Ask about this productRelated genes to: SLD5 antibody
- Gene:
- GINS4 NIH gene
- Name:
- GINS complex subunit 4
- Previous symbol:
- -
- Synonyms:
- MGC14799, SLD5
- Chromosome:
- 8p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2006-05-04
- Date modifiied:
- 2016-03-21
Related products to: SLD5 antibody
Related articles to: SLD5 antibody
- Lung adenocarcinoma (LUAD) is the most prevalent subtype of lung cancer, with lymph node metastasis serving as a key prognostic factor. MUC5B, a member of the mucin family, has been implicated in the progression of various cancers, yet its specific role in LUAD metastasis remains underexplored. This study aimed to investigate the role of MUC5B in LUAD progression and its potential as a biomarker for lymph node metastasis. - Source: PubMed
Publication date: 2025/12/02
Song WeijianYang QianDu MinjunWei JiacongZhou BoxuanShi JianweiLiang LinchuanLiu ZixuLiang MeiLi MianyangGao Yushun - The α5-nicotinic acetylcholine receptor (α5-nAChR) is implicated in nicotine-driven proliferation of lung cancer cells. GINS4 functions as a regulatory factor of the G1/S transition and DNA replication dynamics, closely linking it to proliferative capacity. Profiling of CHRNA5, the gene encoding α5-nAChR, indicated that silencing CHRNA5 reduced GINS4 expression. The mechanistic relationship between α5-nAChR and GINS4 in lung adenocarcinoma (LUAD), however, has not been fully clarified. Analysis in this study revealed that α5-nAChR expression correlated with GINS4 levels, smoking status, and overall survival. In vitro experiments demonstrated that α5-nAChR mediates nicotine-induced GINS4 expression via STAT3, thereby enhancing LUAD cell proliferation, migration, and invasion. The α5-nAChR/GINS4 axis was further validated in both mouse xenograft models and human LUAD tissue samples. Collectively, the results indicate the existence of a novel α5-nAChR/GINS4 signaling pathway contributing to nicotine-associated LUAD progression. - Source: PubMed
Publication date: 2025/11/03
Wang ZengpingCai JiayingYang MengdanYang ShuranWang JingJia YanfeiSun HaijiMa Xiaoli - As a recognized common and severe chronic disease predominantly affecting preterm infants, bronchopulmonary dysplasia (BPD) necessitates meticulous clinical management. Emerging evidence has thoroughly elucidated the role of complex subunit 4 (GINS4) in lung carcinogenesis. Nevertheless, the specific molecular mechanisms underlying GINS4' potential involvement in BPD pathogenesis remain underexplored and require systematic investigation. In this study, we proved that GINS4 expression was significantly upregulated in hyperoxia-induced lung injury. Additionally, in a hyperoxia-induced BPD neonatal rat model, GINS4 was found to upregulate the expression of inflammatory cytokines, including interleukin-6 (IL-6), interleukin-1β (IL-1β), interleukin-18 (IL-18), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-ɑ), concomitantly increasing myeloperoxidase (MPO) activity. Histopathological analyses via Giemsa staining and hematoxylin-eosin (H&E) staining further revealed that GINS4 promoted alveolarization in this experimental context. Analysis of Aquaporin 5 (AQP5) and surfactant-associated protein C (SPC) indicated GINS4 exerted differential effects on alveolar development. Notably, GINS4 was found to directly interact with p65, thereby promoting phosphorylation and acetylation of the p65 NF-κB. Finally, in a preterm rat model, we demonstrate that GINS4 induced BPD-like pathological alterations in lung tissues, characterized by alveolar septal simplification and thickening. Collectively, this study identifies GINS4 as a potential novel therapeutic target for prevention and treatment of BPD. - Source: PubMed
Publication date: 2025/10/27
Chen ShengYuan Tianming - The aim of this study was to evaluate the transcriptome of peripheral blood mononuclear cells (PBMCs) derived from patients affected by psoriasis (PSO) and psoriatic arthritis (PSA) following treatment with guselkumab, an interleukin (IL)-23 inhibitor. - Source: PubMed
Publication date: 2025/09/02
Mastrangelo MircoRuscitti PieroBruni ManfredoLucantonio EleonoraDe Berardinis AndreaBarile AntonioFargnoli Maria ConcettaCipriani PaolaEsposito MariaPellegrini Cristina - While monogenic variants in CDC45-MCM-GINS (CMG) replisome proteins cause human natural killer cell deficiencies (NKDs), family members with the same inherited variants often have variable clinical and cellular phenotypes. We investigated two siblings with inherited compound heterozygous GINS4 variants but variable disease expressivity. Cell cycle impairment and increased apoptosis were detected following NK cell lineage commitment but not in pluripotent cells. While this effect was detected in both siblings, the efficiency of NK cell differentiation was variable and correlated with differential clinical severity of NKD. Further investigation of allelic expression of inherited GINS4 variants demonstrated expected biallelic expression of GINS4 in pluripotent cells and progenitors. However, allelic bias in lineage-committed NK cells led to over- or under-representation of more damaging GINS4 heterozygous variants associated with differential cellular and clinical severity. This study identifies allelic bias that causes phenotypic variation of a monogenic disease and defines additional mechanisms underlying immunodeficiency. - Source: PubMed
Publication date: 2025/08/05
Seo SeungmaeAhn Yong-OonPatil Sagar LArmetta JacquelineSaturne Madrikha DHegewisch-Solloa EverardoGuilz Nicole CPatel AchchheCorneo BarbaraBorowiak MalgorzataMace Emily M