Ask about this productRelated genes to: VEGFR1 antibody
- Gene:
- FLT1 NIH gene
- Name:
- fms related tyrosine kinase 1
- Previous symbol:
- FLT
- Synonyms:
- VEGFR1
- Chromosome:
- 13q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: VEGFR1 antibody
Related articles to: VEGFR1 antibody
- Neuropathic pain (NP) is frequently comorbid with anxiety and depression, yet the underlying molecular mechanisms in the brain remain poorly understood, hindering the development of targeted therapies. This study aimed to identify key transcriptional networks and regulatory pathways in the anterior cingulate cortex (ACC) associated with NP-induced anxiodepression. We analyzed transcriptomic data (GSE92718) from the ACC of a mouse model of chronic NP. By comparing differentially expressed genes at a time point manifesting anxiodepressive-like behavior (8-week post-injury) against those with pain alone (2-week), we constructed a weighted gene co-expression network (WGCNA). A key module (blue module) significantly correlated with the anxiodepressive phenotype was enriched for synaptic signaling (glutamatergic/GABAergic), neuroplasticity, and key pathways like MAPK and Ras. Within this module, we identified 7 pivotal lncRNAs and 5 hub mRNAs (Flt1, Slc38a2, Bmpr1b, Pdgfra, Gng2) via integrated lncRNA-mRNA-pathway and protein-protein interaction network analyses. Furthermore, we established a competing endogenous RNA (ceRNA) network, revealing a core regulatory axis comprising 3 hub lncRNAs, 5 hub mRNAs, and 40 miRNAs. The aberrant expression of the five hub mRNAs in the ACC was specifically validated in mice with anxiodepressive phenotypes using RT-PCR. Our findings unveil a critical ceRNA network and implicate dysregulated synaptic genes in the ACC as key drivers of NP-induced anxiodepression, providing novel insights into its molecular basis and highlighting potential diagnostic biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/23
He YongtaoXu YaoweiXing FeiShi XiaoshanZhang FanXing MingquanLiu YafeiZhang WeiWei XinYuan Jingjing - The development of resistance to anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors and a poor response to immune checkpoint inhibitors (ICIs) remain challenges in ALK-rearranged non-small cell lung cancer (NSCLC). We performed immune-related gene expression profiling (irGEP) for ALK-rearranged NSCLC to assess the characteristics of the tumor microenvironment and explore potential therapeutic avenues. - Source: PubMed
Publication date: 2026/04/19
Kurosaki TakashiSuzuki ShinichiroWatanabe YasutakaKenmotsu HirotsuguItoh ShoichiYamaguchi MasafumiShiono AyakoSuzuki TakujiYokoyama ToshihideToi YukihiroTanaka HisashiOki MasahideTsuda TakeshiIchihara EikiAzuma KoichiTanaka HiroshiArai RyoUchibori KenMiyauchi EisakuKatayama RyoheiHayashi Hidetoshi - Clear cell renal cell carcinoma (ccRCC) is distinguished by the absence of definitive diagnostic markers and efficacious treatment modalities, factors that collectively contribute to its unfavorable clinical prognosis. The targeting of senescent cells has recently emerged as a promising therapeutic strategy. Nevertheless, the precise role of cellular senescence in the pathophysiology of ccRCC has yet to be comprehensively elucidated. This study sought to investigate the role of cellular senescence levels in ccRCC through comprehensive transcriptomic, proteomic, spatial transcriptomic, and single-cell analyses. The study determined that elevated levels of cellular senescence contribute to a suppressed immune microenvironment, thereby exacerbating the prognosis for ccRCC patients. We utilized an extensive array of machine learning algorithms, in conjunction with multi-omics technologies, validated through immunofluorescence, RT-qPCR, and additional techniques, to collectively identify FLT1 as a pivotal single gene driving ccRCC progression. Our work reveals a FLT1-centered network of related factors, where FLT1 acts as the core single gene, closely associated with key factors VEGFA and AKT1. This network mediates crosstalk between endothelial and epithelial cells: endothelial cells expressing FLT1 alone, AKT1 alone, or co-expressing FLT1/AKT1 exhibited enhanced malignancy; among epithelial cells, proximal tubular epithelial cells with high VEGFA expression (a factor closely related to FLT1) represented the most aggressive subtype and acted as "pioneer cells" driving tumor progression. This FLT1-centric mechanism is evolutionarily conserved, as validated in mouse single-cell datasets. Clinically, ccRCC patients with low expression of the FLT1-centered network (particularly low FLT1) showed better responses to immunotherapy. For patients with high FLT1 expression, a combination therapy targeting this network-screened via molecular docking and dynamics simulations-may improve prognosis. This includes FLT1 inhibitors (Sorafenib, Regorafenib, Lenvatinib), supplemented by AKT1 inhibitors (Capivasertib) and VEGFA inhibitors (Bevacizumab) to suppress FLT1-associated malignant cell populations. - Source: PubMed
Sun MouyuanMao HuchaoLuo YaxianYang MeiHe ZhixuLi ShuangyangLiu ZhichaoPeng LianjieZhang QuanjieZhang JingyuZhang Yan - Stillbirth remains a major global health challenge, particularly in low- and middle-income countries. Angiogenic imbalance, characterized by elevated soluble fms-like tyrosine kinase-1 (sFlt-1) and reduced placental growth factor (PlGF), is implicated in placental dysfunction, yet few studies have examined the association between the sFlt-1:PlGF ratio and stillbirth. - Source: PubMed
Publication date: 2026/04/01
Lee Mi-Sun SEum Ki-DoChristiani David C - - Source: PubMed
Publication date: 2026/04/16
Duggan Michael RJacobsen ErinYang ShuojiaZeng XuemeiKandala SridharJoynes Cassandra MKarikari Thomas KNimgaonkar Vishwajit LKamboh M IlyasSnitz Beth EFerrucci LuigiYolken RobertGanguli MaryWalker Keenan A