Camk2a monoclonal antibody, clone 6G9
- Known as:
- Camk2a mab (anti-), clonality 6G9
- Catalog number:
- MAB6626
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- Camk2a monoclonal antibody clone 6G9
Related genes to: Camk2a monoclonal antibody, clone 6G9
- 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 monoclonal antibody, clone 6G9
Related articles to: Camk2a monoclonal antibody, clone 6G9
- 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 - Symptoms of fragile X syndrome (FXS), the leading monogenic cause of intellectual disability and autism, are thought to arise from an excitation/inhibition (E/I) imbalance. Here, we leverage cell-type-specific mRNA sequencing to profile molecular alterations in cortical excitatory (Camk2) and inhibitory (Pvalb) neurons in Fmr1 knockout (KO) mice, integrating transcriptomic results with circuit and behavioral readouts to prioritize novel therapeutic targets. We uncovered significant genotype-by-cell type interactions for differential gene expression in Camk2a and Pvalb translatomes, and, strikingly, the underlying signaling pathways were often altered in opposite directions. Among the 184 differentially expressed genes that were concordantly dysregulated across both cell types, only Rapgef4 (a.k.a., exchange protein direftly activated by cAMP 2 [Epac2]; upregulated in Fmr1 KO) was also a fragile X messenger ribonucleoprotein (FMRP) target, brain-enriched, and associated with neurodevelopmental disorders. Treatment of Fmr1 KO mice with a specific EPAC2 antagonist restored cortical circuit function and ameliorated multiple behavioral phenotypes. Thus, EPAC2 should be considered a potential therapeutic target for FXS. - Source: PubMed
Publication date: 2026/05/18
Suresh AnandKourdougli NazimNomura ToshihiroButh Jessie EMiranda-Rottmann SoledadSánchez-León Carlos AWu Michelle WNelson Sofia MWall Lauren TTran Anne TAraya RobertoContractor AnisGandal Michael JPortera-Cailliau Carlos - - Source: PubMed
Publication date: 2026/05/08
Xu JiahaoXu LianhongHu DieZhang YingWang YongfangYun Zhihua