Masthead

nCounter® Fibrosis Panel

Masthead

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.

01:

Study pathogenesis and identify biomarkers for fibrotic diseases of the lungs, heart, liver, kidney, and skin

02:

Elucidate the mechanism of action behind the four stages of fibrosis: initiation, inflammation, proliferation, and modification

03:

Understand the signaling cascade from cell stress to inflammation

04:

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 pro

Find Your Panel

Product Information

Coverage across Stages of Fibrosis
Functional Annotations
Product Specifications
Immune Cell Profiling
Catalog Information
Coverage across Stages of Fibrosis

Functional Annotations
Product Specifications
Immune Cell Profiling
Catalog Information

Related Resources

View All Related Resources
Fibrosis Product Bulletin

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.

Skysphere

Contact Us

Have questions or simply want to learn more?

Contact our helpful experts and we’ll be in touch soon.

Contact Us