Abcam, ab265311, Human INPP5K (SKIP) knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
INPP5K KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 5 and 32 bp insertion in exon 5. 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, 1 bp insertion in exon 5 and 32 bp insertion in exon 5,
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-INPP5K, 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.
SKIP also known as Splicing Factor Kinase Interacting Protein is a protein with a mass of approximately 45 kDa. It functions mechanically as a transcriptional co-regulator and is critical in the regulation of gene expression. SKIP interacts with various transcription factors aiding in RNA polymerase II's activity. SKIP expression is widespread in multiple tissues including liver and brain with higher expression noted in differentiated cells. It plays an essential role in modulating different signaling pathways by interacting with specific proteins.
Biological function summary
This protein serves multiple roles within the cellular environment. It participates in mRNA splicing as part of the spliceosome complex which is vital for removing introns from pre-mRNA. SKIP modulates the alternative splicing of pre-mRNA thereby affecting the type and function of mRNA that is translated into proteins. Besides its role in splicing SKIP also interacts with other proteins like transcription factors and components of the chromatin remodeling complex. These interactions demonstrate its importance in regulating transcriptional and post-transcriptional processes.
Pathways
SKIP plays integral roles in pathways such as the Wnt signaling pathway and TGF-beta signaling. These pathways regulate various processes including cell proliferation and differentiation. In the Wnt pathway SKIP interacts with proteins such as beta-catenin influencing gene transcription. It affects the stability of transcription complexes by interacting with factors in these pathways ensuring appropriate cellular responses. These interactions highlight SKIP's contribution to maintaining cellular homeostasis and influencing phenotypic outcomes.
Research links SKIP to cancer and neurodegenerative diseases. SKIP dysregulation has associations with cancer development through its impact on the Wnt pathway affecting cell growth and migration. It interacts with proteins like beta-catenin in this context which is often implicated in oncogenesis. SKIP's role in neurodegenerative diseases such as Alzheimer's involves its influence on the alternative splicing of key neuronal proteins. Incorrect splicing can lead to the production of dysfunctional proteins contributing to disease progression. Hence understanding SKIP's regulation and interactions is essential in targeting these pathologies.