura SachiyoJiang TianluXu ZekuanLi Zheng - Heterozygous de novo variants in the transcription factor Activity-Dependent Neuroprotective Protein (ADNP) cause a severe neurodevelopmental disorder, termed Helsmoortel-Van der Aa syndrome (HVDAS), characterised by autism, intellectual disability, and multisystem involvement. The ADNP gene is essential for embryonic development and interacts with components of several chromatin remodelling complexes. However, the precise pathophysiological mechanisms underlying the disorder remain incompletely understood. - Source: PubMed
Publication date: 2026/05/28
D'Incal Claudio PeterCappuyns ElisaPaldi Floravan der Lei Mathijs BAnnear Dale JohnAlastruey Clara MiliánSokolova DimitraElinck EllenDe Man KevinKonings AnthonyHuyghebaert JolienThys SofiePintelon IsabelVerschuuren MarliesCalus ElkeVan Dam DebbyDe Deyn Peter PNguyen SylvieYalcin BinnazHorii TakuroHatada IzuhoMateiu LigiaCavalli GiacomoPasciuto EmanuelaBerghe Wim VandenKooy R Frank - High-altitude hypoxic adaptation in mammals involves complex molecular mechanisms, with non-coding RNAs (ncRNAs) increasingly reported to participate in hypoxia-related regulation. However, the contribution of circRNAs in cardiac adaptation to chronic hypoxia remains largely unexplored. This study performed an integrative competitive endogenous RNA (ceRNA) analysis to investigate circRNA-mediated regulatory networks in the hearts of Tibetan pigs and Yorkshire pigs maintained under high- and low-altitude conditions, using four comparison groups (TH, TL, YH, and YL). Using Ribo-Zero RNA sequencing, we identified 961 circRNAs in heart tissues, with 358 differentially expressed circRNAs (DE-circRNAs) detected across the four groups. Functional enrichment analysis revealed that their host genes were associated with hypoxia-related pathways, including HIF-1, VEGF, AMPK, and autophagy, critical for energy metabolism and mitochondrial function. A HIF-1-specific ceRNA network was constructed, identifying key axes including circDUSP16-ssc-miR-671-5p-, circTLK1-ssc-miR-331-3p-, and circTLK1-novel-miR-624-. JASPAR analysis predicted potential HIF-1α binding sites in the promoters of , , and , supporting their regulatory roles. These findings provide a transcriptomic overview of circRNA expression patterns in pig heart tissues under different altitude conditions and prioritize candidate ceRNA relationships for further functional investigation. - Source: PubMed
Publication date: 2026/05/14
Li PanCheng WeiShang PengTao ZhuZhang HaoZhang Bo - RNA regulation plays a central role in neurodevelopment by coordinating neuronal differentiation, migration, and circuit formation. The CUGBP Elav-like family member 2 (CELF2) is an RNA-binding protein with established roles in alternative splicing and mRNA regulation, yet its function in the developing brain remains poorly defined. Here, we investigated the role of CELF2 during neurodevelopment using a constitutive Celf2 knockout (KO) mouse model. Celf2 knockout pups exhibited neonatal lethality accompanied by impaired neuronal maturation and disrupted cortical organization. Bulk RNA sequencing revealed widespread transcriptional dysregulation, while splicing analyses identified reduced exon inclusion in multiple neurodevelopmental transcripts following CELF2 loss. Notably, Camk2a transcript and protein levels were markedly reduced in knockout brains, consistent with CELF2 binding to the Camk2a 3'UTR. Functional studies in C. elegans demonstrated that expression of human CAMK2A partially rescued synaptic puncta deficits in unc-75 (CELF ortholog) mutants, supporting a conserved role for CELF-family proteins in synaptic maturation. Histological analyses revealed reductions in Nestin- and Doublecortin-positive immature neurons, thinning of upper cortical layers, and decreased CAMK2A expression. Single-nucleus RNA sequencing further revealed selective reductions in upper layer II/III excitatory neuron populations in the cortex. Cellular trajectory and pseudotime analyses revealed delayed maturation in certain cell types but accelerated progression in others in Celf2 KO animals. Together, these findings establish CELF2 as a critical post-transcriptional regulator required for neuronal maturation and architectural stability during early brain development and highlight how disruption of RNA regulatory programs may contribute to neurodevelopmental disorders. - Source: PubMed
Publication date: 2026/05/26
Syed IshanaJiang JingKo Su-HyukChen ShaotingZhang ZhaoLiu ZhijieChen Lizhen