Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 139 bp insertion in exon 2 and 2 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, 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-CDK4, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, 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.
Cdk4 also known as Cyclin-dependent kinase 4 is a serine/threonine kinase involved in cell cycle regulation. Cdk4 has a molecular weight of approximately 34 kDa. This protein mainly locates in the nucleus of the cell and its expression occurs in diverse tissues. Cdk4 partners with D-type cyclins to exert its function which is essential for the transition from the G1 phase to the S phase of the cell cycle. Researchers often study Cdk4 using techniques like immunohistochemistry (IHC) to determine its expression and localization in different tissues.
Biological function summary
Cdk4 plays a fundamental role in cell cycle regulation by forming a complex with D-type cyclins. Together they phosphorylate the retinoblastoma protein (Rb) resulting in the release of E2F transcription factors which promote the expression of genes necessary for DNA replication. The Cdk4/cyclin D complex regulates the cell's commitment to enter S phase and continue cell division. This regulation is key for normal cell proliferation and tissue homeostasis. Cdk4 activity is strictly controlled by INK4 family members acting as inhibitors and adding an extra regulation layer.
Pathways
Cdk4 is an integral part of important signaling pathways like the cell cycle and PI3K/AKT pathways. In the cell cycle pathway Cdk4 relays signals downstream that drive the transition from the G1 to S phase through its interaction with cyclin D and Rb. In the PI3K/AKT pathway signaling can influence cyclin D expression indirectly affecting Cdk4 activity. Proteins such as Cdk6 closely relate to Cdk4 and often compensate or partner with Cdk4 in these pathways to maintain proper cell cycle progression.
Abnormalities in Cdk4 function or regulation relate to cancer and certain metabolic syndromes. Hyperactivity of Cdk4 due to overexpression or mutation frequently occurs in several cancers including melanoma and breast cancer. In these malignancies Cdk4 aberrantly drives excessive cell proliferation. Mutations or alterations in proteins such as p16 an inhibitor of Cdk4 are often found in these cancers highlighting the critical role of Cdk4 in disease progression. Understanding the role of Cdk4 allows researchers to develop targeted therapies such as Cdk4/6 inhibitors offering new treatment options.
