Ask about this productRelated genes to: GUCY1B3 antibody
- Gene:
- GUCY1B1 NIH gene
- Name:
- guanylate cyclase 1 soluble subunit beta 1
- Previous symbol:
- GUC1B3, GUCY1B3
- Synonyms:
- GC-SB3, GC-S-beta-1
- Chromosome:
- 4q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-09
- Date modifiied:
- 2017-11-24
Related products to: GUCY1B3 antibody
Related articles to: GUCY1B3 antibody
- Our previous studies have shown that acid-sensitive ion channel 1a (ASIC1a) promotes lipopolysaccharide (LPS)-induced acute lung injury (ALI), but the exact mechanism is unclear. This study explores the potential mechanism by which ASIC1a promotes ALI and provides new ideas for the development of new drugs. - Source: PubMed
Publication date: 2026/03/13
Zhang AnqiZhu YueqinChen HaoyangLv XiaoyuZhang TingtingRen RuohanWang YuyanXu HuXu ZhouLi ZihaoQian ShishunZhang JingrongLi MengxueHu XiaojieCao ChunAbou-Elnour AmiraDing ZhenxingWang JiajiaHuang Yan - Primary graft dysfunction (PGD) usually occurs within 72 hours after lung transplantation and is primarily caused by ischemia-reperfusion injury (IRI). Patients who develop PGD after lung transplantation tend to have a poor prognosis. However, effective clinical strategies to reduce the incidence of primary graft dysfunction remain limited. Therefore, a comprehensive understanding of the mechanisms underlying lung ischemia-reperfusion injury is essential for improving outcomes in lung transplant recipients. - Source: PubMed
Publication date: 2026/02/25
Zhu LongfeiDing JiaqiWei DongChen Jingyu - Alzheimer's disease (AD) is a progressive neurodegenerative age-related disorder characterized by widespread transcriptional deregulation across multiple brain regions. Among the molecular players involved, the transcription factors (TFs) can regulate the expression of AD-related peptides (β-amyloid and tau). We aim to unveil reconstructed TF-centered networks and their dynamics across multiple brain regions. In this study, we conducted an exhaustive differential gene expression analysis, reconstructed TF-TF-centered regulatory networks, and performed master-regulation analyses across multiple regions. We used bulk RNA-seq data from 2,229 post-mortem samples from the ROSMAP, MAYO, and MSBB cohorts. To place these regulatory programs in a disease-relevant context, we integrated protein-protein interaction (PPI) data, experimental TF-target data, and AD-associated genetic risk loci as a translational layer. We assessed TF-centered regulons for 1,605 TFs and identified 354 master-regulators (MR-TFs) across multiple brain regions, including the parahippocampal gyrus, temporal cortex, and cerebellum, which exhibited the highest numbers of regulons. Overall, regulons fell within a moderate size range (median 55 targets), rather than into extensive large networks. Novel MR-TFs, including ADCYAP1, TEAD2, BCL6, MAFF, NFKBIA, were consistently identified as MR-TFs across tissues in AD. Furthermore, GUCY1B1, RBFOX2, and MEF2C were found conserved in the parahippocampal gyrus, inferior frontal gyrus, and posterior cingulate cortex. Additionally, our work identified the well-known AD-related genes BIN1, EGFR, and SPI1 as MR-TFs, reinforcing their functional roles as susceptibility risk markers in AD. This work established an MR-TF-centered integrated regulatory network map of AD, revealing MR-TFs as factors that orchestrate gene deregulation in a region- and cell-context-dependent approach, and providing a robust foundation for mechanistic and translational investigations in neurodegeneration. - Source: PubMed
Publication date: 2026/02/23
Belém-Souza Marcella VitóriaBarra-Matos Gustavode Araújo Gilderlanio Santana - Radiotherapy often causes severe and irreversible neural damage, including cognitive impairment and depression-like behaviors. Current mitigants are limited, with single-target molecules being ineffective and nanomedicines posing complexity and toxicity risks. Dragon's Blood (DB), a nontoxic, brown-red resin extracted from (Lour.) (S. C. Chen, China), possesses diverse pharmacological properties. Extensive studies demonstrated that the compounds in DB exhibit multiple therapeutic effects, including cardiovascular protection, promotion of blood circulation, and anti-inflammatory effect. Herein, DB's neuronal radiation mitigation effect and mechanism were investigated. In a whole-brain irradiation rat model, DB administration significantly alleviated radiation-induced anhedonia-like behavior, normalized calcium dyshomeostasis, restored mitochondrial membrane potential, mitigated dendritic spine loss, suppressed neuroinflammation (IL-1β and TNF-α), and preserved hippocampal cytoarchitecture. Brain tissue proteomics revealed 23 DB-modulated KEGG pathways, encompassing the glutamatergic/GABAergic synapse, synaptic plasticity, addiction-related pathways, calcium/cAMP signaling, and hormonal regulation. Ensemble analysis integrating proteomics, WGCNA, machine learning, and PPI pinpointed 24 DB radiation mitigation-related proteins. Among these, eight targets (Grin1, Gabra4, Grm2, Grm3, Grm7, Prkcb, Shank3, and Pak7) functioning via ligand-target interactions were dysregulated by radiation and restored by DB. Molecular docking identified three DB ingredients (socotrin-4'-ol, cinnabarone, and 2'-methoxysocotrin-5'-ol) interacted with all eight targets. Plasma proteomics further revealed radiation mitigation-related brain-enriched proteins (Mib1, Gucy1b1, Fkbp1a, Synj1, and Clasp2). PPI between these 5 plasma proteins and 24 brain proteins reveals DB's multitarget radiation mitigation effect on neurotransmission and synaptic regulation, neuroplasticity, and signaling transduction and cellular response. This work nominated DB and its key constituents as promising candidates for mitigating radiotherapy-induced neural injury. - Source: PubMed
Publication date: 2025/11/25
Li BoyangHan ChuZhang HanLi Bo - Cardiovascular diseases (CVDs), including myocardial infarction (MI), heart failure (HF), atrial fibrillation (AF), and arrhythmia, are major contributors to global mortality and often share overlapping risk factors and pathophysiological mechanisms. While genome-wide association studies (GWAS) have identified many loci for individual CVDs, the shared genetic architecture across related traits-particularly in East Asian populations-remains underexplored. - Source: PubMed
Publication date: 2025/06/24
Zhong PengZhang ChumengWu QinfengChang Xiao