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
- 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
Arlt Friederike AMiske RamonaAppeltshauser LuiseZinnow ViktoriaBorowski KathrinStenzel WernerRadbruch HelenaMeisel AndreasRuprecht KlemensEndres MatthiasBlau IgorKirchner MarieluiseMertins PhilippSanchez-Sendin ElisaWernick StephaniePressler HannahStascheit FraukeLinke JanisHümmert SophieWerner Hauke BWibisono Esravila ADoppler KathrinKomorowski LarsSpiliotis Elias TDubey DivyanshuZeckeridou AnastasiaPittock Sean JMills John RMcKeon AndrewScharf MadeleinePrüss Harald - INTRODUCTION: Gastric cancer remains a major global health burden with high incidence and mortality. Despite therapeutic advances, long-term survival remains unsatisfactory. Reliable biomarkers to predict therapeutic efficacy and clinical outcomes are urgently needed. This study aimed to elucidate the heterogeneity of gastric cancer using an integrative bioinformatics approach that combines single-cell RNA-sequencing (scRNA-seq) and bulk RNA-seq data. METHODS: scRNA-seq datasets were obtained from the GEO database, and bulk RNA-seq data were obtained from the TCGA. Cell communication, pseudotime analysis, and cell death scoring (cuproptosis, ferroptosis, autophagy, and pyroptosis) were performed on the basis of the scRNA-seq datasets. Stemness, survival, drug sensitivity and posttranslational modification (PTM) analyses were conducted using TCGA data. RESULTS: Cancer cells were clustered into three molecular subtypes with distinct molecular characteristics, pathway activation profiles and cell death patterns. Cell-cell communication analysis revealed subtype-specific regulatory interactions, whereas pseudotime and cell death scoring demonstrated dynamic cellular states. Bulk RNA-seq revealed five cell death patterns, among which "cell death 2" and high cuproptosis scores emerged as independent risk factors for poor prognosis. Genes such as LMF1-AS1, CAMKV, ERVW-1, ACLY, GAS2L2, RGS8, and RASSF8-AS1 were differentially expressed in the high-risk group. Samples with low stemness and elevated pyroptosis showed enhanced inferred drug resistance, particularly to LBH589. Additionally, ZDHHC22 was identified as a potential protective prognostic factor, and in vitro assays suggested its association with cell death modulation in gastric cancer. CONCLUSION: This study highlights the molecular heterogeneity of gastric cancer, demonstrating how distinct cell death patterns and PTM features shape prognosis and drug sensitivity. The identified biomarkers and resistance profiles may provide valuable guidance for personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/05/30
Wu JiamingChen CongDou GuangjianHuang LiyongZhu YiChen ZhihengMao QileJia JingyiWang PeterLi Jin - Long-term outcome data for stiff person spectrum disorder (SPSD) remain limited and sustained response to treatment varies. - Source: PubMed
Mangioris GeorgiosMcKeon AndrewBower James HVorasoot NisaDubey DivyanshuFlanagan Eoin PPittock Sean JZekeridou Anastasia - We examined the clinical course and risk factors for late onset neurotoxicities, including nerve palsies (IEC-NP) and parkinsonism (IEC-PKS), in patients with relapsed/refractory multiple myeloma (RRMM) treated with ciltacabtagene autoleucel (cilta-cel) in standard-of-care practice (SOC). Among 235 RRMM patients who received cilta-cel, 15 (6.4%) developed IEC-NP and 9 (3.8%) developed IEC-PKS with one patient developing both. Pre-infusion, patients with age >75 years, bone marrow plasma cells ≥20%, or involved free light chain ≥20 mg/dL had increased odds of IEC-PKS. Post-infusion, patients who developed ICANS, received higher cumulative steroid doses or received >1 dose of tocilizumab also had increased odds of IEC-PKS. High peak absolute lymphocyte count (ALCpeak) was a statistically significant predictor on univariate and multivariate analysis for IEC-NP and IEC-PKS. ALC ≥ 3 × 10/L was identified as a meaningful threshold (AUC = 0.838) to predict for late onset neurotoxicity. An ALC ≥ 3 × 10/L conferred a positive predictive value for delayed neurotoxicity of 31% vs a negative predictive value of 98% in patients with ALC < 3 × 10/L. All IEC-NP patients received steroid +/- IVIG; 87% had complete resolution of their cranial neuropathies (median 57 days). Four patients with IEC-PKS received cyclophosphamide (1.5-2 g/m) within 1-13 days of symptom onset and all had observable symptom improvement within 1-2 days. - Source: PubMed
Publication date: 2025/12/31
Lim Kenneth J CTan MelindaParrondo RicardoChhabra SaurabhDooley KatharineDe Menezes Silva Corraes AndreCarabenciov DarinGertz MorieHwa LisaHaily StephensKapoor PrashantKourelis TaxiarchisWarsame RahmaCook JoselleBinder MoritzBergsagel P LeifYadav UditWiedmeier-Nutor ErinGeyer SusanAilawadhi SikanderFonseca RafaelKumar ShajiZekeridou AnastasiaLin Yi