Ask about this productRelated genes to: NEGR1 antibody
- Gene:
- NEGR1 NIH gene
- Name:
- neuronal growth regulator 1
- Previous symbol:
- -
- Synonyms:
- KILON, MGC46680, Ntra, IGLON4
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-09
- Date modifiied:
- 2014-11-19
Related products to: NEGR1 antibody
Related articles to: NEGR1 antibody
- Depot-specific fat deposition influences carcass yield and meat quality in ducks. To explore regulatory mechanisms, we profiled adipogenic progenitor cells (APCs) from pectoral muscle (PM), subcutaneous (SAT), and visceral adipose tissue (VAT) using single-cell RNA sequencing. Nine major cell types were identified, with APCs being most abundant in VAT and least abundant in PM, consistent with histological findings. Transcriptomic comparisons revealed depot-specific microenvironments: PM was enriched with myogenic-related pathways, SAT with immune and inflammatory responses, and VAT with pro-adipogenic signaling. Next, APCs were regrouped into 5 subclusters. Cluster 0 (PI16 PDGFRB) enriched in SAT/VAT showed activated signaling of BMP and glycolysis, indicating strong adipogenic potential. Cluster 1 (PDGFRA F3) enriched in PM was associated with Wnt signaling, which maintains APCs in a progenitor state. Cell cycle, RNA velocity, and pseudotime analyses indicated that APCs of SAT/VAT were more advanced in differentiation, while APCs of PM retained stronger proliferative capacity. Cell-cell communication analysis further revealed more active paracrine regulation within SAT/VAT, while APCs from PM showed limited signaling interactions. Key depot-specific regulators were identified, including NEGR1 (PM), CD36 (SAT), and RSPO2 (VAT), which may contribute to regulations of the adipogenic process. This study provides the first single-cell atlas of duck APCs across depots, revealing molecular heterogeneity, lineage dynamics, and niche-specific regulation. These findings advance understanding of depot-specific adipogenesis and offer targets to enhance IMF while limiting excessive SAT and VAT, thereby improving both meat quality and production efficiency. - Source: PubMed
Publication date: 2026/04/23
Wang ZhixiuYang ChunyanLiu SuliJiang YongBai HaoChang GuobinChen GuohongZhao Liang - Frailty, a clinical state of increased vulnerability to stressors with aging, imposes significant strain on healthcare systems. Its genetic underpinnings remain incompletely explored, highlighting the need to identify novel therapeutic targets for aging. - Source: PubMed
Publication date: 2026/04/01
Zhong JiaYuYuan MingHaoZhou EnHu Shuo - Chagas disease, caused by , affects over seven million people worldwide. Vertical transmission during pregnancy contributes to the urban spread of the disease, including in non-endemic regions. Although the placenta constitutes a critical barrier against fetal infection, the molecular mechanisms underlying congenital transmission remain poorly understood. To identify placental factors associated with transmission, we performed a transcriptomic analysis of placental tissues from deliveries of congenitally infected (M+B+), exposed but uninfected (M+B-), and unexposed/uninfected (M-B-) newborns. Differential gene expression analysis comparing M+B+ and M-B- placentas revealed overexpression of CEMIP (cell migration-inducing hyaluronidase 1), involved in extracellular matrix (ECM) remodeling and intracellular transport, together with ENSG00000304767, a novel long non-coding RNA located intronically within . In contrast, PRRX1 (paired related homeobox 1), CADM3 (cell adhesion molecule 3), and CDH11 (cadherin 11), genes associated with transcriptional regulation and cell-cell adhesion, were underexpressed. In the M+B- versus M-B- comparison, MIR4300HG, a long non-coding RNA hosting , was overexpressed, whereas CGB5 (chorionic gonadotropin subunit beta 5), essential for pregnancy maintenance, was underexpressed. Direct comparison between M+B+ and M+B- placentas showed overexpression of the -associated lncRNA and CGB5, accompanied by downregulation of CADM3, NEGR1, PDPN, and CDH11, implicating altered adhesion and structural pathways in transmission. Overall, these findings indicate that placental cell adhesion and ECM integrity are disrupted in transmitting placentas. Gene set enrichment analysis using the Gene Ontology library revealed alterations of immune-related pathways in both infected mother groups, while highlighting ECM-related processes-particularly collagen organization and metabolism-as key contributors to transmission events. Cell type enrichment analysis showed overrepresentation of extravillous trophoblasts in M+B+ placentas, with the opposite pattern observed in M+B- cases. Conversely, syncytiotrophoblasts and villous cytotrophoblasts were enriched in non-transmitting placentas relative to controls. Immune-associated placental cell types were consistently reduced in both infected groups. Co-expression network analysis further confirmed compromised placental signaling and structural integrity in transmitting cases, identifying ENPP1 and SLC16A10 as central hub genes. Together, these RNA-seq data define key placental transcriptional alterations associated with congenital transmission which, upon future experimental validation may provide insights into molecular mechanisms governing fetal protection or susceptibility. - Source: PubMed
Publication date: 2026/03/18
Apodaca SofiaCampos Emiliano ECalupiña Kevin DDavies CarolinaLucero Raúl HLonghi Silvia AKamenetzky LauraZago Maria PaolaSchijman Alejandro G - Neuronal growth regulator 1 () is an IgLON cell adhesion molecule significantly associated with depression risk in genome-wide association studies. Since the role of NEGR1 in depression pathophysiology remains incompletely understood, we investigated changes in -associated gene expression levels in stress-susceptible male mice exposed to chronic restraint stress. - Source: PubMed
Mingardi JessicaSalluzzo MarcoRimondini RobertoMusazzi LauraCarboni Lucia - NEGR1 (neuronal growth regulator 1) has been genetically linked to metabolic and neuropsychiatric disorders; however, its cellular function in insulin-responsive tissues remains poorly understood. Here, we investigated the role of NEGR1 in regulating actin cytoskeletal dynamics and insulin-stimulated GLUT4 trafficking in skeletal muscle. We found that loss of reduced GLUT4 abundance selectively in predominantly glycolytic skeletal muscles in vivo. Despite preserved insulin-induced Akt phosphorylation, insulin-stimulated GLUT4 translocation was markedly impaired in both Negr1-deficient and NEGR1-overexpressing muscle cells. Mechanistically, deficiency was associated with enhanced PAK-cofilin signaling and excessive intracellular F-actin accumulation that likely impedes GLUT4 vesicle trafficking. In contrast, NEGR1 overexpression did not increase total F-actin content but induced abnormal peripheral actin organization, resulting in constitutive GLUT4 surface localization and elevated basal glucose uptake. Consistent with these findings, both loss and overexpression of NEGR1 disrupted insulin-induced Rac1-dependent actin remodeling without affecting Akt signaling. Collectively, these results identify NEGR1 as a critical modulator of actin homeostasis required for proper insulin-stimulated GLUT4 trafficking and glucose uptake in skeletal muscle, providing mechanistic insight into the metabolic abnormalities associated with NEGR1 dysregulation. - Source: PubMed
Publication date: 2026/03/28
Yun Seo-YoungLee Soojin