Ask about this productRelated genes to: CAMK4 Blocking Peptide
- Gene:
- CAMK4 NIH gene
- Name:
- calcium/calmodulin dependent protein kinase IV
- Previous symbol:
- -
- Synonyms:
- CaMK-GR, CaMKIV
- Chromosome:
- 5q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-24
- Date modifiied:
- 2019-02-07
Related products to: CAMK4 Blocking Peptide
Related articles to: CAMK4 Blocking Peptide
- The dynamic remodeling of the pituitary endocrine state is a critical pivot driving the transition of the reproductive cycle in geese. In this study, pituitary tissues from Wanxi white geese at the onset-of-birth and the laying period were investigated. Using serum hormone assays, transcriptomics, and dual-luciferase reporter assays, the mRNA and miRNA expression profiles of the pituitary during these periods were constructed. The results revealed that serum levels of FSH, LH, E2, and P4 were significantly elevated during the laying compared to the onset-of-birth period. In contrast, the PRL level was significantly decreased. Integrated omics analysis identified 453 differentially expressed genes and 73 differentially expressed miRNAs. Functional enrichment analysis demonstrated that during the laying period, the pituitary mediates the robust synthesis and release of gonadotropins by activating ECM-receptor interaction, calcium and MAPK signaling pathways. Furthermore, it regulates the pituitary tissue microenvironment and upstream signal transduction through a post-transcriptional network centered on miR-32-x and miR-338-y. This network targeted key genes, including NTRK2, CAMK4, COL1A2 and ADCY2. Furthermore, dual-luciferase reporter assays supported a sequence-specific interaction between miR-338-y and the ADCY2 3'UTR. In conclusion, our findings suggest that the synergistic effect of endocrine pathways and the miRNA post-transcriptional network provides a potential multi-dimensional regulatory framework for the transduction of pituitary reproductive signals, which may drive the transition of Wanxi White geese from the onset of birth to the laying period. This study provides preliminary insights into the molecular regulatory network underlying pituitary gonadotropin secretion in poultry and identifies potential candidate targets for future breeding strategies evaluating egg-laying performance in geese. - Source: PubMed
Publication date: 2026/07/28
Li X JYuan XChen SHou M MRen MLi S H - Alzheimer's disease (AD), a progressive neurodegenerative disease with a rising global prevalence, is characterized by amyloid-β (Aβ) aggregation, tau hyperphosphorylation, inflammation, oxidative damage, and neuronal apoptosis. Studies have increasingly recognized epigenetic modifications as key regulators in the development of AD. Epigenetic modifications, particularly histone acetylation, are increasingly recognized as critical regulators of cell survival and AD pathogenesis. Although artemisinin (ART) exhibits potent anti-oxidative, anti-inflammatory, and neuroprotective properties, its impact on histone acetylation in AD remains uncharacterized. This study investigated whether ART regulates histone acetylation to confer neuroprotection and rescue behavioral deficits in Alzheimer's disease models. Using SH-SY5Y cells, primary neurons, and 3xTg-AD mice, we found that ART restores histone acetylation homeostasis by enhancing histone H4 acetylation. Mechanistically, this effect is driven by the activation of the CaMK IV/PKA-CREB signaling cascade. Treatment with ART reduced ROS, improved mitochondrial function, decreased Aβ1-42 deposition, and suppressed neuronal apoptosis. However, these beneficial effects were abolished by PKA or CaMK IV inhibitors. Consequently, ART treatment significantly reduced reactive oxygen species (ROS) generation, restored mitochondrial function, decreased Aβ1-42 deposition, suppressed neuronal apoptosis, and alleviated AD-like neuropathology and cognitive deficits. Crucially, the neuroprotective and epigenetic benefits of ART were entirely abolished by pharmacological inhibitors of PKA or CaMK IV. This study is the first to demonstrate that artemisinin ameliorates AD pathology and behavioral impairments via the CaMK IV/PKA-CREB-Ace-H4 axis, establishing ART as a promising therapeutic candidate for epigenetic intervention in AD. - Source: PubMed
Publication date: 2026/08/19
Chen YitianGe LijunLazarovici PhilipZheng Wenhua - With the increasing frequency of extreme weather events globally, livestock are facing ever-increasing demands for environmental adaptability. Some goat populations have demonstrated remarkable adaptability under long-term extreme environmental stress, and their genomes retain characteristic genetic imprints formed by adaptive evolution. This study integrated whole-genome resequencing data from 496 individuals from 29 endemic goat populations in China, along with data from 11 environmental factors. Through signal selection analysis and genome-environment association analysis, we identified 262 candidate genes associated with environmental adaptation. Subsequently, we screened Chinese goat populations in extreme environments based on environmental data. We used the FST and θπ methods to scan the genomes of these goat populations. In four extreme environments (high elevation, hot, and arid), 95, 74, and 162 candidate genes were identified, respectively. Based on research related to environmental adaptation, we found that genes such as FGF5, CAMK4, COL4A3BP, and CACNG4 may play important roles in goat adaptation to extreme environments. This study not only deepens our understanding of the evolutionary mechanisms of environmental adaptation in Chinese goats, but also provides important theoretical basis for goat stress resistance breeding and germplasm resource conservation. - Source: PubMed
Publication date: 2026/07/21
Yang KaijieDong JieWang WannianCai KeLiu JianhuaQiao LiyingLiu Wenzhong - - Source: PubMed
Publication date: 2026/07/20
- Intracellular Ca transients drive key developmental and physiological processes, yet their role in oncogenesis remains incompletely understood. In glioblastoma (GBM), an aggressive brain malignancy, tumor cellular networks exhibit self-sustaining Ca transients that promote tumor growth through unclear mechanisms. Using patient-derived GBM models, we show that these transients depend primarily on intracellular Ca stores and extend to the nucleus to drive tumorigenesis. A neuromodulator screen identified extracellular purines ATP and ADP as potent inducers of both nuclear and cytosolic Ca transients via activation of metabotropic purinergic P2RY1 receptors, whose knockdown attenuates tumorigenicity and . Mechanistically, Ca transients promote tumorigenesis via the nuclear Ca/calmodulin-dependent kinase CAMK4, which regulates transcriptional and epigenetic programs, as well as ribosomal DNA transcription. From the therapeutic perspective, pharmacologic P2RY1 inhibition suppresses tumor growth and . Collectively, these findings reveal a pharmacologically targetable oncogenic mechanism in GBM and possibly other malignancies. - Source: PubMed
Publication date: 2026/05/14
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