Ask about this productRelated genes to: Jund antibody
- Gene:
- JUND NIH gene
- Name:
- JunD proto-oncogene, AP-1 transcription factor subunit
- Previous symbol:
- -
- Synonyms:
- AP-1
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2016-10-11
Related products to: Jund antibody
Related articles to: Jund antibody
- BACKGROUNDIn European countries, including France, the incidence and costs of whooping cough in people with chronic conditions remains understudied.AIMWe aimed to estimate cumulative incidence and costs of whooping cough hospitalisations in children, adolescents and adults with chronic conditions in France.METHODSWe extracted data from patients hospitalised with whooping cough with or without underlying chronic conditions, asthma, chronic obstructive pulmonary disease (COPD), diabetes and immunocompromising conditions between 2008 and 2020 using the Système National des Données de Santé (SNDS).RESULTSAmong the 10,893 patients hospitalised with whooping cough in 2008-2020, asthma and/or COPD were the most common chronic conditions. Of the 7,212 children and adolescents hospitalised, 1,263 (17.5%) had asthma and 68 (0.9%) had an immunocompromising condition. Of the 3,681 adults, 2,297 (62.4%) had asthma and/or COPD, 594 (16.1%) had an immunocompromising condition and 454 (12.3%) had diabetes. In children and adolescents, the highest cumulative incidence ratio (CIR) was among patients with an immunocompromising condition (adjusted CIR = 3.6; 95% confidence interval (CI): 2.8-4.6) whereas in adults, patients with asthma and/or COPD had the highest adjusted CIR (18.6; 95% CI: 17.4-19.9). Median hospitalisation costs were the highest for patients with an immunocompromising condition (EUR 4,401). No significant changes in healthcare resource utilisation were observed before and after whooping cough hospitalisation in adults.CONCLUSIONChronic conditions are associated with higher cumulative incidence of whooping cough-related hospitalisation in France. This highlights the importance of reducing whooping cough circulation, through strengthening vaccination programmes, particularly for those with chronic conditions. - Source: PubMed
Vargas-Zambrano Juan CArnaud MickaelAntunes AnaKarzazi KhalilDespres JohannaVerdier RegisBoisnard FlorenceJund JeromeJanssen CecilePinquier DidierMacina Denis - The silver pomfret (Pampus argenteus) represents a commercially vital marine fish species. However, its aquaculture potential, especially in temperate northern regions, is critically constrained by pronounced cold sensitivity. Building upon preliminary investigations which demonstrated a significant inverse correlation between dusp5 expression levels and ambient water temperature, this study aimed to elucidate the functional mechanism of dusp5-a cold-inducible dual-specificity phosphatase affecting the MAPK pathway-in mediating cold stress adaptation. Utilizing cellular models subjected to dusp5 knockdown (KO) and overexpression (OE), we systematically evaluated its impact on cold stress responses. Functional analysis revealed that dusp5 OE conferred significant cytoprotection: it effectively suppressed cold-induced DNA fragmentation indicative of apoptosis (quantified by TUNEL assay), ameliorated mitochondrial dysfunction (assessed via JC-1 staining and TEM ultrastructural examination), and diminished oxidative stress (indicated by reduced malondialdehyde/MDA levels). Subsequent qPCR profiling demonstrated that dusp5 OE modulated the expression of selected genes associated with MAPK signaling cascades, apoptotic pathways, endoplasmic reticulum (ER) stress response, and mitochondrial functional integrity under cold duress. Furthermore, employing dual-luciferase reporter assays, we identified atf2, atf4, jund, and stat1 as putative regulators of dusp5 promoter activity. Complementary histidine affinity chromatography facilitated the identification of candidate dusp5-associated proteins predominantly localized to the ER and mitochondrial compartments, with functional annotations implicating roles in ER homeostasis, autophagic processes, and peroxisome metabolism. Collectively, this work provides the preliminary mechanistic insights of dusp5 in promoting cold tolerance within P. argenteus, yielding novel and fundamental insights into the molecular regulators underpinning low-temperature adaptation mechanisms in marine teleosts. - Source: PubMed
Publication date: 2026/08/03
Tang MengkeZhang ManQiu YubeiLi YuanboDai QinqinChen XianglongWang ChongyangXu FangjunZhang LuYuan ZiYan XiaojunHu JiabaoWang Yajun - Angiogenesis is essential for tumor progression, MEN1 gene encodes the menin protein, which is known as a tumor suppressor in lung tissue. Our previous study have shown that vascular density is significantly increased in menin-deficient lung cancer, suggesting that menin deficiency may promote the malignant progression of lung cancer by enhancing angiogenesis. However, whether menin play an important role in angiogenesis of lung cancer and the underlying mechanisms remain unclear. In this study, lung-specific Kras mutation induced mouse lung cancer model, clinical human lung cancer tissues, lung cancer and vascular endothelial cell lines were utilized, RNA-seq, ATAC-seq, ChIP, tube formation, sprouting, invasion and migration experiments were applied to investigate the role and mechanism of MEN1 in lung cancer angiogenesis. The result show menin were negatively related to angiogenesis markers and phenotype. Menin deficiency indirectly upregulates MMP10 transcription through activation of the transcription factor JunD. The expression of MMP10 further activates the EGFR receptor in vascular endothelial cells, thereby initiating the AKT/ERK signaling pathway. Inhibition MMP10 reversed menin low expression induce angiogenic phenotype and tumor progress. In conclusion, menin deficiency promotes angiogenesis through upregulates MMP10, targeting MMP10 with inhibitor represent an effective anti-angiogenic strategy for treating MEN1-deficient lung cancer. - Source: PubMed
Publication date: 2026/07/21
Wei ChengyuLiu XiangyuHu ShiminShen XiaodieLiu YingliQin XinxinZhou YeZheng JianqiTian BingkeHong JingfangSong YongxiaWang DiPeng LinlinDing JinxiaWang FangZhang HuiZhang ShihaoQiu Huan - Caspases are cysteine proteases that cleave specific proteins to control a range of cellular processes including cell death, inflammation, and differentiation. Proteomic approaches, like N-terminomics, have been central to identifying both cleaved proteins and where they are cleaved. We recently reported N-terminomics on differentiating and dying C2C12 myoblasts, identifying many new caspase substrates and cleavage sites. Here, we present a further analysis of this dataset demonstrating that there are caspase substrates "hidden" in our and in other N-terminomics datasets. We propose that for a subset of proteins, caspase cleavage is followed by removal of two amino acids from the neo-N-terminus by a dipeptidyl peptidase (DPP). As the peptide sequence of the neo-N-terminus is used to identify the cleavage site, this hides the caspase-mediated cleavage event. The implications of this are that N-terminomics datasets can be used to reveal hitherto unidentified caspase substrates and provide more information on cell-fate decisions. In C2C12 myoblasts, we have shown that cleavage of "hidden" substrates in apoptotic myoblasts that is absent from differentiating myoblasts (which also contain active caspase-3), suggesting that cleavage may identify apoptotic cells. A better understanding of the interplay between caspases and other proteases and their sequential action on caspase substrates may allow further elucidation of cell fate decisions. - Source: PubMed
Fotouhi FatemehGomez-Cardona ErikPatel JainilkumarJulien OlivierFearnhead Howard - Multiple myeloma (MM) exhibits an exhausted CD8 T cell state. Therefore, this study aimed to investigate exhausted CD8 T cell-related signatures and the underlying mechanisms in MM. - Source: PubMed
Publication date: 2026/05/14
Zhan HuienLai JingChen JieXu YingZhong Liye