Target Name: CDK8
NCBI ID: G1024
Review Report on CDK8 Target / Biomarker Content of Review Report on CDK8 Target / Biomarker
CDK8
Other Name(s): mediator of RNA polymerase II transcription subunit CDK8 | Mediator complex subunit CDK8 | cyclin dependent kinase 8 | Cyclin-dependent kinase 8 (isoform 1) | Mediator of RNA polymerase II transcription subunit CDK8 | CDK8 protein kinase | CDK8_HUMAN | K35 | cell division protein kinase 8 | IDDHBA | MGC126074 | Protein kinase K35 | MGC126075 | Cyclin-dependent kinase 8 | mediator complex subunit CDK8 | protein kinase K35 | Cyclin dependent kinase 8, transcript variant 1 | CDK8 variant 1 | Cell division protein kinase 8

CDK8: A promising drug target for cancer treatment

CDK8, a member of the cyclin-dependent kinase 8 (CDK8) family, is a key regulator of cell proliferation and differentiation. CDK8 plays a crucial role in the transcription of RNA polymerase II (RNA polymerase II), which is responsible for producing virtually all RNA in the cell. CDK8 has been implicated in various cellular processes, including cell cycle progression, apoptosis, and tissue repair. As a result, targeting CDK8 has been identified as a promising strategy for cancer treatment.

CDK8 as a drug target

CDK8 has been identified as a potential drug target due to its involvement in various cellular processes that are associated with cancer development. Several studies have shown that inhibition of CDK8 can lead to the inhibition of cancer cell growth and the triggering of apoptosis.

One of the key reasons for the potential of CDK8 as a drug target is its involvement in the regulation of cell proliferation. CDK8 is known to play a role in the G1-S transition, which is a critical phase of the cell cycle where cell growth and differentiation occur. In G1, CDK8 promotes the loading of the RNA polymerase II complex onto the nuclear envelope and facilitates the opening of the nuclear channels that allow the entry of RNA and the initiation of transcription. In S, CDK8 promotes the separation of the RNA polymerase II complex from the nuclear envelope and facilitates the closure of these channels.

In addition to its role in cell proliferation, CDK8 has also been implicated in the regulation of apoptosis. CDK8 has been shown to play a role in the regulation of cell apoptosis, which is a natural process that is involved in the elimination of damaged or dysfunctional cells. Studies have shown that CDK8 promotes the production of pro-apoptotic proteins, such as Bcl-2, which can inhibit the inhibition of cell apoptosis.

Another potential mechanism by which CDK8 may contribute to cancer development is its involvement in tissue repair. CDK8 has been shown to play a role in the regulation of tissue repair, which is a critical process that is essential for the maintenance of tissue homeostasis. studies have shown that CDK8 promotes the production of pro-inflammatory cytokines, such as TNF-alpha, which can contribute to the development of cancer.

CDK8 inhibition as a cancer treatment

CDK8 inhibition has been shown to be an effective strategy for cancer treatment. Several studies have shown that inhibition of CDK8 can lead to the inhibition of cancer cell growth and the triggering of apoptosis.

One of the key advantages of CDK8 inhibition as a cancer treatment is its selectivity. Unlike many other kinases, CDK8 inhibitors have been shown to have a low toxicity and a high therapeutic index. This means that they can be used at relatively low concentrations to achieve effective cancer treatment.

Another advantage of CDK8 inhibition is its ability to cross-resist. Many CDK8 inhibitors have been shown to be cross-resist, which means that they can inhibit CDK8 activity even in cells that are resistant to inhibition. This may be important for cancer treatment, as some cancers may become resistant to traditional cancer treatments.

CDK8 inhibition has been shown to be effective in a variety of cancer types, including breast, ovarian, and colorectal cancers. For example, a study by the National Cancer Institute found that CDK8 inhibitors were effective in treating breast cancer in both pre- and post-menopausal women. The study showed that the overall treatment effect was associated with the inhibition of

Protein Name: Cyclin Dependent Kinase 8

Functions: Component of the Mediator complex, a coactivator involved in regulated gene transcription of nearly all RNA polymerase II-dependent genes. Mediator functions as a bridge to convey information from gene-specific regulatory proteins to the basal RNA polymerase II transcription machinery. Mediator is recruited to promoters by direct interactions with regulatory proteins and serves as a scaffold for the assembly of a functional pre-initiation complex with RNA polymerase II and the general transcription factors. Phosphorylates the CTD (C-terminal domain) of the large subunit of RNA polymerase II (RNAp II), which may inhibit the formation of a transcription initiation complex. Phosphorylates CCNH leading to down-regulation of the TFIIH complex and transcriptional repression. Recruited through interaction with MAML1 to hyperphosphorylate the intracellular domain of NOTCH, leading to its degradation

The "CDK8 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about CDK8 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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CDK9 | CDKAL1 | CDKL1 | CDKL2 | CDKL3 | CDKL4 | CDKL5 | CDKN1A | CDKN1B | CDKN1C | CDKN2A | CDKN2A-DT | CDKN2AIP | CDKN2AIPNL | CDKN2AIPNLP1 | CDKN2B | CDKN2B-AS1 | CDKN2C | CDKN2D | CDKN3 | CDNF | CDO1 | CDON | CDPF1 | CDR1 | CDR2 | CDR2L | CDRT15 | CDRT15L2 | CDRT4 | CDRT7 | CDS1 | CDS2 | CDSN | CDT1 | CDV3 | CDX1 | CDX2 | CDX4 | CDY1 | CDY1B | CDY2A | CDYL | CDYL2 | CEACAM1 | CEACAM16 | CEACAM16-AS1 | CEACAM18 | CEACAM19 | CEACAM20 | CEACAM21 | CEACAM22P | CEACAM3 | CEACAM4 | CEACAM5 | CEACAM6 | CEACAM7 | CEACAM8 | CEACAMP1 | CEACAMP10 | CEACAMP3 | CEACAMP4 | CEACAMP5 | CEBPA | CEBPA-DT | CEBPB | CEBPB-AS1 | CEBPD | CEBPE | CEBPG | CEBPZ | CEBPZOS | CECR2 | CECR2-containing remodeling factor complex | CECR3 | CECR7 | CEL | CELA1 | CELA2A | CELA2B | CELA3A | CELA3B | CELF1 | CELF2 | CELF2-AS1 | CELF2-AS2 | CELF3 | CELF4 | CELF5 | CELF6 | CELP | CELSR1 | CELSR2 | CELSR3 | CEMIP | CEMIP2 | CEMP1 | CENATAC | CEND1 | CENP-A-nucleosome distal (CAD) centromere complex