Ask about this productRelated genes to: NNAT Blocking Peptide
- Gene:
- NNAT NIH gene
- Name:
- neuronatin
- Previous symbol:
- -
- Synonyms:
- Peg5
- Chromosome:
- 20q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-29
- Date modifiied:
- 2019-04-23
Related products to: NNAT Blocking Peptide
Related articles to: NNAT Blocking Peptide
- Neuronatin (NNAT) is small transmembrane protein involved in a wide range of physiological processes, such as white adipose tissue browning and neuronal plasticity, as well as pathological ones, such as Lafora disease caused by the formation of NNAT aggregates. However, its 3D structure is unknown, and its mechanism of action is still unclear. In this study the two most well-known NNAT isoforms (α and β) were modelled and the interaction with the SERCA2b calcium pump was assessed using computational methods. First, molecular docking identified the same binding region as the one described for phospholamban, a thoroughly described SERCA inhibitor. Then, analyses of the flux of water molecules during molecular dynamics simulations highlighted significant similarities between the behavior of SERCA2b when in complex with phospholamban, and when in complex with either NNAT isoform. These results suggest that NNAT could be considered a "regulin-like" protein. Additional all-atom and coarse-grained simulations of multiple copies of NNAT highlighted a significant aggregation potential of both NNAT isoforms, supporting experimental data. - Source: PubMed
Publication date: 2026/04/09
Ben Mariem OmarCoppi LaraDe Fabiani EmmaEberini IvanoCrestani Maurizio - Idiopathic recurrent pregnancy loss (IRPL), defined as two or more consecutive pregnancy losses without an identifiable cause, affects 1-2 % of couples in their reproductive years. While maternal factors have been extensively studied, paternal contributions remain underexplored. Paternally imprinted genes are essential for spermatogenesis, embryonic development, and placental function, and their epigenetic dysregulation may contribute to IRPL. - Source: PubMed
Publication date: 2025/12/14
Hashemi Karoii DanialNajafi S Mahmoud AFavaedi RahaEsmaeili Borzabadi VahidSabbaghian MarjanAmirchaghmaghi ElhamShahhoseini Maryam - Growing evidence has established the imprinted gene neuronatin (NNAT) as a key regulator in human metabolic disorders, particularly obesity and type 2 diabetes. Its expression is prominently detected in major neuroendocrine and metabolic tissues, including the hypothalamus, pancreas, adipose tissue, and skeletal muscle. NNAT orchestrates diverse cellular processes through its regulation of intracellular calcium dynamics and pathological insulin secretion. Notably, NNAT exhibits nutrient-responsive regulation and is a crucial modulator of glucose homeostasis, adaptive thermogenesis, and overall energy balance. These pleiotropic functions position NNAT as an attractive therapeutic target for obesity-related metabolic disorders. This comprehensive review systematically evaluates the multifaceted roles of NNAT in metabolic regulation, with a particular focus on its tissue-specific mechanisms in both physiological and pathological states while integrating the current understanding of its contributions to systemic metabolic homeostasis. - Source: PubMed
Zhang TingJu WantaoHan XinyuLiu Yanjun - This study aims to delineate the mechanisms through which intraperitoneal injection of gentamicin (GEN) influences the inner ear cells of mice by employing single-cell RNA sequencing (scRNA-seq) technology. - Source: PubMed
Publication date: 2025/11/21
Bao XiaolinWang YuanLiu WeiTang HuilingGuo Yufen - Cerebral ischemia-reperfusion injury (CIRI) involves oxidative stress, inflammation, and regulated cell death, among which ferroptosis has emerged as a key contributor. However, therapeutic strategies targeting ferroptosis remain limited. This study investigated whether Ciwujianoside C (CC), a triterpenoid saponin from Acanthopanax senticosus, protects against CIRI by modulating ferroptosis via the NNAT/NF-κB pathway. In MCAO/R rats, CC reduced infarct size, improved neurological scores, and ameliorated oxidative stress and ferroptosis markers. In BV2 microglia and HT22 cells (a mouse hippocampal neuronal cell line) subjected to OGD/R, CC enhanced cell viability, decreased iron accumulation, and restored GPX4 and FTH1 expression while inhibiting NF-κB activation. Importantly, NNAT knockdown abolished these protective effects, demonstrating NNAT as a critical mediator. These findings reveal that CC protects against CIRI by suppressing ferroptosis through the NNAT/NF-κB axis, highlighting NNAT as a potential therapeutic target in CIRI. - Source: PubMed
Publication date: 2025/11/29
Dai WeichuanChen YingxianCai WenhuaZhu YuyanGuo Xieli