c1qtnf3 duo set elisa  (R&D Systems)

Journal: Molecular Medicine

Article Title: Panx3 deficiency in mice impairs bone fracture healing and causes transient hypoglycemia in neonatal animals

doi: 10.1186/s10020-026-01458-9

Figure Lengend Snippet: Panx3 deficiency results in altered glucose metabolism markers. A Serum levels of glucose and insulin in mice of the indicated genotypes at 3, 7 and 14 postoperative days ( N = 6). Relative fold changes to controls were plotted. B Heatmap of 30 differentially regulated genes with highest fold changes in the callus of Panx3 +/+ ( N = 5) and Panx3 −/− ( N = 4) mice 3 days after the osteotomy. Each column represents one individual sample and gene, respectively. Z-scores were calculated based on the expression level of each gene and visualized in a color scale (blue = downregulated, red = upregulated). Genes associated with glucose metabolism were highlighted in red. C Expression of the indicated genes ( Slc = solute carrier family, C1qtnf3 = C1q tumor necrosis factor-related protein 3) in the callus of Panx3 +/+ and Panx3 −/− mice at the indicated postoperatively time points ( N = 6). D Representative alizarin red–stained images of isolated calvarial osteoblasts from Panx3 + / + and Panx3 −/− mice and quantification of extracellular matrix mineralization after 10 days of osteogenic differentiation ( N = 6). E Expression of the indicated genes ( Bglap = bone gamma-carboxylglutamic acid-containing protein, osteocalcin, Dmp1 = dentin matrix acidic matrix phosphoprotein 1, Panx3 = pannexin 3, C1qtnf3 = C1q tumor necrosis factor-related protein 3, Slc = solute carrier) in calvarial osteoblasts from Panx3 + / + and Panx3 −/− mice after 10 days of osteogenic differentiation ( N = 4). Unpaired Student’s t test was used to determine statistical differences between groups at each time point or for each gene. Data are presented as box plots that represent median with minimum and maximum whiskers

Article Snippet: C1qTNF3 duo set ELISA (#DY7925-05, R&D Systems Inc., Minneapolis, USA) was used to determine the concentration in human patients.

Techniques: Expressing, Staining, Isolation

Journal: Molecular Medicine

Article Title: Panx3 deficiency in mice impairs bone fracture healing and causes transient hypoglycemia in neonatal animals

doi: 10.1186/s10020-026-01458-9

Figure Lengend Snippet: Panx3 -deficient mice display impaired glucose homeostasis. A Body weight of Panx3 + / + ( N = 4–6) and Panx3 −/− ( N = 3–4) mice and B serum glucose of Panx3 + / + ( N = 6) and Panx3 −/− ( N = 3–5) mice at the indicated ages. C Glucose and D insulin tolerance test of adult mice of the indicated genotypes ( N = 7). Relative alterations to the baseline level were plotted. E Serum levels of insulin and C1qtnf3 in Panx3 + / + and Panx3 −/− mice at the indicated ages ( N = 3 for P3, N = 7 for P600). F Serum concentration of C1qtnf3 in healthy individuals as control ( N = 10), patients displayed adequate fracture healing (Fx, N = 16) and nonunion formation (NU, N = 19). Unpaired Student’s t test was used to determine statistical differences between groups at each time point. Data are presented as box plots that represent median with minimum and maximum whiskers

Article Snippet: C1qTNF3 duo set ELISA (#DY7925-05, R&D Systems Inc., Minneapolis, USA) was used to determine the concentration in human patients.

Techniques: Concentration Assay, Control

Journal: Frontiers in Cardiovascular Medicine

Article Title: CTRP3 attenuates myocardial lipotoxicity via suppression of lipid accumulation, inflammation, apoptosis, and mitochondrial oxidative stress

doi: 10.3389/fcvm.2025.1575929

Figure Lengend Snippet: (A,B) Compared to the high-fat diet (HFD) group, supplementation with CTRP3 significantly improves cardiac function in mice, as evidenced by enhanced left ventricular ejection fraction. (C,D) Histological examination of myocardial tissue reveals substantial lipid droplet accumulation in the HFD group. However, CTRP3 supplementation reduces lipid droplet accumulation, improves myocardial tissue structure, and alleviates the degree of fibrosis. (E–M) Immunofluorescence results indicate that CTRP3 supplementation mitigates myocardial inflammation, apoptosis, and oxidative stress in mice. (N–Q) Serum ELISA assays demonstrate that levels of triglycerides (TG), total cholesterol (TCHO), inflammatory markers, apoptotic factors, and oxidative stress indicators are significantly improved in the CTRP3 group compared to the HFD group ( n ≥ 3, p < 0.05).

Article Snippet: The recombinant CTRP3 protein (rCTRP3, Catalog Number: CSB-EP883621HU) was commercially procured from Wuhan Cusabio Biotech Co., Ltd. (Hubei, China).

Techniques: Immunofluorescence, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Cardiovascular Medicine

Article Title: CTRP3 attenuates myocardial lipotoxicity via suppression of lipid accumulation, inflammation, apoptosis, and mitochondrial oxidative stress

doi: 10.3389/fcvm.2025.1575929

Figure Lengend Snippet: (A–F) Lipid testing results demonstrate that palmitic acid (PA) induces lipid accumulation in myocardial cells, while CTRP3 supplementation significantly reduces lipid droplet accumulation. (G) CTRP3 intervention improves the expression of genes related to fatty acid uptake, fatty acid oxidation, and lipid efflux in myocardial cells ( n ≥ 3, p < 0.05). (H) Quantitative PCR (q-PCR) results indicate that CTRP3 mitigates inflammation, apoptosis, and oxidative stress in myocardial cells stimulated by PA ( n ≥ 3, p < 0.05).

Article Snippet: The recombinant CTRP3 protein (rCTRP3, Catalog Number: CSB-EP883621HU) was commercially procured from Wuhan Cusabio Biotech Co., Ltd. (Hubei, China).

Techniques: Expressing, Real-time Polymerase Chain Reaction

Journal: Frontiers in Cardiovascular Medicine

Article Title: CTRP3 attenuates myocardial lipotoxicity via suppression of lipid accumulation, inflammation, apoptosis, and mitochondrial oxidative stress

doi: 10.3389/fcvm.2025.1575929

Figure Lengend Snippet: (A–E) RNA sequencing analysis of myocardial tissue from the control group, HFD group, and CTRP3 group indicates that CTRP3 likely exerts its effects within myocardial mitochondria, playing a role in the metabolic regulation of myocardial lipotoxicity.

Article Snippet: The recombinant CTRP3 protein (rCTRP3, Catalog Number: CSB-EP883621HU) was commercially procured from Wuhan Cusabio Biotech Co., Ltd. (Hubei, China).

Techniques: RNA Sequencing, Control

Journal: Frontiers in Cardiovascular Medicine

Article Title: CTRP3 attenuates myocardial lipotoxicity via suppression of lipid accumulation, inflammation, apoptosis, and mitochondrial oxidative stress

doi: 10.3389/fcvm.2025.1575929

Figure Lengend Snippet: (A,B) JC-1 staining results demonstrate a decrease in mitochondrial membrane potential in myocardial cells of the PA group. (C,D) Mito-Tracker staining results show a reduction in mitochondrial number in the PA group. (E) PA intervention in myocardial cells leads to decreased ATP production, while CTRP3 intervention improves ATP generation. (F) Transmission electron microscopy reveals increased mitochondrial damage and autophagy in myocardial cells following PA intervention. CTRP3 can mitigate mitochondrial damage and autophagy in myocardial cells.

Article Snippet: The recombinant CTRP3 protein (rCTRP3, Catalog Number: CSB-EP883621HU) was commercially procured from Wuhan Cusabio Biotech Co., Ltd. (Hubei, China).

Techniques: Staining, Membrane, Transmission Assay, Electron Microscopy

Journal: Heliyon

Article Title: Obesity alters adipose tissue response to fasting and refeeding in women: A study on lipolytic and endocrine dynamics and acute insulin resistance

doi: 10.1016/j.heliyon.2024.e37875

Figure Lengend Snippet: Key resources table

Article Snippet: Human CTRP3 ELISA DuoSet Kit , R&D systems Biotechne , Cat# DY7925-05.

Techniques: Clinical Proteomics, Recombinant, Enzyme-linked Immunosorbent Assay, Software