Ask about this productRelated genes to: CAMKV antibody
- Gene:
- CAMKV NIH gene
- Name:
- CaM kinase like vesicle associated
- Previous symbol:
- -
- Synonyms:
- MGC8407, VACAMKL
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-04
- Date modifiied:
- 2018-06-04
Related products to: CAMKV antibody
Related articles to: CAMKV antibody
- High-risk (HR) neuroblastoma (NB) remains a leading cause of pediatric cancer mortality, frequently driven by MYCN amplification or MYC overexpression. Despite their central role, direct pharmacological targeting of these transcription factors remains clinically challenging. Here, we identify CaM kinase-like vesicle-associated protein (CAMKV) as a MYCN/MYC-regulated effector of NB pathogenesis. Although previously classified as a nonfunctional pseudokinase, we demonstrate that CAMKV possesses intrinsic kinase activity that is essential for tumor growth. Analysis of patient datasets and primary tumors shows that elevated CAMKV expression correlates with advanced disease stage and poor overall survival. Through integrated transcriptomics, ChIP-seq, and phosphoproteomics, we establish CAMKV as a central signaling hub that coordinates metabolic and proliferative pathways. Both genetic depletion and small-molecule inhibition of CAMKV significantly impair NB cell proliferation in vitro and suppress tumor growth in vivo. Collectively, our findings establish CAMKV as a unifying therapeutic vulnerability and highlight this functional kinase as a promising target for translational development in HR NB. - Source: PubMed
Publication date: 2026/09/25
Yu YangZhao YanlingShi ZhongchengWang Larry LCheng FengCecil AmberRudra NimeshChoi Jong MinLi KanSilverman DanielQi DanPrakash AnilWu ZhixingWang JunMei ShenglinZhang AnqingIchii KeitaNguyen Hanh-XuanRood Brian RDome Jeffrey SFabbri MullerYi Joanna SWu ErxiLu DaiJung Sung YunAgarwal SaurabhZhang ChunchaoYang Jianhua - High post-infusion absolute lymphocyte count (ALC) following ciltacabtagene autoleucel (cilta-cel) therapy is associated with an increased risk of immune effector cell-associated delayed neurotoxicity (IEC-DNT), including parkinsonism (IEC-PKS) and cranial nerve palsies (IEC-NP). Between December 2024 and August 2025, we evaluated a prophylactic strategy using a short course of dexamethasone (DEX) in 57 patients with high-ALC, defined as a post-infusion ALC of ≥3 × 10⁹/L on serial monitoring after CAR-T infusion. DEX was administered at 10 mg twice daily for a minimum of three days. Outcomes were compared with a historical control cohort of 104 patients with high-ALC treated between February 2022 and November 2024. While DEX appeared to attenuate the severity of facial nerve palsy, it did not significantly improve event-free survival for IEC-DNT, IEC-PKS, or IEC-NP, nor did it reduce the severity of IEC-PKS. Analysis of ALC kinetics demonstrated no statistically or biologically meaningful reduction in lymphocyte expansion, suggesting that the dose and duration of dexamethasone may be insufficient, or that additional immune and host factors contribute to the risk of IEC-DNT. These findings highlight the limited role of corticosteroid prophylaxis and underscore the need for more mechanistically targeted strategies to mitigate this challenging complication of BCMA-directed CAR-T therapy. - Source: PubMed
Publication date: 2026/08/10
Lim Kenneth JcTan MelindaParrondo RicardoChhabra SaurabhSchaefers ChristophDooley KatharineDe Menezes Silva Corraes AndreGupta MalvikaCarabenciov DarinGertz MorieHwa LisaHaily StephensKapoor PrashantKourelis TaxiarchisWarsame RahmaCook JoselleBinder MoritzAbdallah NadineZanwar SaurabhBergsagel P LeifYadav UditWiedmeier-Nutor ErinGeyer SusanAilawadhi SikanderFonseca RafaelKumar ShajiZekeridou AnastasiaLin Yi - This review aims to provide a summary of the latest novelties in the field of paraneoplastic neurological syndromes (PNS), emphasizing relevant clinical updates on epidemiology, antibody discovery, and testing. - Source: PubMed
Publication date: 2026/09/09
Berzero Giulia - Once rabies virus (RABV) gains access to the central nervous system, infection almost inevitably results in fatal outcomes, and our incomplete understanding of viral pathogenesis remains a major barrier to effective therapeutic intervention. Here, we identify as an interferon-stimulated gene (ISG) that drives the macroautophagic/autophagic degradation of RABV phosphoprotein (P), thereby potently suppressing viral replication . Notably, overexpression of CAMKV significantly delays disease progression in mice challenged with a street strain of RABV. Mechanistically, CAMKV interacts with both RABV P and SQSTM1, promoting SQSTM1-mediated selective autophagic clearance of P and thereby restricting RABV transcription and replication. Collectively, our findings establish CAMKV as a critical host antiviral effector that functions through selective autophagy, highlighting CAMKV as a promising molecular target for the development of novel therapeutics against lethal RABV infection. 3-MA: 3-methyladenine; ABLV: Australian bat lyssavirus; ATG: autophagy related; AKT: AKT serine/threonine kinase; Baf-A1: bafilomycin A1; CAMKV: CaM kinase like vesicle associated; CAMK2: calcium/calmodulin dependent protein kinase II; co-IP: co-immunoprecipitation; CQ: chloroquine; DUVV: Duvenhage virus; DMSO: dimethyl sulfoxide; EBLV-1: European bat lyssavirus 1; ISG: interferon stimulated gene; LAMP1: lysosome associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; Mdivi-1: mitochondrial division inhibitor-1; MLD50: 50% mouse lethal dose; MOI: multiplicity of infection; MTOR: mechanistic target of rapamycin kinase; qPCR: quantitative real-time polymerase chain reaction; RABV: rabies virus; SQSTM1/p62: sequestosome 1; WT: wild type. - Source: PubMed
Publication date: 2026/07/13
Wang JinmingHuo HongTao YutingWang JinliangWang XijunWen ZhiyuanGe JinyingChen WeiyeBu ZhigaoShuai Lei - Severe neuropathies with predominant involvement of motor fibres can resemble lower motor neuron disease (LMND) phenotypes. Given the fatal prognosis of LMND, identifying underlying autoimmune syndromes is crucial to provide treatment options to patients. We investigated a novel autoantibody binding pattern observed on murine teased sciatic nerve fibres. Target antigens were identified using immunoprecipitation combined with mass spectrometry. Target specificity of these autoantibodies was validated in cell-based assays, neutralization assays and knock-out models. A retrospective study cohort consisting of different neuropathies (chronic inflammatory demyelinating polyradiculopathy n = 86, Guillain-Barré syndrome n = 37, multifocal motor neuropathy n = 18, diabetic neuropathy n = 30, other inflammatory neuropathies n = 10), amyotrophic lateral sclerosis (n = 50), multiple sclerosis (n = 50) and healthy controls (n = 50) was negative for septin multimer autoantibodies. Histopathological analysis of skin and the sural nerve including electron microscopy was performed in one seropositive patient, and autoantibody binding was characterized in vitro. Extensive immunotherapy was initiated in one patient, with clinical and serological follow-up over 4 years. Among 3543 total samples tested, three patients (two male, one female)-diagnosed with the LMND variant of amyotrophic lateral sclerosis (aged 65, 72 and 79 years, respectively)-showed a novel and distinct autoantibody binding pattern of indirect immunofluorescence staining on peripheral nerves, targeting Schmidt-Lanterman incisures (SLIs), paranodes and the abaxonal myelin. Target identification and validation revealed septin multimers as autoantibody epitopes. Despite the primarily intracellular location of septins, autoantibody binding was evident in living myelinated dorsal root ganglia, primarily at SLIs ('incisuropathy'). Septin multimer autoantibodies further initiated complement deposition on fixed and permeabilized cell-based assays. Sural nerve and skin biopsies showed inflammation, myelin and axonal pathology. Extensive immunotherapy in one patient was followed by disease stabilization over 3 years. The other two patients died of rapid disease progression: one of them received no immunotherapy while the other had ineffective treatments with single administrations of intravenous immunoglobulin and rituximab. Our data suggest that septin multimer autoimmunity occurs in severe motor-predominant neuropathies which can clinically resemble a neurodegenerative LMND. Screening for septin multimer autoantibodies should be considered in patients presenting with this phenotype. Follow-up studies need to determine the direct pathogenicity of septin multimer autoantibodies, their potential as a biomarker of an autoimmune syndrome and responses to immunotherapy in larger cohorts. - Source: PubMed
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