Ask about this productRelated genes to: RAVER1 antibody
- Gene:
- RAVER1 NIH gene
- Name:
- ribonucleoprotein, PTB binding 1
- Previous symbol:
- -
- Synonyms:
- KIAA1978
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-22
- Date modifiied:
- 2016-04-06
Related products to: RAVER1 antibody
Related articles to: RAVER1 antibody
- Craniopharyngiomas are rare benign pathologies but clinically challenging tumours because of their intimate relationship with critical brain structures, leading to severe endocrine-deficiencies/comorbidities. Therefore, identifying alternative prognostic/therapeutic tools is crucial. Although dysregulated splicing is a molecular feature that characterizes almost all tumour/cancer types, the dysregulation of the components belonging to the molecular machinery controlling the splicing-process (spliceosome) remains unknown in craniopharyngiomas. Here, we uncover a profound dysregulation in the expression of relevant spliceosome-components and splicing-factors in craniopharyngiomas versus control non-tumour tissues, identifying PRPF8 and RAVER1 as key tumour suppressor factors associated with relevant oncogenic processes. Moreover, we demonstrate that the spliceosome activity inhibition using pladienolide-B in primary patient´s derived cell-cultures might serve as a potential therapeutic tool worth to be explored in humans. Altogether, our results demonstrate a drastic and clinically relevant spliceosome-associated molecular dysregulation in craniopharyngiomas, which could serve as a potential source of novel diagnostic/prognostic biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2025/06/28
Fuentes-Fayos Antonio CG-García Miguel ESánchez-Medianero TeresaApps JohnFlores-Martínez ÁlvaroDe la Rosa-Herencia Ana SGil-Duque IgnacioOtto GeorgVenegas-Moreno EvaRuiz-Valdepeñas Eugenio CárdenasHerrera-Martínez Aura DSolivera JuanGahete Manuel DCano David AOrtega RosaSoto-Moreno AlfonsoGálvez-Moreno María AMartínez-Barberá Juan PedroLuque Raúl M - COVID-19 severity has been linked to immune factors, with excessive immune responses like cytokine storms contributing to mortality. However, the genetic basis of these immune responses is not well understood. This study aimed to explore the genetic connection between COVID-19 severity and blood cell traits, given their close relationship with immunity. - Source: PubMed
Publication date: 2025/02/17
Meng ZiangZhang ChumengLiu ShuaiLi WenWang YueZhang QingyiPeng BichenYe WeiyiJiang YueSong YingchaoGuo MiaoChang XiaoShao Lei - Multiple cell death and inflammatory signaling pathways converge on two critical factors: receptor-interacting serine/threonine kinase 1 (RIPK1) and caspase-8. Careful regulation of these molecules is critical to control apoptosis, pyroptosis, and inflammation. Here, we found a pivotal role of Raver1 as an essential regulator of pre-mRNA splicing, expression, and functionality and the subsequent caspase-8-dependent inflammatory cell death. We show that Raver1 influences mRNA diversity primarily by repressing alternative exon inclusion. Macrophages from -deficient mice exhibit altered splicing of . As a result, -deficient primary macrophages display diminished cell death and decreased interleukin-18 and interleukin-1ß production, when infected with bacteria, or by restraining TGF-ß-activated kinase 1 or IKKβ in the presence of lipopolysaccharide, tumor necrosis factor family members, or interferon-γ. These responses are accompanied by reduced activation of caspase-8, Gasdermin D and E, and caspase-1 in the absence of . Consequently, -deficient mice showed heightened susceptibility to infection. Raver1 and RIPK1 also controlled the expression and function of the C-type lectin receptor Mincle. Our study underscores the critical regulatory role of Raver1 in modulating innate immune responses and highlights its significance in directing in vivo and in vitro inflammatory processes. - Source: PubMed
Publication date: 2025/02/13
Zhang BoyaoOrning PontusLehman Jesse WDinis AlexandreTorres-Ulloa LeslieElling RolandKelliher Michelle ABertin JohnProulx Megan KGoguen Jon DRyan LivKandasamy Richard KEspevik TerjePai Athma AFitzgerald Katherine ALien Egil - In this study, we analyzed the potential associations of selected laboratory and anamnestic parameters, as well as 12 genetic polymorphisms (SNPs), with clinical COVID-19 occurrence and severity in 869 hospitalized patients. The SNPs analyzed by qPCR were selected based on population-wide genetic (GWAS) data previously indicating association with the severity of COVID-19, and additional SNPs that have been shown to be important in cellular processes were also examined. We confirmed the associations of COVID-19 with pre-existing diabetes and found an unexpected association between less severe disease and the loss of smell and taste. Regarding the genetic polymorphisms, a higher allele frequency of the LZTFL1 and IFNAR2 minor variants significantly correlated with greater COVID-19 disease susceptibility (hospitalization) and severity, and a similar tendency was observed for the RAVER1 and the MUC5B variants. Interestingly, the ATP2B4 minor haplotype, protecting against malaria, correlated with an increased disease susceptibility, while in diabetic patients disease susceptibility was lower in the presence of a reduced-function ABCG2 transporter variant. Our current results, which should be reinforced by larger studies, indicate that together with laboratory and anamnestic parameters, genetic polymorphisms may have predictive value for the clinical occurrence and severity of COVID-19. - Source: PubMed
Publication date: 2025/01/03
Mózner OrsolyaSzabó EditKulin AnnaVárady GyörgyMoldvay JuditVass VivienSzentesi AndreaJánosi ÁgostonHegyi PéterSarkadi Balázs - Multiple cell death and inflammatory signaling pathways converge on two critical factors: receptor interacting serine/threonine kinase 1 (RIPK1) and caspase-8. Careful regulation of these molecules is critical to control apoptosis, pyroptosis and inflammation. Here we discovered a pivotal role of Raver1 as an essential regulator of pre-mRNA splicing, expression, and functionality, and the subsequent caspase-8-dependent inflammatory cell death. Macrophages from -deficient mice exhibit altered splicing of , accompanied by diminished cell death and reduced activation of caspase-8, Gasdermin D and E, caspase-1, as well as decreased interleukin-18 (IL-18) and IL-1ß production. These effects were triggered by bacteria, or by restraining TAK1 or IKKβ in the presence of LPS, TNF family members, or IFNγ. Consequently, animals lacking showed heightened susceptibility to infection. Raver1 and RIPK1 also controlled the expression and function of the C-type lectin receptor Mincle. Our study underscores the critical regulatory role of Raver1 in modulating innate immune responses and highlights its significance in directing and inflammatory processes. - Source: PubMed
Publication date: 2024/11/29
Zhang BoyaoOrning PontusLehman Jesse WDinis AlexandreTorres-Ulloa LeslieElling RolandKelliher Michelle ABertin JohnProulx Megan KRyan LivKandasamy RichardEspevik TerjePai Athma AFitzgerald Katherine ALien Egil