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
- 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
Wang ShuaiRichter JennaKim Claire DRonnen RebeccaCai JuliaSong YunfeiHaddock SaraStoessel Mark BDada HannahGross SuzanneGuerrero AdlerKarnavas TheodorisStephan GabrieleBelizaire GregBonanni LukeGolub DanielleSabio JonathanSchwarz HannaJiang AlbertMaleeha NawshinGhosh AnuvaYung MadelynnGrossman-Glover EricTang JocelynGherghina LauraDonovan AlexLeonard AndreaChiriboga LuisJones DrewSong Soomin CMazzoni EstebanVincent TheresaSchneider Robert JZagzag DavidMiura YukiBasu JayeetaBrand Andrea HPlacantonakis Dimitris G - Aldosterone-producing adenomas (APA) are a major cause of primary aldosteronism. While gene mutations in APA trigger aldosterone overproduction via calcium signaling, their precise regulatory mechanisms remain unclear. Our prior proteomic analysis identified significant upregulation of tumor protein D52 (TPD52), an oncogene protein implicated in cancer progression, in APA. This study investigates the role of TPD52 in regulating aldosterone synthesis and its molecular mechanism. - Source: PubMed
Xie LingMa LinqiangKang BingChen ZhihaoQi ShuangxinDu ManmanLi JiayuLi JunlongHe YifanXu YongHuang WeiGao RufeiHu JinboYang ShuminLi QifuPeng Chuan - Cholinergic dysfunction is a key contributor to cognitive impairment observed in aging and neurodegenerative disorders such as Alzheimer's disease (AD). Although acetylcholinesterase (AChE) inhibitors have been the mainstay of symptomatic treatment for over two decades, their limited efficacy and adverse effects underscore the need for alternative therapeutic approaches. Recent evidence indicates that mechanical stimulation can modulate neuronal and glial signaling through mechanotransduction, suggesting a potential strategy to enhance cognitive function via non-pharmacological means. Here, we developed a head-mounted vibrotactile stimulation system (HVSS) that delivers controlled vibration to the cranium and evaluated its effects in a pharmacological model of acute cholinergic dysfunction induced by scopolamine. To this end, male C57BL/6 mice received scopolamine (1 mg/kg, i.p.; on days 7, 14, and 28) and were exposed to daily vibrotactile stimulation at 20, 40, or 80 Hz for 28 days. Behavioral performance was assessed using passive avoidance and Morris water maze tests, followed by biochemical and histological analyses. HVSS at 40 Hz and 80 Hz significantly improved cognitive performance, enhanced hippocampal cholinergic function, reduced oxidative damage, and upregulated memory-related signaling genes, including BDNF, PI3K, AKt, ERK1/2, CREB, and CAMK4. These findings suggest that high-frequency HVSS improves memory hippocampal cholinergic function via activation of memory-related signaling pathways, highlighting its potential as a safe, non-pharmacological neuromodulatory strategy for cholinergic dysfunction-related cognitive decline. - Source: PubMed
Publication date: 2026/04/22
Kim Ok-HyeonShin Chang-HoCho Min-WooHa Jae-YoungChoung Jai JunSong Dong-KeunChoi Jae-YeongChang Eun SeoLee Hyun JungKu Sae-Kwang - Current treatment of lupus nephritis (LN) relies on broad immunosuppression and often fails to eradicate intrarenal immune niches that sustain inflammation. Tertiary lymphoid structures (TLS)-organized aggregates of immune cells forming in chronically inflamed non-lymphoid tissues-are increasingly recognized as drivers of local immune activation and tissue injury in LN. We previously showed that genetic CaMK4 deficiency suppresses autoimmunity and nephritis in lupus-prone mice. Here, we tested whether CaMK4 regulates renal TLS-like organization. Using kidneys from MRL/ mice that were CaMK4-deficient or treated with KN93-loaded nanoparticles targeted to CD4 T cells or podocytes (anti-podocin), we compared findings with vehicle-treated controls. TLS-associated inflammation and maturation were quantified by mean fluorescence intensity of CD3, CD20, Ki67, and α-SMA. Across genetic and targeted-treatment arms, CaMK4 inhibition reduced all assessed markers, with uniform suppression of CD20 signal, highlighting a key role for B cells in TLS maintenance. Notably, podocyte-targeted KN93 most strongly suppressed TLS-like formation, implicating podocyte-driven pathways in interstitial inflammation and lymphoid neogenesis through previously underappreciated mechanisms. These data identify CaMK4 as a regulator of TLS-like architecture in LN and support the translational potential of cell-targeted CaMK4 inhibition to disrupt local immune recruitment while limiting systemic toxicity. - Source: PubMed
Publication date: 2026/03/31
Jamaly SiminRakaee MehrdadIchinose KunihiroMaeda KayahoOtomo KotaroKoga TomohiroTsokos Maria GTsokos George C - Atherosclerosis represents a chronic inflammatory disease of the arterial wall and remains a principal cause of cardiovascular morbidity and mortality. Macrophages critically govern lesion initiation, progression, and destabilization, and accumulating evidence indicates that protein kinases are key regulators of their phenotype and function. This systematic review synthesizes data from 162 publications encompassing 76 kinases to delineate the contribution of macrophage-associated kinase signaling to atherogenesis. The identified kinases span major families, including AGC, CaMK, CMGC, Ste20, and tyrosine kinases, each exerting distinct regulatory effects on macrophage survival, polarization, lipid handling, efferocytosis, and inflammatory activation. Several kinases, such as CaMK2γ, CaMK4, DCLK1, Trib1, and STK25, exhibit pro-atherogenic activity by promoting foam cell formation, expanding the necrotic core, and propagating inflammatory pathways. Conversely, kinases, including STK11 and the context-dependent mediator Akt1, exhibit protective or dual functions that contribute to metabolic homeostasis and reparative macrophage states. Despite substantial mechanistic insights and the established therapeutic utility of kinase inhibitors in oncology, clinical translation in the context of atherosclerosis remains limited. This review consolidates current knowledge, identifies critical gaps, and outlines prospective avenues to target macrophage-specific kinase pathways as novel therapeutic strategies for atherosclerosis. - Source: PubMed
Publication date: 2026/03/27
Müller Jana Svan der Vorst Emiel P C