Description
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 1 bp insertion in exon 2
Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-FXYD5, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Zygosity-Homozygous, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Dysadherin also known as FXYD domain-containing ion transport regulator 5 (FXYD5) is a small protein with a mass of approximately 20 kDa. It localizes on the cell surface as a glycoprotein. The protein has wide expression across various tissues including epithelial tissues and certain cancerous cells. Dysadherin has been primarily identified in cells involved in malignancy and metastasis which suggests its role in cancer biology.
Biological function summary
Dysadherin contributes to cell-cell adhesion disruption facilitating the metastatic spread of cancer cells. It is not part of a known protein complex but it interacts with the extracellular matrix to alter cellular cohesion and mobility. By influencing the cellular adhesion properties dysadherin may play a part in the invasive characteristics of some epithelial tumors. This alteration can drive processes leading to carcinoma progression by reducing cell-cell interaction stability.
Pathways
Disruptions in cell adhesion mediated by proteins like dysadherin can impact the epithelial-mesenchymal transition (EMT) pathway significantly. Within this pathway dysadherin decreases E-cadherin expression which weakens cellular adhesion enhancing cell motility and invasiveness. Also it may engage in the PI3K/AKT signaling pathway by affecting cellular growth and survival. Dysadherin might act together with other regulatory proteins that modulate cell adhesion and mobility impacting tumor behavior and progression.
Dysadherin's expression links closely with metastatic cancers including colorectal cancer and breast cancer. Its role in reducing E-cadherin function means it connects to diseases where diminished cell adhesion contributes to cancer metastasis. Dysadherin has associations with other proteins implicated in these diseases such as integrins which also influence metastatic cell movement and invasion. Understanding dysadherin's function and interactions may provide insight into therapeutic strategies for tackling metastatic disease.
