Abcam, ab265366, Human CTDSPL knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
CTDSPL KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, Homozygous: 14 bp deletion in exon 2. 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: 14 bp deletion in exon 2,
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 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-CTDSPL, 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.
The CTDSPL protein also known as CTDSP1 or Small C-terminal domain phosphatase 1 has a notable role in transcriptional regulation. It is a 29 kDa protein that is part of the SCP (small C-terminal domain phosphatase) family. CTDSPL is expressed in various tissues including the brain lung and liver. Its primary mechanical function involves dephosphorylation of the RNA polymerase II C-terminal domain which can regulate the transcription process.
Biological function summary
The CTDSPL protein influences the cell cycle and neuronal differentiation. It functions as a negative regulator of cell proliferation by dephosphorylating retinoblastoma protein (pRb) leading to cell cycle exit and differentiation. CTDSPL does not typically function as part of a larger complex but interacts directly with its substrates. It thereby regulates gene expression associated with cell growth and differentiation.
Pathways
The protein CTDSPL is essential in the regulation of the retinoblastoma (Rb) pathway and TGF-beta signaling pathway. In these pathways CTDSPL contributes to cell cycle control and tissue homeostasis. Through the TGF-beta pathway it interacts with proteins such as SMADs which are critical mediators of signal transduction. In the Rb pathway CTDSPL impacts various cell cycle stages by modulating the activity of retinoblastoma protein.
Variations in CTDSPL expression have been linked to cancer and neurological disorders. Its role in dephosphorylating pRb connects it to cancer biology particularly in the context of tumor suppressor mechanisms. CTDSPL also associates with alternative splicing factors involved in some neurodegenerative diseases. It is closely studied alongside proteins like retinoblastoma protein and SMADs that are implicated in these disorders.