Ask about this productRelated genes to: NEO1 antibody
- Gene:
- NEO1 NIH gene
- Name:
- neogenin 1
- Previous symbol:
- -
- Synonyms:
- NGN, HsT17534, IGDCC2, NTN1R2
- Chromosome:
- 15q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-26
- Date modifiied:
- 2016-10-05
Related products to: NEO1 antibody
Related articles to: NEO1 antibody
- Restoration of vascular structure and function is pivotal for neurological recovery following spinal cord injury (SCI), yet repairing the blood-spinal cord barrier (BSCB) remains a significant challenge. In this study, we demonstrate that exosomes (Exos) derived from endothelialized human umbilical cord mesenchymal stem cells (E‑UCMSCs) markedly enhance angiogenesis, improve vascular function, and promote neurological recovery. Human umbilical cord mesenchymal stem cells were induced to differentiate into endothelial‑like cells, and RNA‑sequencing revealed upregulation of genes associated with angiogenesis and vascular barrier integrity, alongside activation of relevant signaling pathways. In a co‑culture system, E‑UCMSC‑derived Exos significantly enhanced bEnd.3 cell migration and BSCB stability. To enable targeted delivery to neovasculature, Exos were engineered with RGD peptides (RGD‑E‑UCMSC‑Exos) via lentiviral modification. In vivo, these modified Exos preferentially localized to neovascular endothelial cells, promoted angiogenesis, reinforced BSCB integrity, and improved neurological outcomes in SCI mouse models. Proteomic profiling identified key angiogenic and barrier‑stabilizing factors carried by RGD‑E‑UCMSC‑Exos, including MMP2, FLT1, TIMP1, GAS6, CTHRC1, and NEO1, which likely mediate their therapeutic effects. Collectively, these findings provide novel mechanistic insights and establish a novel strong preclinical foundation for exosome‑based therapies in SCI. - Source: PubMed
Publication date: 2026/03/26
Liu QuanboZhang WentaoXue JingboLi XuelinTan JinghuaXu ZhunWang MingLi YunlongOuyang ZhihuaWang ChengYan YiguoJiang LiyuanXie Yong - Cerebral microbleeds (CMBs) are small vascular lesions detectable on MRI and are associated with increased stroke risk and cognitive decline. However, imaging-based diagnosis is limited by cost and accessibility. This study aimed to identify serum protein biomarkers for early CMB diagnosis and to elucidate molecular mechanisms underlying CMB subtypes. - Source: PubMed
Publication date: 2026/03/05
Yin Wu-MengHe Liu-ChangHan Guang-YiLi An-MingZhu Hang-HangCao YuanXue Xin-LiZhang LeiShi Chang-HeXu Yu-MingWang Yun-Chao - Astrocytes coordinate vascular homeostasis and tissue clearance in the brain, yet how these functions are mechanistically integrated remains unclear. Here, we identify neogenin (NEO1) as a cortex-specific astrocytic regulator that links angiogenesis with phagocytosis. Astrocyte-specific deletion of NEO1 in the mouse cortex, but not the hippocampus, leads to elevated HIF1/2α levels, increased expression of the angiogenic factor VEGFa, and reduced expression of the phagocytic receptor MEGF10. Mechanistically, loss of NEO1 induces intracellular iron deficiency, resulting in impaired prolyl hydroxylase-dependent degradation of HIF1/2α. This iron dysregulation is associated with reduced hepcidin expression and increased levels of the iron exporter ferroportin. Stabilized HIF1/2α preferentially engages HIF1β-p300 complexes at the VEGFa promoter to promote angiogenesis while reducing HIF1β-p300 occupancy at the MEGF10 promoter, thereby suppressing phagocytic gene expression. Together, these findings establish NEO1 as a critical cortical astrocytic regulator that balances vascular remodeling and phagocytic capacity through control of iron homeostasis and HIF-dependent transcription. - Source: PubMed
Publication date: 2026/03/10
Yao Ling-LingLee DaehoonWu Min-YiZou Wen-JunRen XiaoHu Jin-XiaWu AnikaXiong LeiMei LinXiong Wen-Cheng - The influence of paternity on progeny quality, particularly during early developmental stages, has long been underappreciated. However, altered sperm phenotypes are increasingly recognized as effective tools for identifying paternal-effect-associated genes (PEAGs), whose expression in the progeny is influenced by genetic or non-genetic factors carried by the sperm. This study investigated the impact of post-thaw sperm storage (PTS) as a stressor to verify its effect on larval performance in common garden rearing trial and to reveal PEAGs in Eurasian perch (Perca fluviatilis) progeny. In vitro fertilizations were performed using cryopreserved sperm that was either used immediately after thawing (0 min; CON) or after 30 min of post-thaw storage at 4 °C. - Source: PubMed
Publication date: 2026/02/20
Panda AbhipsaWałdowska SylwiaPalińska-Żarska KatarzynaDebernardis RossellaNynca JoannaRożyński RafałMajewska Anna MJastrzębski Jan PŻarski Daniel - Neogenin (NEO1) is a ubiquitously expressed multifunctional receptor. It binds members of the repulsive guidance molecules (RGM), RGMa, RGMb, and hemojuvelin (HJV). While RGMa and RGMb binding to NEO1 are necessary for neural development, more recent studies demonstrated that the Neo1-Hjv interaction in hepatocytes plays a pivotal role in iron homeostasis by facilitating hepcidin expression through the bone morphogenetic protein (BMP)-signaling pathway. Hepcidin is an iron regulatory hormone. In mice, ablation of Neo1 or Hjv reduces hepcidin and causes iron overload. Similar effects occur upon disruption of the Neo1-Hjv association. Besides HJV, NEO1 also interacts with matriptase-2 (MT2), a key suppressor for hepcidin expression. MT2 mutations result in an inappropriately high hepcidin and iron-refractory iron-deficiency anemia in humans. MT2 is a membrane-anchored serine protease. It can cleave multiple components of the hepcidin induction pathway in vitro, including HJV. In this study, we investigated the roles of Neo1-Mt2 interaction in hepcidin expression in vivo. In contrast to the observations that Mt2 cleaves Neo1 and markedly reduces Neo1 levels in cultured hepatoma cells, we found that Mt2 stabilizes Neo1 in murine liver. Studies in mice suggest that Mt2 suppression of hepcidin relies on the presence of Neo1. Additional investigations imply that the major function of hepatic Neo1 is to set the basal levels of hepcidin expression. Together, these data along with the evidence that Mt2 also suppresses the function of Hjv, support the model that Mt2 suppression of hepatic hepcidin is achieved by inhibiting the Neo1/Hjv-induced Bmp-signaling pathway. - Source: PubMed
Publication date: 2026/01/12
Enns Caroline AJue ShallZhang An-Sheng