LCN2
- Known as:
- LCN2
- Catalog number:
- ENZ-297
- Product Quantity:
- 2µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- LCN2
Related genes to: LCN2
- Gene:
- LCN2 NIH gene
- Name:
- lipocalin 2
- Previous symbol:
- -
- Synonyms:
- NGAL, 24p3
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-29
- Date modifiied:
- 2016-10-05
Related products to: LCN2
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- Essential thrombocythemia (ET) is a myeloproliferative disorder characterized as excessive platelet production. Early and accurate diagnosis is critical to manage the disease and prevent progression to serious myeloid neoplasms like myelofibrosis or acute myeloid leukemia, though definitive diagnosis remains challenging. - Source: PubMed
Publication date: 2026/04/29
Li YeqiongChen XiangguoGuo YingSha RongrongHao HuichengZhang JinSong HonghongWei YupingYe Xiupeng - Prostate cancer (PCa) is a hormone-dependent tumor and one of the most prevalent cancers in men worldwide. PCa progression is influenced by its interaction with the surrounding tumor microenvironment, highlighting the role of periprostatic adipose tissue (PPAT), which modulates PCa behavior through the secretion of bioactive molecules (e.g., adipokines). However, the influence of this complex cell communication, particularly under altered metabolic conditions, remains to be fully elucidated. - Source: PubMed
Publication date: 2026/05/14
Pérez-Gómez Jesús MPrats-Escribano AntonioGil-Duque IgnacioArroyo-Millán LauraHuertas-Cabrera HugoNúñez-Santos Miguel ALópez-Ruiz Daniel JMata-Ordoñez FernandoGonzález-Serrano TeresaOrtea IgnacioPorcel-Pastrana FranciscoÁlvarez-Benito MarinaPlanque MélanieCarrasco-Valiente JuliaGómez-Gómez EnriqueGuzmán-Ruiz RocíoFuentes-Fayos Antonio CFendt Sarah-MariaGahete Manuel DSarmento-Cabral AndréMalagón María Del MarLuque Raúl M - Dysregulated iron handling-including catalytic iron and ferroptosis, hepcidin-ferroportin signaling, ferritin dynamics, and neutrophil gelatinase-associated lipocalin (NGAL)-mediated siderophore transport-has been implicated in the initiation and propagation of acute kidney injury (AKI) across ischemia-reperfusion, sepsis, and nephrotoxic contexts. To provide a SANRA-aligned narrative synthesis of mechanistic and translational evidence on iron biology in AKI, clarifying biomarker readiness and therapeutic prospects while explicitly separating preclinical from human findings. PubMed, Scopus, and Web of Science (1 January 2000 to 30 September 2025), plus appraised grey literature (guidelines/registries) using predefined criteria (authority, update recency, and methodological transparency). Narrative review with comprehensive database searches, single-reviewer screening/extraction (acknowledged as a limitation), and qualitative synthesis. Evidence is organized by pathway (catalytic iron/ferroptosis, transferrin (Tf)/transferrin receptor (/TfR), ferritin/ferritin heavy chain (FtH), hepcidin-ferroportin and NGAL) and translational domain (biomarkers and therapeutics). Statements are tagged as [Preclinical] or [Human]. Robust signals support roles for catalytic iron and ferroptosis, protection by iron chelation, hepcidin modulation, heme oxygenase 1 (HO-1)/FtH induction, and apotransferrin/NGAL-based strategies. Biomarkers such as NGAL show clinical utility for kidney injury detection, whereas catalytic iron assays (labile plasma iron [LPI]/bleomycin-detectable iron [BDI]) remain investigational with limited standardization. Observational links between iron-regulatory pathways and AKI risk exist, but interventional trials are sparse; dose, timing, and safety of iron-targeted strategies in defined AKI settings remain to be established. Iron-handling pathways are compelling targets for AKI prevention/mitigation, yet high-quality human trials are limited. Priorities include standardized catalytic-iron assays, biomarker-guided enrichment, and pragmatic trials of tractable interventions (e.g., peri-contrast or cardiopulmonary bypass settings). Until such evidence accumulates, recommendations beyond standard care should be avoided. - Source: PubMed
Publication date: 2026/04/24
Annamalai ChandrashekarViswanathan Pragasam - Ovarian cancer (OC) is a highly aggressive malignancy with poor prognosis and limited response to immunotherapy. Ribosomal stress, a cellular response to disrupted ribosome biogenesis, has been increasingly implicated in tumorigenesis and immune regulation, yet its contribution to OC remains unclear. - Source: PubMed
Publication date: 2026/05/11
Han XuechuanYu YanFan YangZhang Miao - Colchicine (COL) is known to ameliorate severe acute pancreatitis (SAP), yet the precise molecular mechanisms remain elusive. This study integrates bioinformatics with in vivo experimentation to elucidate the mechanism by which COL attenuates SAP. An SAP rat model was established via sodium taurocholate injection. Key therapeutic targets were screened using transcriptomics and network pharmacology. Mechanistic validation utilized AAV-mediated lipocalin-2 (LCN2) overexpression, the ferroptosis inhibitor ferrostatin-1 (Fer-1), and the ERK inhibitor PD98059. COL treatment significantly ameliorated pancreatic pathological injury, inflammatory cell infiltration, and cytokine release. LCN2 was identified as a pivotal target markedly upregulated in SAP but downregulated by COL. Crucially, LCN2 overexpression reversed COL's therapeutic benefits and restored ferroptosis markers (COX2, Fe2+, ROS) while suppressing anti-ferroptotic indices. Notably, this reversal was effectively abrogated by co-treatment with either Fer-1 or PD98059, confirming the involvement of the MAPK/ERK pathway. This study is the first to elucidate that COL inhibits ferroptosis in pancreatic acinar cells by downregulating LCN2 and subsequently suppressing the LCN2/MAPK/ERK signaling axis. These findings provide a novel molecular basis for COL and highlight a potential target for therapeutic intervention in SAP. - Source: PubMed
Publication date: 2026/05/11
Yang LiuZheng XiaoyiZhang YangLi YueLi LeiLiu Feng