APLP1 ELISA kit
- Known as:
- APLP1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-APLP1-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- APLP1 ELISA kit
Related genes to: APLP1 ELISA kit
- Gene:
- APLP1 NIH gene
- Name:
- amyloid beta precursor like protein 1
- Previous symbol:
- -
- Synonyms:
- APLP
- Chromosome:
- 19q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-18
- Date modifiied:
- 2016-01-21
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- Prostate cancer (PCa) progression to treatment-related neuroendocrine PCa (t-NEPC) often involves an early neuroendocrine differentiation (NED) phase lacking identified biomarkers. We utilized GeoMx Digital Spatial Profiling and single-cell RNA sequencing on human PCa tissues ranging from hormone-naïve (HNPC) to t-NEPC, with extensive multi-omics validation. Our results established early NED as a distinct, prognostically adverse subtype. We identified and validated 6 NED markers (FMN2, APLP1, SCG2, SCG3, CHGB, and RIMBP2), demonstrating specificity for NE cells and consistent upregulation throughout NEPC progression. Notably, the Hedgehog (Hh) pathway was specifically activated in early NED, manifested by high SHH ligand in neuroendocrine cells, GLI1 upregulation, and intercellular communication mediated via the SHH-Hh axis. Conversely, in late-stage t-NEPC, Hh pathway activity was significantly downregulated, while MYC-driven proliferation pathways predominated. A risk score derived from the 6-gene NED markers effectively stratified patients, correlating with pronounced NE features and shorter progression-free survival in 86 endocrine-treated patients and externally in The Cancer Genome Atlas (TCGA). In conclusion, this study delineates the dynamic molecular landscape of early NED, establishing a clinically promising biomarker panel and highlighting the Hh pathway as a stage-specific therapeutic target. - Source: PubMed
Publication date: 2026/05/06
Zhu WenhaoGao XiaomeiWang YinzhaoTang GuyuChen MinfengQi LinCai Yi - Hospitalization in older adults often leads to disability in daily living activities, thereby increasing the risk of functional and cognitive impairments. Thisrandomized controlled trial analyzed the serum protein profile of patients admitted to an acute geriatric unit who engaged in supervised multicomponent functional exercise program compared with a control group. Potential protein biomarkers were assessed using the Olink serum proteomics platform employing two predefined panels: Cardiometabolic and Inflammation. Notably, the short-term exercise intervention was associated with moderate but consistent changes in the serum proteome. Nominal differences (p < .05, unadjusted) were observed for amyloid beta precursor-like protein 1 (APLP1), complement C1q tumor necrosis factor-related protein 1 (C1QTNF1), interleukin-8 (CXCL8), interleukin-7 (IL-7), M-phase phosphoprotein 8 (MPHOSPH8), neurotrophin 3 (NTF3), tissue-type plasminogen activator (PLAT), SFRS1-interacting protein (PSIP1), pleiotrophin (PTN), cardiac-type troponin I (TNNI3), and von Willebrand factor (vWF); conversely, levels of CD40 ligand (CD40LG) were reduced. These findings suggest that short-term multicomponent functional exercise during acute hospitalization can induce changes in the serum proteome. These molecular alterations provide exploratory insights into the biological processes associated with the functional benefits observed following the intervention in hospitalized older adults. - Source: PubMed
Izco-Cubero MaiteLachén-Montes MercedesChenhuichen ChenhuiCedeno-Veloz Bernardo AbelEcheverría-Beistegui IcíarZambom-Ferraresi FabricioZambom-Ferraresi Fabiolade la Riva María Luisa Fernández-GonzálezÁlvarez-Rodríguez PatriciaSantamaría EnriqueMartínez-Velilla Nicolás - This study explored protein expression in B-cell acute lymphoblastic leukemia (B-ALL) patients with and without elevated weight or obesity and controls to understand global proteomic differences between newly diagnosed B-ALL patients and controls as well as the influences of elevated body mass index (BMI) on pretreatment inflammatory and immune-related protein expression in B-ALL patients. Protein expression was measured in serum samples of pediatric patients (aged 1-21 years) with newly diagnosed B-ALL ( = 39), and age and sex-matched controls ( = 41) using OLink panels. We examined normalized protein expression data clustered by patient information in -unsupervised hierarchical clustering and principal component analysis. Of 239 assays, 128 assays differed significantly based on B-ALL diagnosis and 4 assays (APLP1, CDHR5, GHRL, SEZ6L) varied significantly as a function of BMI. In healthy individuals, oncology marker furin (p.adjust = 0.016) was more highly expressed in the high-BMI category; this trend was reversed for B-ALL individuals. Furin expression is often upregulated in malignancies and obesity; however this suggests its expression may follow unique patterns in pediatric B- ALL patients with elevated BMI. - Source: PubMed
Publication date: 2026/04/28
Werk Rachel SChacón Jeremy MTurcotte Lucie MRyder Justin R - Amyloid precursor protein (APP) is associated with both familial and sporadic forms of Alzheimer's disease. We previously reported that APP and its family members, amyloid precursor-like proteins 1 and 2 (APLP1 and APLP2), regulate intrinsic neuronal excitability and synaptic plasticity in excitatory principal neurons, though APP family is dispensable for neuronal survival. However, the physiological role of APP family in inhibitory interneurons remains poorly understood. Here, we use our previously characterized floxed APP, APLP1, APLP2 and GAD2-Cre alleles to generate inhibitory neuron-specific conditional triple knockout (IN-APP/APLP1/APLP2 cTKO) mice. Our electrophysiological analysis of acute hippocampal slices revealed that IN-APP/APLP1/APLP2 cTKO CA1 pyramidal neurons exhibit increased amplitudes of evoked GABA receptor-mediated inhibitory postsynaptic currents (IPSCs), while basal spontaneous IPSC frequency and amplitude remain unchanged. At Schaffer collateral (SC)-CA1 synapses, short-train frequency facilitation is enhanced in slices from IN-APP/APLP1/APLP2 cTKO mice, whereas paired-pulse facilitation (PPF) and long-term potentiation (LTP) are normal. Consistent with a cell-autonomous interneuron defect, basal excitatory transmission, measured by spontaneous and miniature excitatory postsynaptic currents (EPSCs) in CA1 pyramidal neurons, is unaltered. These data show that APP family in inhibitory interneurons regulates activity-dependent inhibitory output without overtly perturbing baseline glutamatergic transmission and thus, indirectly shapes short-term facilitation at SC-CA1 synapses. Together with our earlier findings in excitatory neuron-specific APP/APLP1/APLP2 cTKO mice showing intrinsic hyperexcitability, enhanced short-term facilitation, and impaired LTP, these results suggest that the APP family modulates inhibitory and excitatory functions at SC-CA1 synapses through complementary mechanisms in principal neurons and interneurons. - Source: PubMed
Publication date: 2026/03/29
Lee Sang HunKang JongkyunZhang ChenBolshakov Vadim YShen Jie - Cerebral microbleeds (CMBs) are small vascular lesions detectable on MRI and are associated with increased stroke risk and cognitive decline. However, imaging-based diagnosis is limited by cost and accessibility. This study aimed to identify serum protein biomarkers for early CMB diagnosis and to elucidate molecular mechanisms underlying CMB subtypes. - Source: PubMed
Publication date: 2026/03/05
Yin Wu-MengHe Liu-ChangHan Guang-YiLi An-MingZhu Hang-HangCao YuanXue Xin-LiZhang LeiShi Chang-HeXu Yu-MingWang Yun-Chao