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: 19 bp deletion 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 and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-NIBAN2, 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.
FAM129B also known as NIBAN2 functions as a protein implicated in cell survival signaling. It weighs approximately 75 kDa. Expression of FAM129B is detected in various tissues with prominence in the lymphoid tissues and central nervous system. Researchers have highlighted its role in apoptosis regulation where it interacts with other molecules to affect cell fate decisions under stress conditions.
Biological function summary
FAM129B engages in apoptosis modulation and cell survival playing a significant part in cellular stress response. The protein often partners with other components to form complexes that influence intracellular signaling pathways. Specifically by interacting with protein tyrosine phosphatases it affects the delicate balance between survival and programmed cell death providing cells the ability to adapt to fluctuating environmental challenges.
Pathways
FAM129B integrates into the MAPK and PI3K/AKT signaling pathways which are vital for regulating cell survival proliferation and differentiation. Within these pathways FAM129B associates with proteins like AKT and ERK that mediate its impact on cell survival signaling. Its involvement in these pathways suggests a regulatory role in cellular responses to external stimuli contributing to the maintenance of homeostasis.
Abnormal expression or dysfunction of FAM129B links to the pathophysiology of cancers and neurodegenerative diseases. For instance in cancer its interaction with AKT has been implicated in enhancing cell survival potentially leading to tumorigenesis. Additionally the altered regulation of FAM129B has connections to Alzheimer's disease where it may interact with other proteins like tau contributing to neurodegenerative processes.
