Ask about this productRelated genes to: NPDC1 antibody
- Gene:
- NPDC1 NIH gene
- Name:
- neural proliferation, differentiation and control 1
- Previous symbol:
- -
- Synonyms:
- DKFZp586J0523, CAB-, CAB1
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-08-11
- Date modifiied:
- 2016-09-09
Related products to: NPDC1 antibody
Related articles to: NPDC1 antibody
- Myocardial infarction (MI) remains a leading cause of global morbidity, often progressing to irreversible ischemic cardiomyopathy due to the limitations of current pharmacological interventions in arresting adverse remodeling. Here, we combined whole-transcriptome sequencing with bioinformatic prioritization in a murine MI model to identify circClint1 as a pivotal, upregulated mediator within the infarcted microenvironment. Mechanistically, luciferase reporter assays and RNA pull-down confirmed that circClint1 functions as a competitive endogenous RNA (ceRNA) for miR-378b, thereby sequestering the miRNA and preventing the targeted degradation of its downstream effector, NPDC1. Notably, both in vivo Western blot and immunofluorescence revealed that ischemic stress triggers a dramatic and spatiotemporal accumulation of NPDC1 protein, particularly within the cytoplasm of peri-infarct cardiomyocytes. Functionally, we established an AAV9-mediated myocardial-specific overexpression model to evaluate the pathological consequences of sustained NPDC1 elevation. Our results demonstrated that NPDC1 accumulation significantly exacerbates post-infarction damage by promoting TUNEL-positive cardiomyocyte apoptosis, intensifying fibrotic remodeling, and impairing the myocardial microcirculation. Conversely, siRNA-mediated genetic silencing of NPDC1 in HL-1 cardiomyocytes effectively attenuated hypoxia-induced oxidative stress, preserved mitochondrial membrane potential, and improved cell viability. Collectively, this study provides definitive evidence that the circClint1/miR-378b/NPDC1 axis is a master detrimental driver of post-MI progression. By elucidating the multi-dimensional role of NPDC1 in coordinating cell death and impaired revascularization, our findings identify this axis as a promising therapeutic target for mitigating myocardial injury and improving long-term cardiovascular outcomes. - Source: PubMed
Publication date: 2026/05/08
Zhang XinZhu XingyuDang ZijianChen MingzheTian JiayinGuo XiaoqingGuo RuxingHan ChutongShen NanaLi XinggeLiu JieWu XiaopengYang YangChang HuiJin Zhenxiao - Autoimmune liver diseases (AILDs), including primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and autoimmune hepatitis (AIH), pose significant diagnostic and therapeutic challenges due to poorly understood mechanisms. While most studies focus on absolute protein levels, protein-protein ratios (PPRs), reflecting the relative abundance of paired plasma proteins, emerge as critical yet understudied biomarkers for decoding disease-specific network perturbations. To harness this potential, we integrated protein quantitative trait loci (pQTLs), ratio QTLs (rQTLs), and mediation Mendelian randomization (MR) to map causal proteomic networks, aiming to unravel pathogenic networks and identify therapeutic targets in AILDs. Using two-sample MR, we analyzed 2821 plasma PPRs and 2923 individual proteins from the UK Biobank Pharma Proteomics Project. The primary analysis employed the inverse-variance weighted (IVW) method, complemented by MR-Egger regression, weighted median, simple mode, and weighted mode methods, all within a random-effects model. Sensitivity analyses were performed to validate the findings, including Cochran's Q test, MR-Egger intercept analysis, MR-PRESSO, and Steiger filtering. Cross-trait linkage disequilibrium score regression (LDSC) quantified genetic correlations, while the MR approach based on Bayesian model averaging (MR-BMA) prioritized independent causal PPRs. Two-step mediation MR identified mechanistic pathways. Functional enrichment and protein-protein interaction (PPI) networks were constructed using STRING and the clusterProfiler package. Finally, we investigated the associations between the causal PPRs and AILD-related symptoms/complications, as well as the influence of modifiable lifestyle factors on these PPRs. CD74 exhibited dual roles in AILDs. Elevated plasma CD74 levels were associated with an increased risk of PSC (OR = 1.54, 95% CI 1.24-1.90), whereas CD74-PPRs exhibited robust protection. Specifically, CD74/JAM2 reduced risks of PSC (OR = 0.70, 95% CI 0.59-0.83) and AIH (OR = 0.53, 95% CI 0.39-0.71), while CD74/NPDC1 conferred protection against PSC (OR = 0.66, 95% CI 0.54-0.80). Mediation MR identified TRY3 as the dominant mediator of CD74/JAM2 in AIH (91.52% proportion mediated, P = 0.017), with GREM1 and TEK mediating CD74/NPDC1 effects in PSC. PPI networks implicated interactions among CD74, amyloid precursor protein (APP), and endoglin (ENG). Notably, CD74/JAM2 demonstrated cross-disease relevance, significantly lowering PSC-associated ulcerative colitis risk (OR = 0.35, 95% CI 0.22-0.54). This study pioneers the integration of pQTLs, rQTLs, and mediation MR to map dynamic proteomic interactions in AILDs. Our findings revealed the multifaceted impact of CD74 on AILDs: its direct elevation may promote disease, whereas its protein interactions appear to mitigate risk. These results advance understanding of AILD pathogenesis and pave the way for developing novel biomarkers and targeted therapies. - Source: PubMed
Publication date: 2026/03/12
Tian DianzheYang ZuyiZhao LvyuxingZhao HaitaoSang XintingDu ShundaLuo YunpingZhang LeiXu YiyaoLu Xin - Heart failure (HF) and its main subtypes, heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF), impose an enormous health burden on elders. Assessment of the circulating proteome to illuminate pathogenesis could open new opportunities for treatment. - Source: PubMed
Publication date: 2026/02/04
Njoroge Joyce NSanders van Wijk SandraAustin Thomas RBrody Jennifer ASitlani Colleen MHamerton EmilyBis Joshua CHenry AlbertLumbers R Thomas Seshaiah TaliaShojaie AliYang YiminLamberson VictoriaYu BingShah Amil MBansal NishaShah Sanjiv JTracy Russell PGerszten Robert EJennings Lori LGudmundsdottir ValborgGudnason VilmundurEmilsson ValurPsaty Bruce MKizer Jorge R - Colorectal cancer (CRC) ranks as one of the leading causes of cancer-related mortality globally. NPDC1 is a novel regulator involved in cell proliferation and is upregulated in CRC. However, the biological function and mechanism of NPDC1 driving CRC progression have not been investigated. - Source: PubMed
Publication date: 2026/01/24
Qin QingZhang DapengXie YusaiZhang FanHuang YulanDeng RenchaoYang MinliZhang LiliLiang HoujieShi Rongchen - α-Synuclein (α-syn) fibrils accumulate in Parkinson's disease, spreading between cells to template misfolding and drive neurodegeneration. α-Syn fibril entry into healthy neurons is a key step. Here, we comprehensively assessed the membrane proteome for α-syn fibril binding. We identified mGluR4 and NPDC1 as nigral surface proteins binding and internalizing α-syn fibrils. While striatal α-syn fibril injection led to nigral dopamine neuron loss in wild type mice, deletion of either Grm4 or Npdc1 provided protection of dopamine neurons. We observed mGluR4 and Npdc1 to form a complex regulating mGluR4 function. Cultured neurons lacking both Grm4 and Npdc1 fail to bind α-syn fibrils, to accumulate phosphorylated α-syn and to lose synapses. Transheterozygous Grm4, Npdc1 mice showed protection of nigral neurons from α-syn fibrils, demonstrating genetic interaction. For transgenic α-syn A53T mice, double Grm4, Npdc1 heterozygosity increased mouse survival, motor function and spinal motoneuron number. Thus, a cell surface mGluR4-NPDC1 complex participates in α-syn neurodegeneration. - Source: PubMed
Publication date: 2025/12/25
Perez-Canamas AzucenaChen MingmingAlmandoz-Gil LeireKhan NababTang Si JieHo AllysonGunther Erik CStrittmatter Stephen M