CAMK2A (CAMK2 alpha) Antibody (C_term)
- Known as:
- CAMK2A (CAMK2 a) Antibody (C_term)
- Catalog number:
- AP7206b
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- CAMK2A (CAMK2 alpha) Antibody (C_term)
Related genes to: CAMK2A (CAMK2 alpha) Antibody (C_term)
- Gene:
- A4GNT NIH gene
- Name:
- alpha-1,4-N-acetylglucosaminyltransferase
- Previous symbol:
- -
- Synonyms:
- alpha4GnT
- Chromosome:
- 3q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-12
- Date modifiied:
- 2016-10-05
- Gene:
- ABCB5 NIH gene
- Name:
- ATP binding cassette subfamily B member 5
- Previous symbol:
- -
- Synonyms:
- EST422562, ABCB5beta, ABCB5alpha
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2016-10-05
- Gene:
- AGPAT1 NIH gene
- Name:
- 1-acylglycerol-3-phosphate O-acyltransferase 1
- Previous symbol:
- -
- Synonyms:
- LPAAT-alpha
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-07
- Date modifiied:
- 2016-10-05
- Gene:
- AKR1C4 NIH gene
- Name:
- aldo-keto reductase family 1 member C4
- Previous symbol:
- CHDR
- Synonyms:
- DD4, HAKRA, C11, 3-alpha-HSD, CDR, MGC22581
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-26
- Date modifiied:
- 2016-06-03
- Gene:
- ARHGEF6 NIH gene
- Name:
- Rac/Cdc42 guanine nucleotide exchange factor 6
- Previous symbol:
- MRX46
- Synonyms:
- alphaPIX, Cool-2, KIAA0006, alpha-PIX, Cool2
- Chromosome:
- Xq26.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-27
- Date modifiied:
- 2016-10-05
Related products to: CAMK2A (CAMK2 alpha) Antibody (C_term)
Related articles to: CAMK2A (CAMK2 alpha) Antibody (C_term)
- Compared to lean pig genotypes, the local Krškopolje pig is characterised by a greater capacity for lipid and lower capacity for protein deposition, along with lower dietary protein requirements. The aim of the present study was to unravel the transcriptomic differences in subcutaneous adipose tissue between the local Krškopolje pig and modern hybrids, as well as to study the impact of the reduced protein diet in both genotypes. Differential gene expression analysis between local and modern pigs revealed 375 differentially expressed genes, with 189 upregulated and 186 downregulated in Krškopolje pig. Among the upregulated genes, several suggested more pronounced adipogenesis (SLC7A10, ADIRF, INHBB, and SFRP2) in the Krškopolje pig. In addition, genes encoding collagen proteins and extracellular matrix remodelling (e.g., COL6A5, COL4A5, COL2A1), calcium signalling (TRPV4, CAMK2A, CALML5), pro-inflammatory cytokines (e.g., IL1A, TNFSF9, CXCL8, PTGS2 etc.) and cholesterol metabolism (CYP1A1, CYP2A19, CES1 etc.) were differentially expressed. The reduced protein diet induced only minor changes in gene expression at the individual gene level. However, gene set enrichment analysis revealed that, in Krškopolje pigs, dietary effects were associated with biological processes related to immune response, intracellular protein transport, and extracellular matrix organisation. In the case of modern hybrids, a reduced protein diet resulted in enrichment of gene sets related to oxidative phosphorylation, mitochondrial function, and energy metabolism. In conclusion, this study demonstrated that the adipose tissue of Krškopolje pigs compared with modern hybrids exhibited greater adipogenic potential, being also supported by higher expression of genes involved in extracellular matrix remodelling and inflammation. The impact of a reduced protein diet on adipose-tissue gene expression was relatively small in both breeds, particularly in Krškopolje pig, suggesting a metabolic adaptability of this breed. - Source: PubMed
Publication date: 2026/05/27
Poklukar KČandek-Potokar MSavić BŠkrlep M - 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 - Painful diabetic neuropathy (PDN) is frequently accompanied by anxiety, yet the neural circuit mechanisms associated with nociceptive hypersensitivity to affective dysfunction remain unclear. Here we combined brain-wide c-Fos mapping, viral tracing, in vivo fiber photometry, whole-cell recordings, and projection-specific opto/chemogenetics in a mouse model of streptozotocin-induced PDN to define a thalamo-cortex circuit for pain-anxiety comorbidity. Within the posterior insular cortex (pIC), CaMKIIα⁺ excitatory neurons were recruited in PDN mice with comorbid anxiety, exhibiting heightened neuronal excitability and enhanced excitatory synaptic input. Bidirectional chemogenetic modulation of pIC neurons oppositely regulated anxiety-like behavior and mechanical hypersensitivity without locomotor or glycemic confounds. Circuit mapping identified a monosynaptic excitatory projection from the paraventricular thalamus (PVT) to the pIC; PVT neurons were hyperactive in PDN, and projection-defined manipulation of the PVT to pIC pathway bidirectionally controlled the behavioral phenotypes. Cacna1c was upregulated in the PVT of PDN mice; its knockdown in pIC-projecting PVT neurons attenuated both pain and anxiety-like behaviors. Together, these results delineate a thalamo-cortex excitatory pathway that couples nociceptive and affective dimensions of PDN and suggest that selective targeting of the PVT to pIC circuit may provide coordinated relief of pain and anxiety-related symptoms. - Source: PubMed
Publication date: 2026/05/27
Wei MinShou JiayinYang JingCai SiqingBai QiyuanHou JinwenJiang YeShen ShixiongYu ZhuoyingZhao XinruHan YongzhengCai JieYang Xue-WeiLi ZhengqianMa DaqingXing Guo-GangLi Min