Abcam, ab265197, Human PHLDA3 knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
PHLDA3 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:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 1 bp insertion in exon 1,
Disease:Adenocarcinoma

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-PHLDA3, 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.
PHLDA3 also known as PHLDA family member 3 is a small protein with a molecular mass of about 15 kDa. It functions mechanically as an antagonist of the AKT signaling pathway. PHLDA3 can inhibit AKT by binding to its pleckstrin homology (PH) domain preventing AKT's interaction with other molecules. This protein is expressed in various tissues throughout the body including the brain lungs and liver indicating its role in diverse cellular functions.
Biological function summary
The protein acts as a tumor suppressor through its ability to regulate cell growth and apoptosis. PHLDA3 does this by modulating the AKT pathway inhibiting cell survival and promoting apoptosis. It is not part of a larger complex but interacts directly with other proteins to execute its function. The influence of PHLDA3 on cell cycle processes suggests it plays roles in maintaining normal cellular functions and preventing uncontrolled proliferation.
Pathways
Several studies have shown PHLDA3 integrates into the p53 signaling pathway a critical pathway for cellular stress responses and tumor suppression. It interacts with the AKT pathway which connects it to proteins like PI3K and PTEN influencing cellular growth and apoptosis. PHLDA3 effectively bridges interaction between the p53 pathway and AKT pathway which balances cell fate decisions under stress conditions.
PHLDA3 exhibits a significant impact on cancer development and progression. Loss of PHLDA3 expression has been observed in various tumors suggesting its role in cancer development. Additionally it relates to diabetes where altered AKT signaling affects insulin response. In cancer PHLDA3 connects to the tumor suppressor protein p53 influencing its regulatory functions while in diabetes its relation to AKT pathway points to disturbances in glucose homeostasis.