Human CDK4 Knockout Cell Line-HCT116
Cat.No. : CSC-RT2742
Host Cell: HCT116 Target Gene: CDK4
Size: 1x10^6 cells/vial, 1mL Validation: Sequencing
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Cell Line Information
Cell Culture Information
Safety and Packaging
| Cat. No. | CSC-RT2742 |
| Cell Line Information | This cell is a stable cell line with a homozygous knockout of human CDK4 using CRISPR/Cas9. |
| Target Gene | CDK4 |
| Host Cell | HCT116 |
| Size Form | 1 vial (>10^6 cell/vial) |
| Shipping | Dry ice package |
| Storage | Liquid Nitrogen |
| Species | Human |
| Revival | Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media. |
| Mycoplasma | Negative |
| Format | One frozen vial containing millions of cells |
| Storage | Liquid nitrogen |
| Safety Considerations |
The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach. |
| Ship | Dry ice |
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Background
Applications
CDK4 (Cyclin-dependent kinase 4) is an essential protein in humans, encoded by the CDK4 gene. The main function of CDK4 is to participate in the G1-S phase of the cell cycle, acting as a catalytic subunit in a protein kinase complex. The activity of CDK4 is tightly regulated by its binding to D-type cyclins and the CDK inhibitor p16INK4a. More specifically, CDK4 phosphorylates the retinoblastoma protein (Rb), an important step in regulating cell cycle progression. This phosphorylation event dissociates the E2F transcription factor from the Rb/E2F complex and subsequently initiates transcription of E2F target genes responsible for G1 phase progression.
In addition to its role in normal cell cycle regulation, CDK4 has important clinical implications, especially in cancer. Mutations in CDK4 and its associated regulatory proteins, including D-type cyclins, p16INK4a, CDKN2A, and Rb, have been implicated in various cancers. A specific mutation, CDK4 (R24C), was initially identified in melanoma patients. This mutation has been extensively studied in animal models, confirming its role as an oncogene. Due to its widespread involvement in tumorigenesis, CDK4 has emerged as a promising target for cancer therapy. Various CDK4 inhibitors are currently in clinical trials to evaluate their efficacy in treating different types of cancer.
Cancer Research: This cell line is useful for studying the role of CDK4 in cancer cell proliferation. By comparing the proliferation rates of CDK4 knockout cells to wild-type HCT116 cells, researchers can better understand how CDK4 promotes tumor growth, potentially identifying new targets for cancer treatment.
Drug Development: The CDK4 knockout HCT116 cell line can be used as a model for screening and evaluating CDK4 inhibitors and other therapeutic agents. It provides insight into the efficacy and specificity of potential drugs, allowing researchers to identify compounds that specifically target the CDK4 pathway without affecting other cellular mechanisms.
Cell Cycle Regulation Studies: CDK4 plays a critical role in the cell cycle, specifically the transition from G1 to S phase. This knockout cell line is useful for elucidating the molecular mechanisms involved in cell cycle regulation and determining how CDK4 loss affects cell cycle progression.
Genomic Studies: This cell line can be used for genetic studies, including studying gene regulation, expression, and the effects of CDK4 loss on the broader genomic landscape. It can be used to study compensatory mechanisms that cells may employ in the absence of CDK4.
Signal Transduction Studies: CDK4 is part of several signal transduction pathways. By using CDK4 knockout cell lines, researchers can dissect these pathways and understand how the loss of CDK4 affects various signaling cascades.
For research use only. Not intended for any clinical use.
