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nCounter® Fibrosis Panel

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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

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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
Blog Q&A with Metabolic Pathways Panel Grant Winner Teresa Cardoso Delgado, Ph.D.: The Metabolomics of Non-Alcoholic Fatty Liver Disease (NAFLD)
Webinar Murine March Madness: Genetics of Osteoarthritis: From Man to Fish to Mouse

Publications

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Spatial transcriptomics and proteomics technologies for deconvoluting the tumor microenvironment.

The tumor microenvironment (TME) harbors heterogeneous contents and plays critical roles in tumorigenesis, metastasis, and drug resistance. Therefore, the deconvolution of the TME becomes increasingly essential to every aspect of cancer research and treatment.

Decreased ATM Function Causes Delayed DNA Repair and Apoptosis in Common Variable Immunodeficiency Disorders.

PURPOSE: Common variable immunodeficiency disorders (CVID) is characterized by low/absent serum immunoglobulins and susceptibility to bacterial infection. Patients can develop an infections-only phenotype or a complex disease course with inflammatory, autoimmune, and/or malignant complications.

A SARS-CoV-2 targeted siRNA-nanoparticle therapy for COVID-19.

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in humans. Despite several emerging vaccines, there remains no verifiable therapeutic targeted specifically to the virus.

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