nCounter® Fibrosis Panel
Helping Your Research
The cellular and molecular basis for fibrotic disease is still poorly understood, and the lack of biomarkers for progression and therapeutic response have hampered efforts to develop treatments. The nCounter Fibrosis Panel helps uncover the mechanisms of disease pathogenesis, identify biomarkers of progression, and develop signatures for therapeutic response. This gene expression panel combines hundreds of genes involved in the initial tissue damage response, chronic inflammation, proliferation of pro-fibrotic cells, and tissue modification that leads to fibrotic disease of the lungs, heart, liver, kidney, and skin.
How it Works
Profile 770 genes across 51 annotated pathways in human or mouse.
Study pathogenesis and identify biomarkers for fibrotic diseases of the lungs, heart, liver, kidney, and skin
Elucidate the mechanism of action behind the four stages of fibrosis: initiation, inflammation, proliferation, and modification
Understand the signaling cascade from cell stress to inflammation
Quantify the relative abundance of 14 different immune cell types
Panel Selection Tool
Find the gene expression panel for your research with easy to use panel proFind Your Panel
NanoString Technology for Human Papillomavirus Typing.
High-throughput HPV typing assays with increased automation, faster turnaround and type-specific digital readout would facilitate studies monitoring the impact of HPV vaccination. We evaluated the NanoString nCounter((R)) platform for detection and digital readout of 48 HPV types in a single reaction.
Stepwise Reversal of Immune Dysregulation Due to STAT1 Gain-of-Function Mutation Following Ruxolitinib Bridge Therapy and Transplantation.
PURPOSE: Patients with heterozygous gain-of-function (GOF) mutations in STAT1 frequently exhibit chronic mucocutaneous candidiasis (CMC), immunodeficiency and autoimmune manifestations. Several treatment options including targeted therapies and hematopoietic stem cell transplantation (HSCT) are available for STAT1 GOF patients but modalities and outcomes are not well established.
Tissue-specific endothelial cell heterogeneity contributes to unequal inflammatory responses.
Endothelial cells (EC) coordinate vascular homeostasis and inflammation. In organ transplantation, EC are a direct alloimmune target.