CAMK2A
- Known as:
- CAMK2A
- Catalog number:
- Y214313
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- 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
- Understanding synapse-specific effects of neuroinflammation can provide mechanistic and therapeutically relevant insights across the spectrum of neurological diseases. - Source: PubMed
Publication date: 2026/03/24
Espinosa-Garcia ClaudiaSrivastava UpasnaKumar PrateekKour DilpreetMalepati SnehaTobin Brendan RXiao HailianSunna SydneyBowen Christine ACheng LihongBagchi PrithaDuong Duc MWhitworth Ted JLiu XinranSeyfried Nicholas TWood Levi BFaundez VictorRangaraju Srikant - Fluoxetine (Flx), a selective serotonin reuptake inhibitor, and St. John's Wort extract (SJW), a herbal remedy, are common treatments for depression. However, a comprehensive comparison of their molecular mechanisms remains elusive. This study aimed to systematically elucidate and compare their therapeutic actions using an integrated proteomics and metabolomics approach. Behavioral and pharmacological effects of both treatments were assessed through behavioral tests. Proteomics and metabolomics analyses were performed on cortical tissue to identify differentially expressed proteins and metabolites. Furthermore, Mass Spectrometry Imaging (MSI) was employed to visualize the spatial distribution of key metabolites within the cortex. Bioinformatic analysis and integrated multi-omics analysis were used to map the signaling pathways and key molecular targets. Both Flx and SJW induced behavioral changes in locomotor activity as observed through behavioral tests. Multi-omics analysis revealed that both treatments share common regulatory patterns involving neuroplasticity-related pathways and Nicotinate and nicotinamide metabolism. Flx showed a more focused effect on synaptic plasticity. In contrast, SJW exhibited a broader modulation involving inflammatory pathways and amino acid metabolism. MSI analysis confirmed the localized accumulation of key differential metabolites, such as N-Acetyl-l-aspartate, ADP and l-Glutamine. Integrated analysis identified Rhoa, Scn1a, and Camk2a as key shared hub proteins. SIGNIFICANCE: Flx and SJW are widely used antidepressants in clinical practice. This multi-omics study deciphers the convergent and divergent molecular modulations of Flx and SJW, providing insight into their potential mechanisms relevant to depression treatment. While both promote neuroplasticity, Flx's action is more centered on synaptic remodeling, whereas SJW possesses additional strong anti-inflammatory and amino acid metabolism-modulating properties. These findings provide a detailed molecular basis for their clinical efficacy and suggest distinct therapeutic strengths. - Source: PubMed
Publication date: 2026/03/06
Zhang JialeCai YuhangZhang PanpanHao XuruiGuo BowenZhang WanningWu YiyingSun JiawenXu XiangLi WantingZhang BowenZhang ShuaiZhang WeiKong Dezhi - 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 - Spinal cord injury (SCI) induces severe neurological impairment, exacerbated by secondary inflammation and disrupted neural circuitry. Inspired by the spinal cord's electromechanical microenvironment, we developed a biomimetic conductive nerve scaffold via directional freeze-casting of gelatin methacryloyl (GelMA) hydrogel incorporated with N-acetylcysteine-modified silver nanowires (NAC-AgNWs). The scaffold exhibits axially aligned microchannels, tunable mechanical strength, and conductivity akin to native spinal tissue. In a rat model of complete spinal cord transection (2 mm), the scaffold exhibited dual therapeutic effects: (1) early-stage anti-inflammatory modulation (mediated by the synergistic interplay between AgNWs and NAC), and (2) sustained neural reconstruction, evidenced by robust axonal bridging across the lesion, synapse reformation, and significant functional recovery. Integrated transcriptomic analyses revealed the FGF13/Ca/CaMK2A/CREB axis as the activated pathway driving neurite outgrowth and neural circuit reconstruction. This biomaterial design establishes a novel therapeutic paradigm for SCI repair, integrating structural guidance, immunomodulation, and activation of pro-regenerative signaling. - Source: PubMed
Publication date: 2026/02/16
Jiang MinghaoLu WenjieZhuang JunyuSong JiahuiZhao YanfangZhou ChengZhou YangboShu WeizhiZhu ZhongweiJiang LelinWu PingWu AiminSheng SunrenZhu SipinWang Zhouguang - The microtubule-stabilizing drug paclitaxel remains the standard of care for various solid malignancies but frequently leads to chemotherapy-induced peripheral neuropathy (CIPN). CIPN is a leading cause for premature treatment termination and a significantly reduced quality of life in long-term cancer survivors. The molecular mechanisms of neuro-axonal degeneration, neuroinflammation, and pain in patients treated with paclitaxel remain incompletely understood, and there are currently no predictive biomarkers or preventive treatments. We used human iPSC-derived sensory neurons exposed to paclitaxel to comprehensively model the pathophysiology of CIPN. Neurotoxicity was assessed over time using viability assays and sequential RNA sequencing, as well as deep proteome and lipidomic analyses. We observed a time and dose-dependent decline of cell viability at clinically relevant paclitaxel doses. Sequential RNA sequencing defined JUN as an early immediate gene, followed by the overexpression of genes of the neuronal stress response (e.g., ARID5A, WEE1, DUSP16, GADD45A), neuronal injury and apoptotic pathways (e.g., ATF3, HRK, BBC3 [PUMA], BCL2L11 [BIM], CASP3), neuroinflammation and nociception (CALCB, MMP10, IL31RA, CYSLTR2, C3AR1, TNFRSF12A) and neuronal transduction (e.g., CAMK2A, STOML3, PIRT), while key enzymes of lipid biosynthesis were markedly downregulated (e.g., LSS, HMGCS1, HMGCR, DHCR24). Deep proteome analyses following 48 h of exposure to 100 nM paclitaxel revealed a strong correlation of differentially expressed RNA with proteins, and a marked degradation of essential axonal transport proteins such as kinesins, stathmins, and scaffold proteins. Consistent with the downregulation of rate-limiting enzymes of lipid biosynthesis, lipidome analysis confirmed deregulation of neuronal lipid homeostasis. In summary, paclitaxel induces transcriptomic and proteomic signatures of the neuronal stress response, neuroinflammation, nociception, and disturbed metabolism. These may explain, in part, the clinical phenotype of sensory loss, hypersensitivity, and neuropathic pain frequently observed in patients suffering from CIPN, but constitute pharmacologically addressable targets. - Source: PubMed
Publication date: 2026/02/10
Schinke ChristianMaierhof Smilla KHew LoisFernandez Vallone ValeriaFrahm SilkeTelugu Narasimha SwamyDiecke SebastianIvanov AndranikKovács RichardBeule DieterKirchner MarieluiseMertins PhilippBrüning UlrikeKirwan Jennifer AStachelscheid HaraldEndres MatthiasHuehnchen PetraBoehmerle Wolfgang