CDK2: A Promising Drug Target and Biomarker for Cancer Treatment

Target Name: CDK2

NCBI ID: G1017

CDK2

CDK2: A Promising Drug Target and Biomarker for Cancer Treatment

CDK2 (Chromatin-Driven Kinesin 2) is a protein that plays a crucial role in cell division and growth. It is a key regulator of the G1/S transition, which is a critical step in the cell cycle where cells prepare for cell division. CDK2 has also been implicated in the regulation of cell survival and has been linked to the development and progression of various diseases, including cancer. As a result, CDK2 has emerged as a promising drug target and biomarker for cancer treatment.

CDK2 as a Drug Target

CDK2 has been identified as a potential drug target for cancer treatment due to its involvement in cell division and the regulation of the cell cycle. Many studies have shown that inhibiting CDK2 can lead to a reduction in cancer cell proliferation and survival.

One of the main reasons for the potential of CDK2 as a cancer drug is its role in the regulation of the G1/S transition. The G1/S transition is a critical step in the cell cycle where cells prepare for cell division. CDK2 is involved in the regulation of the G1/S transition by promoting the assembly and disassembly of chromatin-bound kinetin proteins, which are essential for the G1/S transition.

In addition, studies have shown that CDK2 is involved in the regulation of cell survival. CDK2 has been shown to play a role in the regulation of cell survival by promoting the association of CDK2 with the protein p53, which is a well-known tumor suppressor protein. The association between CDK2 and p53 has been shown to promote the expression of anti- apoptotic genes, such as Bcl-2, which can protect cells from apoptosis.

CDK2 as a Biomarker

CDK2 has also been shown to be a potential biomarker for cancer diagnosis and treatment. The expression of CDK2 has been shown to be elevated in various types of cancer, including breast, ovarian, and colorectal cancers. Additionally, the expression of CDK2 has been shown to be associated with the poor prognosis of cancer patients.

One of the main reasons for the potential of CDK2 as a biomarker is its role in the regulation of cell growth and the association with cancer cell proliferation. Studies have shown that CDK2 is involved in the regulation of cell growth and has been shown to promote the association of CDK2 with the protein p21, which is a well-known tumor suppressor protein. The association between CDK2 and p21 has been shown to promote the expression of anti-proliferative genes, such as p21, which can inhibit cell proliferation.

In addition, studies have shown that the expression of CDK2 is associated with the poor prognosis of cancer patients. Studies have shown that the expression of CDK2 is associated with poor prognosis in various types of cancer, including breast, ovarian, and colorectal cancers.

Conclusion

In conclusion, CDK2 is a protein that has been shown to play a crucial role in the regulation of cell division and growth. The potential of CDK2 as a drug target and biomarker for cancer treatment is due to its involvement in the regulation of the cell cycle and its association with the regulation of cell survival. Further research is needed to fully understand the role of CDK2 in cancer treatment and to develop safe and effective drugs that target CDK2.

Protein Name: Cyclin Dependent Kinase 2

Functions: Serine/threonine-protein kinase involved in the control of the cell cycle; essential for meiosis, but dispensable for mitosis. Phosphorylates CTNNB1, USP37, p53/TP53, NPM1, CDK7, RB1, BRCA2, MYC, NPAT, EZH2. Triggers duplication of centrosomes and DNA. Acts at the G1-S transition to promote the E2F transcriptional program and the initiation of DNA synthesis, and modulates G2 progression; controls the timing of entry into mitosis/meiosis by controlling the subsequent activation of cyclin B/CDK1 by phosphorylation, and coordinates the activation of cyclin B/CDK1 at the centrosome and in the nucleus. Crucial role in orchestrating a fine balance between cellular proliferation, cell death, and DNA repair in human embryonic stem cells (hESCs). Activity of CDK2 is maximal during S phase and G2; activated by interaction with cyclin E during the early stages of DNA synthesis to permit G1-S transition, and subsequently activated by cyclin A2 (cyclin A1 in germ cells) during the late stages of DNA replication to drive the transition from S phase to mitosis, the G2 phase. EZH2 phosphorylation promotes H3K27me3 maintenance and epigenetic gene silencing. Phosphorylates CABLES1 (By similarity). Cyclin E/CDK2 prevents oxidative stress-mediated Ras-induced senescence by phosphorylating MYC. Involved in G1-S phase DNA damage checkpoint that prevents cells with damaged DNA from initiating mitosis; regulates homologous recombination-dependent repair by phosphorylating BRCA2, this phosphorylation is low in S phase when recombination is active, but increases as cells progress towards mitosis. In response to DNA damage, double-strand break repair by homologous recombination a reduction of CDK2-mediated BRCA2 phosphorylation. Phosphorylation of RB1 disturbs its interaction with E2F1. NPM1 phosphorylation by cyclin E/CDK2 promotes its dissociates from unduplicated centrosomes, thus initiating centrosome duplication. Cyclin E/CDK2-mediated phosphorylation of NPAT at G1-S transition and until prophase stimulates the NPAT-mediated activation of histone gene transcription during S phase. Required for vitamin D-mediated growth inhibition by being itself inactivated. Involved in the nitric oxide- (NO) mediated signaling in a nitrosylation/activation-dependent manner. USP37 is activated by phosphorylation and thus triggers G1-S transition. CTNNB1 phosphorylation regulates insulin internalization. Phosphorylates FOXP3 and negatively regulates its transcriptional activity and protein stability (By similarity). Phosphorylates CDK2AP2 (PubMed:12944431). Phosphorylates ERCC6 which is essential for its chromatin remodeling activity at DNA double-strand breaks (PubMed:29203878)

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•   general information;
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•   protein biological mechanisms;
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•   the target screening and validation;
•   expression level;
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