Anti-DDX19B antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

DDX19B also known as DEAD (Asp-Glu-Ala-Asp) box helicase 19B is an RNA helicase enzyme that assists in RNA metabolism by unwinding RNA molecules. It is part of the DEAD-box protein family characterized by the conserved motif Asp-Glu-Ala-Asp (DEAD). This protein has a molecular weight of approximately 48 kDa. DDX19B is expressed in various human tissues most prominently in the liver and brain. This wide expression pattern suggests its involvement in essential cellular processes.

Biological function summary

DDX19B plays a vital role in RNA processing and transport. It is involved in the export of mRNA from the nucleus to the cytoplasm a critical step in gene expression. DDX19B interacts with large protein complexes such as the nuclear pore complex which facilitates the movement of molecules across the nuclear envelope. By engaging in these interactions DDX19B ensures the proper communication between the nucleus and cytoplasm maintaining cellular homeostasis.

Pathways

DDX19B is integral to the mRNA export pathway working closely with proteins such as NUP214 a nucleoporin essential for the export process. Additionally DDX19B participates in the nonsense-mediated mRNA decay (NMD) pathway which controls mRNA quality by degrading erroneous mRNA molecules. In this pathway DDX19B interacts with proteins UPF1 a critical regulator of NMD reflecting its importance in maintaining proper gene expression and preventing accumulation of faulty proteins.

Associated diseases and disorders

DDX19B has been linked to certain cancers such as liver cancer and neurodegenerative diseases like amyotrophic lateral sclerosis (ALS). In liver cancer DDX19B has shown aberrant expression patterns pointing to its potential role in tumorigenesis. In relation to ALS its interaction with FUS an RNA-binding protein associated with the disorder highlights its involvement in the disease's molecular mechanisms. These connections emphasize the need to further explore DDX19B as a therapeutic target in managing such conditions.