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
- MicroRNA-122 (miR-122) is the most abundant liver-specific microRNA, comprising ~ 70% of the hepatic miRNA pool, and a central regulator of lipid metabolism, inflammation, fibrosis, viral replication, and hepatocarcinogenesis. This review synthesizes experimental, clinical, and molecular evidence on the role of miR-122 across the spectrum of liver disease, including metabolic dysfunction-associated fatty liver disease (MAFLD) and steatohepatitis (MASH), drug-induced acute liver injury, hepatitis B and C virus (HBV/HCV) infection, hepatocellular carcinoma (HCC), and colorectal cancer liver metastasis. Mechanistically, miR-122 governs hepatic lipogenesis through the Sirt1/LKB1/AMPK axis, modulates inflammation via LPS/TLR-4/FoxO3 signaling, and exerts tumor-suppressive and antiviral effects through Cyclin G1/p53, HO-1, NDRG3, GALNT10, PEG10, and NEGR1. A recurring theme is the compartment- and stage-dependent behavior of miR-122: hepatic expression declines with disease progression, whereas circulating levels rise with hepatocyte injury, reconciling apparently contradictory reports and underscoring the importance of specimen source and disease stage in biomarker interpretation. We further contrast the etiology-specific regulation of miR-122 in HBV- versus HCV-associated disease, in which epigenetic silencing and interferon-linked mechanisms drive divergent expression. Finally, we critically appraise the failed clinical translation of anti-miR-122 therapeutics (miravirsen, RG-101), highlighting viral resistance, safety liabilities, and the tumor-suppressor paradox that constrains inhibition-based strategies. Collectively, miR-122 emerges as a minimally invasive biomarker and a biologically informative, though therapeutically challenging, target in liver disease. - Source: PubMed
Publication date: 2026/09/19
Ahmadova SaraWicik ZofiaMucha JoannaPalatini JeffZiętal KatarzynaMirowska-Guzel DagmaraPrzybylkowski AdamEyileten Ceren - Feeding behavior is a key factor influencing growth performance and feed efficiency in poultry, yet its complex phenotypes remain difficult to quantify accurately, limiting the application of large-scale behavioral data in genetic and molecular analyses. In this study, feeding behavior and feed efficiency-related phenotypes were recorded in 829 Tianfu Nonghua ducks using an automated feeding monitoring system integrated with radio frequency identification (RFID) technology. Genetic parameter estimation indicated that the heritability of feeding behavior traits ranged from 0.25 to 0.39. Individuals were classified into high-frequency feeding (HFF) and low-frequency feeding (LFF) groups. Phenotypic analysis showed that ducks in the HFF group had significantly higher residual feed intake (RFI) and feed conversion ratio (FCR) than those in the LFF group. Based on this grouping, transcriptome sequencing was performed on the hypothalamus, pituitary, and liver tissues. A total of 266, 181, and 94 differentially expressed genes (DEGs) were identified in the three tissues, respectively. Enrichment analysis highlighted tissue-specific pathways, including neuroactive ligand-receptor interaction and calcium signaling in the hypothalamus, the Apelin signaling pathway in the pituitary, and steroid hormone biosynthesis in the liver. Appetite-related genes in the hypothalamus (PMCH, HCRT, and CCKAR) and endocrine and metabolic genes in the pituitary and liver (TRH and NEGR1) showed differential expression between feeding strategies. Weighted gene co-expression network analysis further identified hub genes (ITPKB, BAMBI, and BCKDHB) associated with total feeding bouts (TFB). These findings provide new insights into the genetic architecture of feeding behavior traits and the molecular differences associated with divergent feeding patterns in ducks. - Source: PubMed
Publication date: 2026/04/28
Guo ShihaoLiu XingXi YangQi JingjingYang ZhaoHan XuLing WeikangBai LiliHuang AnqiHu JiweiLi LiangLiu Hehe - Traumatic brain injury (TBI) can cause severe neurological damage. Ferroptosis, a recently discovered form of iron-regulated cell death, is closely associated with TBI. Cannabidiol (CBD) has been demonstrated to exhibit neuroprotective effects. However, the antiferroptotic role of CBD in TBI remains unclear. Investigating whether CBD inhibits ferroptosis after brain injury and its underlying mechanisms is of great significance. We find that ferroptosis can be induced in rats after TBI, and CBD significantly inhibits ferroptosis in TBI rats both and . MicroRNAs (miRNAs) are highly expressed in the brain. Differentially expressed miRNAs and mRNAs after TBI are detected by RNA sequencing, and miR-320-3p, Negr1, and the ERK/MEK pathway are screened out due to their strong correlations. The results show that CBD inhibits miR-320-3p expression, increases Negr1 expression, and suppresses the ERK/MEK pathway both and . Mechanistically, transfection with miR-320-3p mimics or siNegr1 inhibits the intervention effect of CBD on ferroptosis and the ERK/MEK pathway. Additionally, gene silencing reverses the effect of the miR-320-3p inhibitor on ferroptosis factors in PC12 cells, which suggests that miR-320-3p can target . In conclusion, our findings indicate that CBD can inhibit TBI-induced ferroptosis through the miR-320-3p/Negr1/ERK signaling axis. - Source: PubMed
Publication date: 2026/01/25
Li JialiCao YanLing TenghanLuo XinyuanLi HengxiYin AipingJiang HongyanGuo XiaobingYang LiWu HaiyingLi Ping - Integrated genomic evidence on shared genetic architecture between obesity and psychiatric disorders remains limited. This work utilized multi-level genomic analytic approaches to identify pleiotropic loci, variants, and genes between 14 adiposity traits and 7 psychiatric disorders, including genetic correlation and bidirectional causality as well as gene expression, functional pathway, and druggability, using genome-wide association study data from up to 806,834 individuals of European descent. Based on 67 genetically correlated trait pairs established between the two groups, we identified 17 causal shared genes across 26 tissues, which were enriched in neurodevelopment, neuronal function, cellular transport, and developmental biology. Of these, , , , and were located in the druggable genome, and and were clinically actionable. Mendelian randomization further supported extensive bidirectional causal associations. These findings provide robust evidence for a shared genetic etiology between adiposity and psychiatric disorders, underscoring mechanistic links and prioritizing actionable targets for comorbidity intervention. - Source: PubMed
Publication date: 2026/04/22
Liu DongDou ChunYe ChaojieChen MinglingKong LijieZhu ZhengZheng JieXu MinXu YuLi MianZhao ZhiyunLu JieliChen YuhongYuan ZhongshangNing GuangWang WeiqingBi YufangWang Tiange - Obesity, characterized by abnormal fat accumulation with comorbidities, continues to increase dramatically, particularly in the pediatric population. Identifying the environmental and genetic causes underlying the development of obesity during early childhood is crucial for establishing preventive and protective treatments for this complex disease. We aimed to investigate genetic variants related to non-syndromic early-onset childhood obesity. - Source: PubMed
Publication date: 2026/04/29
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