Ask about this productRelated genes to: CD117 antibody
- Gene:
- KIT NIH gene
- Name:
- KIT proto-oncogene, receptor tyrosine kinase
- Previous symbol:
- PBT
- Synonyms:
- CD117, SCFR, C-Kit
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: CD117 antibody
Related articles to: CD117 antibody
- Cardiovascular diseases are the leading global cause of mortality but remain underaddressed in complex emergencies where health responses focus on infectious diseases and acute care. This scoping review mapped public health interventions addressing cardiovascular disease in complex emergencies and identified intervention types, epidemiological findings, and research gaps. - Source: PubMed
Publication date: 2026/09/21
Sotomayor Centeno AidaGan Rick KyeFernández García AndreaCernuda Martínez José AntonioArcos González Pedro - Currently, there exists no definitive standardized therapy for radiation enteritis. This study unveils Metrnl as a pivotal regulator of intestinal radioprotection through multi-dimensional single-cell profiling and mechanistic dissection. We first demonstrate that radiation dynamically reprograms Metrnl expression in a time-dependent manner, revealing its role as a radiation-responsive mediator. Crucially, Metrnl confers potent protection against radiation-induced intestinal injury through double mechanisms; Metrnl safeguards label-retaining cells (LRCs) rather than conventional Lgr5 intestinal stem cells, and activates a novel c-KIT-WNT signaling axis ERK/GSK3-mediated pathway crosstalk, both revitalizing intestinal epithelial regeneration. Therapeutically, recombinant Metrnl emerges as a potential biotherapeutic, effectively attenuating radiation enteritis. These findings establish Metrnl as a key mediator bridging radiation biology and regenerative medicine, offering a transformative potential for radiation injury management. - Source: PubMed
Publication date: 2026/06/18
Zhang SailongChen SiminGuo BingjieLing QishengWang ShulingMiao ZhuweiWang ZhiWei YuchenZheng SiliLi ZhiyongFeng An-QiangQian Feng-HuaMiao Chao-Yu - Tyrosine kinase inhibitors (TKIs) have significantly improved outcomes in gastrointestinal stromal tumors (GIST), but acquired resistance remains a major clinical obstacle. The underlying mechanisms that sustain oncogenic KIT signaling in TKI-refractory GIST are not fully understood. Here, we identify a previously unrecognized epigenetic-epitranscriptomic regulatory axis involving SETD2, FTO, and KIT that promotes TKI resistance by stabilizing mRNA. FTO, a key -methyladenosine (mA) RNA demethylase, was found to be markedly overexpressed in high-risk and recurrent GIST samples and correlated with poor prognosis. Mechanistically, FTO enhances mRNA stability by erasing mA modification in its 3' untranslated region (UTR), thereby preventing YTHDF2-mediated degradation and sustaining oncogenic KIT expression. Furthermore, the histone methyltransferase SETD2 activates transcription H3K36 trimethylation at the promoter, establishing a self-reinforcing loop that maintains FTO overexpression. Functional experiments using knockout and pharmacological inhibition (CS1 and entacapone) demonstrated that disrupting FTO activity suppresses tumor proliferation, reduces KIT expression, and restores sensitivity to imatinib both and . In KIT-Asp818Tyr/+ genetically engineered GIST mouse models, the combination of entacapone and imatinib led to significant tumor regression. Most importantly, preliminary clinical results from a Phase I trial (ClinicalTrials.gov: NCT04006769) showed that treatment with entacapone plus imatinib resulted in partial remission in two out of three evaluable TKI-refractory GIST patients, supporting the translational relevance of this strategy. Collectively, our findings establish the SETD2-FTO-KIT axis as a critical mechanism driving drug resistance in GIST and reveal mA demethylation as a key regulator of mRNA stability. Targeting FTO represents a promising and actionable therapeutic strategy to overcome TKI resistance and improve outcomes for patients with advanced GIST. - Source: PubMed
Publication date: 2026/07/15
Li ZhiHe JunjuCao ZhenZhou ShishanZhu YongweiDuan YumeiJiang AnfengGuan YidiGao JieTian JianLiu LiyuRong ZhuoxianLiu HeliLiu XiaoweiXiao HengyiDeng YuezhenLi BinSun Lunquan - To assess the clinical value of differential expression of BBOX1-AS1 in non-small cell lung cancer (NSCLC), and to explore its function and mechanism in disease progression through regulating tumor cells. Reverse transcription-quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expression of BBOX1-AS1. The chi-square test was used to analyze the relationship between BBOX1-AS1 and clinicopathological characteristics of patients (patients diagnosed with NSCLC at Pangang Group General Hospital from January 2018 to January 2021). The clinical diagnostic value of BBOX1-AS1 and miR-3940-3p was evaluated by receiver operating characteristic (ROC) curve. Kaplan-Meier survival curve and Cox regression analysis were used to evaluate the prognostic value of BBOX1-AS1. Cell counting kit-8 (CCK-8) assay was used to analyze the effect of BBOX1-AS1 on the biological function of tumor cells. Bioinformatics tools and dual luciferase reporter system were used to investigate the downstream miRNAs and target genes mediating the function of BBOX1-AS1. BBOX1-AS1 expression was significantly upregulated in NSCLC tumor tissues, serum, and cell lines (all ＜0.05). High BBOX1-AS1 expression was significantly correlated with larger tumor diameter, lymph node metastasis, and advanced TNM stage (all ＜0.05). NSCLC patients with high BBOX1-AS1 expression had a significantly lower 5-year survival rate (36.7%) than those with low expression (61.1%), and high BBOX1-AS1 expression was identified as an independent prognostic factor for NSCLC (=0.496, 95% : 0.272, 0.904, =0.022). MiR-3940-3p expression was downregulated in NSCLC serum (＜0.05) and negatively correlated with BBOX1-AS1 levels (=-0.646,＜0.001). Both BBOX1-AS1 [area under the curve (AUC)=0.858] and miR-3940-3p (AUC=0.852) exhibited high diagnostic value for NSCLC. Knockdown of BBOX1-AS1 inhibited A549 cell proliferation [the absorbance value of the BBOX1-AS1-siRNA group at 72 hours was 0.67±0.05, which was lower than those of the Mock group (1.17±0.06) and the siRNA-NC group (1.06±0.03), ＜0.001]. MiR-3940-3p directly interacted with BBOX1-AS1 and might be involved in mediating the function of BBOX1-AS1. Bioinformatics analysis predicted 10 potential target genes of miR-3940-3p: , , , , , , , , , and . BBOX1-AS1 is highly expressed in NSCLC patients, and its high expression indicates a poor prognosis. Knockdown of BBOX1-AS1 leads to a decrease in tumor cell proliferation. This study screens potential functional target genes and prognostic biomarkers for NSCLC. - Source: PubMed
Zeng X WLuo H FHe X YYang KGuo T P - The leaves of Perilla frutescens (L.) Britt. have long been topically used in Asian folk medicine to alleviate inflammatory and allergic skin disorders. Modern pharmacology confirms its anti-inflammatory, antioxidant, anti-allergic and skin-repairing activities. Nevertheless, the volatile active ingredients and molecular mechanisms of perilla leaves for skin-protective effects remain unclear. This work represents the first systematic stratified investigation comparing epidermal barrier repair between perilla leaf essential oil (PLEO) and its major constituent perillaldehyde, integrating in-silico prediction and in-vitro validation to dissect the multi-terpenoid synergistic mechanism of PLEO. - Source: PubMed
Publication date: 2026/09/20
Wang WencuiLi HonyingWang SenShan WenjieZhao WenjuanLiu HuanyanYao LeiLi YuhongWei Guodong