Abcam, ab266752, Human TIPRL knockout HEK-293T cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
TIPRL KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, Homozygous: 1 bp insertion in exon 1. To order both knockout and wild-type control cells: select 2 x 1000000Cells/vial. To order only knockout cells: select 1000000Cells/vial.
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 1

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-TIPRL, 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.
TIPRL also known as TIP41-like protein weighs approximately 39 kDa. It functions by interacting with the alpha subunit of protein phosphatase 2A (PP2A) which acts as a negative regulator within various cellular processes. TIPRL is expressed in a variety of tissues with notable presence in the liver kidney and brain. Its modulation role occurs through binding to other proteins and influencing catalytic activities important for maintaining balance in cellular signaling.
Biological function summary
TIPRL serves a regulatory role by inhibiting phosphatase activities within the cell contributing significantly to protein dephosphorylation processes. This protein is a part of the PP2A holoenzyme complex where it serves to fine-tune its activity affecting signaling pathways that rely on phosphorylation status. Through associating with PP2A and related phosphatases TIPRL ensures proper cellular phosphoprotein turnover an important factor for healthy cellular function and response to external stimuli.
Pathways
Interaction between TIPRL and other proteins influences the mTOR signaling pathway and MAPK signaling pathways. Through these pathways TIPRL affects cellular growth proliferation and survival. TIPRL influences mTOR pathway by modulating the activity of PP2A which can affect downstream proteins like AKT and S6K1. The MAPK pathway is impacted similarly where TIPRL's interaction with PP2A alters phosphorylation state of proteins such as ERK creating implications for cell cycle progression and stress response.
TIPRL is linked to neurological disorders and certain cancers. TIPRL's regulation of pathways like mTOR and MAPK associates it with the development of glioblastomas where dysregulated signaling contributes to tumorigenesis. Additionally in neurodegenerative conditions altered TIPRL function affects phosphatase activity impacting proteins like Tau which play a role in diseases like Alzheimer's. Understanding TIPRL's modulation could provide insights into therapeutic targets for these conditions.