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, 2 bp deletion in exon 3 and Insertion of the selection cassette in exon 3
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-CDV3, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
CDV3 also known as Cell Death-Inducing DFFA-Like Effector B is a small protein with a mass of around 16 kDa. CDV3 is expressed in various tissues but appears more in the testes and heart. It functions mechanically by modulating cellular apoptosis and might have roles in regulating other cellular processes too. Although comprehensive studies on this protein are limited its expression profile suggests functions in maintaining tissue homeostasis.
Biological function summary
CDV3 influences cell death processes particularly apoptosis. It interacts with different effector molecules but does not function as part of a larger protein complex which implies it could exert its biological effects independently. There is evidence it might have a role in regulating non-apoptotic functions such as cell differentiation or stress responses although these functions need further investigation.
Pathways
CDV3 interacts mainly within the apoptosis signaling pathways. It participates in pathways that involve molecules such as BCL-2 family proteins which regulate mitochondrial membrane permeabilization an important step in the apoptotic process. Another associated pathway could involve stress response protein kinases which are related to cell survival and apoptosis although direct interactions require more precise mapping.
Alterations in CDV3 expression or function might relate to cancer and cardiomyopathy. In cancer dysregulation of apoptosis is a common feature and CDV3 could alter the apoptotic balance. In cardiomyopathy CDV3 expression changes might contribute to cardiac cell death possibly in coordination with BCL-2 proteins which are important factors in cardiomyocyte apoptosis. Further research is needed to clarify its exact roles in these disorders but the connection indicates that it might influence disease progression or treatment response.
