Ask about this productRelated genes to: Shc1 antibody
- Gene:
- SHC1 NIH gene
- Name:
- SHC adaptor protein 1
- Previous symbol:
- SHC
- Synonyms:
- p66, ShcA
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-02-17
- Date modifiied:
- 2016-10-05
Related products to: Shc1 antibody
Related articles to: Shc1 antibody
- is a major opportunistic fungal pathogen, and increasing azole resistance poses a challenge for aspergillosis treatment. Squalene is an upstream precursor of ergosterol biosynthesis and may also be utilized by SHC-like triterpene cyclases, suggesting a potential link between squalene-associated metabolism, membrane adaptation, and azole response. However, the roles of SHC-like triterpene cyclase genes in remain unclear. Here, we characterized three candidates, , , and , using comparative bioinformatic analysis, gene deletion, phenotypic assays, azole susceptibility testing, transcriptomics, and host-interaction models. Sequence, genomic-context, phylogenetic, and structural analyses suggested divergence among the three candidates. Individual deletion caused limited effects on vegetative growth, whereas loss of mildly reduced susceptibility to voriconazole and posaconazole, as reflected by twofold MIC increases and lower inhibition rates. Transcriptomic analysis revealed distinct remodeling patterns, with showing the broadest transcriptional changes despite no detectable MIC shift. Targeted metabolite profiling and PI uptake analysis further supported an association between deletion, sterol/hopane-type triterpenoid balance, and membrane-associated properties. deletion also altered epithelial cell interaction phenotypes, while Δ showed reduced lethality in . In clinical isolates, elevated transcription was associated with azole-resistant backgrounds. These findings suggest functional diversification among SHC-like triterpene cyclase genes and indicate that may contribute to azole-associated adaptation and virulence-related traits in . - Source: PubMed
Publication date: 2026/09/05
Ye KeruiChen FangyanHu LingxueHan JinghuiLi DingchenHu MandongWang ChangjunZeng JumeiHan Li - Diabetic kidney disease (DKD) represents one of the most severe complications of diabetes. Although EZH2 (Enhancer of Zeste Homolog 2) has been implicated in renal injury and diabetes, its specific function within renal tubular cells in DKD remains unclear. Here, we explored the role and downstream mechanism of tubular EZH2 in DKD progression. Renal EZH2 expression was significantly upregulated in DKD. Single-nucleus RNA sequencing and immunofluorescence analyses verified that such elevation was restricted to proximal tubular epithelial cells. Conversely, tubular-specific deletion of Ezh2 exacerbated renal dysfunction and fibrosis in DKD mice. In vitro gain- and loss-of-function experiments in high glucose-stimulated HK2 cells further validated that EZH2 plays a renoprotective role under diabetic conditions. Mechanistically, we demonstrated that EZH2 epigenetically suppresses the pro-oxidative mediator SHC1. In the DKD mouse model, renal SHC1 protein abundance was markedly increased upon tubular Ezh2 knockout, accompanied by reduced levels of antioxidant enzymes SOD1 and SOD2, significantly elevated MDA, and depleted GSH. Consistent with these in vivo observations, in vitro functional assays further validated that EZH2 epigenetically downregulates SHC1 and alleviates such oxidative stress perturbations. Finally, we verified that SHC1 inhibition rescues the exacerbated fibrotic response and oxidative damage triggered by pharmacological EZH2 suppression under high-glucose conditions. In conclusion, tubular EZH2 protects against DKD via inhibiting SHC1-driven oxidative stress. - Source: PubMed
Publication date: 2026/08/10
Xu QimingLin PinglanChen SijunLu JianraoLi LinMoghadasali RezaYang XuejunHu JingWu MingChen Dongping - Beyond established rare fusions, such as ALK and ROS1, emerging ultrarare fusions involving receptor tyrosine kinases or their ligands, including EGFR-SHC1, further guide us to uncover novel mechanisms of oncogenic activation and corresponding treatment strategies. Collectively, rare and ultrarare genomic events are driving precision oncology toward an increasingly individualized era of "ultraprecision" cancer therapy. See related article by Zheng et al., p. 1573. - Source: PubMed
Le XiuningWolf Jürgen - The functional plasticity of tumor-associated macrophages (TAMs) is a critical determinant of the immunosuppressive microenvironment in cervical cancer, yet its integration into actionable prognostic frameworks remains limited. This study aimed to establish a TAM polarization-centered model and elucidate the mechanisms of underlying tumor-immune crosstalk. - Source: PubMed
Publication date: 2026/07/17
Chen YushaWang LingLi SuyuHuang JimiaoZhu LeileiHuang XiqiZheng XiangqinPan DilingHuang Chuanzhong - To investigate the mechanisms underlying benzo[a]pyrene-induced esophageal cancer (EC), and to screen and identify the key targets and biomarkers associated with benzo[a]pyrene-related EC. - Source: PubMed
Publication date: 2026/07/15
Lan XuyanHuang ZuqiangLin YukunSun XiaoyuGuo BinghanLi GenglinWang JintaoLin JinlanZhu LihuanGuo Tianxing