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
- - Source: PubMed
Publication date: 2026/03/31
Naz MaheenBatool MaryamShah Syed AbdullahTalha MuhammadFatima Mahnoor - The class 3 semaphorin SEMA3A is a secreted glycoprotein that serves as an evolutionary conserved axon repellent with proposed vascular functions. In mice, SEMA3A is dispensable for developmental brain, limb or trunk blood vessel patterning, but restricts vessel branching in the zebrafish embryo trunk. Whereas neuropilin 1 (NRP1) is thought to be the SEMA3A receptor in the mouse, prior reports identified Plexin D1 as the Sema3a receptor in zebrafish trunk vessel patterning, with previous knockdown and knockout studies yielding contradictory results on Nrp1 requirement for vessel patterning in zebrafish. To resolve these discrepancies, we have refined the prior knockdown strategy to limit off target effects and generated mutant zebrafish embryos lacking both Nrp1a and Nrp1b paralogues to show that Nrp1 restricts trunk vessel patterning in a Sema3a-dependent manner. In agreement, we found that NRP1 is required in human endothelial cells for SEMA3A-induced repulsion. Moreover, we show that SEMA3A action via NRP1 does not involve the splicing regulation of , previously proposed to act downstream of Plexin D1. Instead, sustained NRP1 activation independent of SEMA3A increases the expression of the anti-angiogenic soluble FLT1 (sFLT1), establishing a feedback mechanism to limit endothelial proliferation. Together, these findings demonstrate a dual role for NRP1 in shaping physiological vascular morphogenesis. Thus, NRP1 mediates repulsive SEMA3A cues in endothelial cells, in analogy to its role in axon guidance, and further restricts angiogenesis by promoting the release of sFLT1 in a SEMA3A-independent manner. - Source: PubMed
Publication date: 2026/05/03
Spreafico MarcoGuzzolino ElenaFanuele FrancescaGestri GaiaTacconi CarlottaPalermo SaraTricco MatildeCatroppa ValeriaAiypova AyazhanDenti LauraPellet-Many CarolineRuhrberg ChristianaFantin Alessandro - - Source: PubMed
Publication date: 2026/04/27
Owari KensukePiao HaishunHori MiyukiFutami Kazunobu - 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