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
Remodeling of the tumor microenvironment via disrupting Blimp1(+) effector Treg activity augments response to anti-PD-1 blockade.
BACKGROUND: Accumulation of Foxp3(+) regulatory T (Treg) cells in the tumor often represents an important mechanism for cancer immune evasion and a critical barrier to anti-tumor immunity and immunotherapy. Many tumor-infiltrating Treg cells display an activated phenotype and express the transcription factor Blimp1.
Gene expression of oxidative stress markers and lung function: A CARDIA lung study.
BACKGROUND: Circulating markers of oxidative stress have been associated with lower lung function. Our objective was to study the association of gene expression levels of oxidative stress pathway genes (ALOX12, ALOX15, ARG2, GSTT1, LPO, MPO, NDUFB3, PLA2G7, and SOD3) and lung function forced expiratory volume in one second (FEV1 ), forced vital capacity (FVC) in Coronary Artery Risk Development in Young Adults study.
Circadian dynamics of the teleost skin immune-microbiome interface.
Background: Circadian rhythms of host immune activity and their microbiomes are likely pivotal to health and disease resistance. The integration of chronotherapeutic approaches to disease mitigation in managed animals, however, is yet to be realised.