Ask about this productRelated genes to: CLEC4G antibody
- Gene:
- CLEC4G NIH gene
- Name:
- C-type lectin domain family 4 member G
- Previous symbol:
- -
- Synonyms:
- UNQ431, LSECtin
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-09
- Date modifiied:
- 2015-12-16
Related products to: CLEC4G antibody
Related articles to: CLEC4G antibody
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), remains a major public health threat, particularly in vulnerable populations. SARS-CoV-2 spike proteins interact with the human angiotensin-converting enzyme 2 (ACE2) receptor, together with accessory molecules that facilitate viral entry, through its spike receptor-binding domain (RBD). Although ACE2 is the primary receptor required for viral replication, its expression patterns do not fully correlate with viral distribution or tissue pathology. Moreover, SARS-CoV-2 has been shown to infect cells and tissues lacking detectable ACE2 expression. Viral entry via ACE2-independent pathways may also confer resistance to some monoclonal antibodies (Abs) targeting the spike RBD that block ACE2-mediated binding. These observations highlight the potential significance of ACE2-independent entry factors in SARS-CoV-2 infection, particularly in vaccinated individuals with Abs directed against ACE2-dependent viral entry. In this review, we discuss the emerging roles of ACE2-independent entry factors in SARS-CoV-2 infection and the immune responses. These factors include CD147, AXL, CD169/Siglec-1, CD209L, CD209, CLEC4G, ASGR1, LDLRAD3, TMEM30A, TMEM106B, transferrin receptor 1, GPR78, integrin α5β1, KREMEN1, LFA-1, and CD4. While ACE2 remains central to viral replication, ACE2-independent entry appears sufficient to elicit immune responses. Therefore, future investigations are warranted to elucidate the roles of ACE2-independent mechanisms in immune-mediated pathology and viral evolution, independent of immune pressure targeting ACE2-mediated entry in previously infected or vaccinated individuals. - Source: PubMed
Publication date: 2025/12/22
Sun YiyuWong Lok-Yin RoyChang Theresa L - The objective was to analyze the effect of () on hepatocellular carcinoma (HCC) and investigate its impact on lenvatinib (Lenva) resistance as well as the underlying action pathway. - Source: PubMed
Publication date: 2025/12/11
Xiao KeminYan JinHe GuangxiHe BinWang Qi - Bladder cancer (BC) is a prevalent urinary tract malignancy with high morbidity and mortality. Despite advances in therapeutic modalities, early diagnosis and precise treatment remain challenging, highlighting the need for reliable biomarkers and therapeutic targets. This study aims to identify molecular targets and drug candidates for BC by integrating cross-omics quantitative trait loci (xQTLs), OLINK proteomics (a high-throughput plasma protein measurement platform), and transcriptomics data, alongside prospective cohort studies and multi-omics analyses. - Source: PubMed
Publication date: 2025/11/26
Han KunWei ChengchengLi YunfanLuo YuSong LiangdongHe JingkeJiang LincenWen JunSu ShuaiZhang JindongWang Delin - In recent years, the impact of ultraviolet (UV) radiation on skin photoaging and its underlying mechanisms have garnered increasing attention. Our previous study identified Acein, an angiotensin-converting enzyme 1 (ACE1)-targeting peptidethat ameliorates aging phenotypes and significantly extends lifespan in Caenorhabditis elegans by downregulating C-type lectin domain-containing protein CLEC-126 expression. However, the therapeutic potential of Acein in human skin photoaging and the roles of ACE1 and CLEC4G (C-type lectin domain family 4 member G, the human homolog of CLEC-126) remains unclear. In this study, photoaging models in vitro were established and Acein (1 μM) reduced UV-induced oxidative stress and inflammatory markers, suppressed MMPs expression while effectively mitigating collagen III (COL3) degradation and decreased β-galactosidase accumulation. Additionally, functional assays demonstrated Acein enhanced cell viability and migration while reducing G1 arrest and apoptosis. Mechanistically, UV irradiation upregulated ACE1 and CLEC4G expression, which was reversed by Acein. Further investigations revealed that ACE1- knockdown alleviated UV-induced oxidative stress, inflammation and senescence, whereas CLEC4G- overexpression exacerbated these effects. Co-Immunoprecipitation and molecular docking confirmed the interaction between ACE1 and CLEC4G, with Western blotting assays identifying CLEC4G as a key downstream mediator of ACE1-driven photoaging. Moreover, Acein was found to attenuate photoaging by inhibiting the p38-MAPK and NF-κB p65 pathways. In vivo studies using acute photodamage model and photoaging mice model demonstrated that topical Acein application reduced oxidative stress, inflammation, and collagen degradation while mitigating mitochondrial autophagy. Collectively, these findings suggest that Acein represents a novel candidate compound for protecting human skin against UV-induced photoaging. - Source: PubMed
Publication date: 2025/11/13
Zhou TianxiongWang YunfanWang JiaqiWu YixinSetrerrahmane SarraZhang RuohuiSun BaogangZhu YanzhiXu Hanmei - Liver sinusoidal endothelial cells (LSECs) are highly specialized components of the hepatic vascular niche, regulating liver function and disease pathogenesis through angiocrine signaling. Recently, we identified GATA4 as a key transcription factor controlling LSEC development and protecting against liver fibrosis. As the transcription factor c-Maf was strongly downregulated in -deficient LSECs, we hypothesized that c-Maf might be an important downstream effector of GATA4 in LSEC differentiation and liver fibrogenesis. - Source: PubMed
Publication date: 2025/06/06
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