Rat F2rl3 (Proteinase-activated receptor 4) ELISA Kit (DEIA-FN463)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
serum, plasma, cell culture supernatants, tissue homogenate
Species Reactivity
Rat
Intended Use
For quantitative detection of Rat F2rl3 (Proteinase-activated receptor 4) in serum, plasma, tissue homogenates and other biological fluids.
Contents of Kit
1. 96-well strip plate (Dismountable), 1 plate
2. Lyophilized Standard, 2 vials
3. Sample/Standard dilution buffer, 20 mL
4. Biotin-detection antibody (Concentrated), 120 uL
5. Antibody dilution buffer, 10 mL
6. HRP-Streptavidin Conjugate(SABC), 120 uL
7. SABC dilution buffer, 10 mL
8. TMB substrate, 10 mL
9. Stop solution, 10 mL
10. Wash buffer (25X), 30 mL
11. Plate Sealer, 5 pieces
12. Product Manual, 1 copy
Storage
Store the unopened product at 2 - 8 °C. Do not use past expiration date.
Precision
Intra-Assay: CV<8%
Inter-Assay: CV<10%
Detection Range
0.625-40 ng/mL
Sensitivity
0.375 ng/mL
Standard Curve

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References


The Expressed Genome in Cardiovascular Diseases and Stroke: Refinement, Diagnosis, and Prediction A Scientific Statement From the American Heart Association

CIRCULATION-CARDIOVASCULAR GENETICS

Authors: Musunuru, Kiran; Ingelsson, Erik; Fornage, Myriam; Liu, Peter; Murphy, Anne M.; Newby, L. Kristin; Newton-Cheh, Christopher; Perez, Marco V.; Voora, Deepak; Woo, Daniel

There have been major advances in our knowledge of the contribution of DNA sequence variations to cardiovascular disease and stroke. However, the inner workings of the body reflect the complex interplay of factors beyond the DNA sequence, including epigenetic modifications, RNA transcripts, proteins, and metabolites, which together can be considered the "expressed genome." The emergence of high-throughput technologies, including epigenomics, transcriptomics, proteomics, and metabolomics, is now making it possible to address the contributions of the expressed genome to cardiovascular disorders. This statement describes how the expressed genome can currently and, in the future, potentially be used to diagnose diseases and to predict who will develop diseases such as coronary artery disease, stroke, heart failure, and arrhythmias.

IDENTIFICATION OF POTENTIAL KEY GENES ASSOCIATED WITH CARDIAC FIBROSIS BY RNA SEQUENCING DATA ANALYSIS

ACTA MEDICA MEDITERRANEA

Authors: Liu, Dandan; Wang, Haizhu; Han, Mao; Han, Caiplng; Ren, Fengbo

Introduction: Cardiac fibrosis is central to a broad constellation of cardiovascular diseases with similar pathophysiologic companions, and is associated with cardiac dysfunction, arrhythmogenesis, and adverse outcome. However, the option of effective treatment strategies is limited due to the insufficient understanding of the mechanisms for cardiac fibrosis. Materials and methods: The RNA sequencing data (GSE97358) comprising 84 TGF-beta 1 -stimulated samples and 84 paired unstimulated samples of cultured primary human cardiac fibroblast from GEO database was used to explore crucial genes and pathways involved in cardiac fibrosis. The differentially expressed genes (DEGs) were identified using edgeR package in R. Protein-protein interaction (PPI) network and module analyses were performed and visualized using STRING and Cytoscape. GO (geneontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analyses were performed by clusterprofiler. The hub genes extracted from PPI were identified by the CytoHubba plug-in and the transcription factor(TF)-hub gene network was further constructed by the iRegulon plug-in. Results: Totally, 647 DEGs were initially screened out in TGF-beta 1-stimulated primary human cardiac fibroblast. Twenty hub genes (9 up-regulated: S1PR5, F2RL3, GPR68, CXCR5, KISS1, GAL, LPAR5, HTR1D, PLCB4; 11 down-regulated: CXCL1, GPR65, CYSLTR2, EDNRA, CXCL6, F2R, GNG2 F2RL2, SSTR1, TAS2R1, HTR2B) were further identified. Wnt signaling and neuroactive ligand-receptor interaction signaling pathways enriched were ultimately identified as the key pathways involved in cardiac fibrosis. Seven TFs (RELB, FOS, SREBF2, PURA, TBX21, IRF1 and IRF4) were identified for the TF-hub gene networks. Conclusions: Our results may provide novel insights into the molecular mechanisms and treatments of cardiac fibrosis. However, further molecular biological experiments are required to confirm these findings.

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