Uses
All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project
(www.proteinatlas.org)and as a result, are supported by the most extensive characterization in the industry.
The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. To view these
protocols and other useful information about Prestige Antibodies and the HPA, visit .
General Description
HOPX (homeodomain only protein x) gene is mapped in human chromosome 4q12. Unlike HOX proteins, it lacks a DNA-binding domain that is required for protein-DNA interactions. HOPX is widely expressed, but not in malignant tissues including choriocarcinoma, lung, uterine endometrial and gastrointestinal cancers. The gene contains 3 transcript variants HOPX- α, β, γ encoding the same protein.
Biochem/physiol Actions
HOPX (homeodomain only protein x) is involved in cardiac and skeletal muscle development by recruiting histone deacetylases. It controls the SRF (serum response factor)-dependent gene expression for the regulation of cardiac development. Downregulation of HOPX leads to cardiac hypertrophy in mice. In advanced human heart failure, HOPX expression is reduced. It acts as co-chaperone and organises the Hsp70-Hsp90 (heat shock proteins) proteins. It serves as a maker for a number of stem cell types. Studies show that HOPX inhibits tumour cell proliferation rate, migration and invasion in lung cancer. It also increase cell death by the activation of oncogenic Ras (GTPase) and the downstream MAPK (mitogen activated protein kinase) pathway.
