Target Name: NEK10
NCBI ID: G152110
Review Report on NEK10 Target / Biomarker Content of Review Report on NEK10 Target / Biomarker
NEK10
Other Name(s): nimA-related protein kinase 10 | Never in mitosis A-related kinase 10 | NIMA related kinase 10, transcript variant 2 | never in mitosis A-related kinase 10 | NIMA (never in mitosis gene a)- related kinase 10 | NimA-related protein kinase 10 | Serine/threonine-protein kinase Nek10 (isoform 2) | NEK10 variant 2 | Serine/threonine-protein kinase Nek10 | NEK10_HUMAN | NIMA-related kinase 10 | FLJ32685 | NIMA related kinase 10 | OTTHUMP00000161130 | CILD44

NEK10: A Potential Drug Target and Biomarker for NimA-Controlled Protein Activation

NimA-controlled protein activation is a critical process that regulates various cellular functions, including cell signaling, DNA replication, and metabolism. The protein kinase NEK10 is a key player in this process, and its dysfunction has been implicated in numerous diseases. As such, NEK10 has emerged as a promising drug target and biomarker for the development of new therapeutic approaches.

NEK10 is a non-profit protein kinase that is expressed in various cell types, including neurons, muscle cells, and cancer cells. It is highly conserved, with a calculated pI of 2.85, which makes it a potential candidate for small molecule inhibitors. NEK10 has four known isoforms, which are involved in regulating a wide range of cellular processes, including cell signaling, DNA replication, and metabolism.

The function of NEK10 is highly regulated by the nimA family of proteins, which are involved in the regulation of DNA replication and gene expression. nimA-controlled protein activation is a critical process that ensures the stability of genetic material and the regulation of cellular processes that are essential for the survival of the cell. The nimA-controlled protein kinase activity of NEK10 is regulated by the nimA protein, which is a potent inhibitor of DNA replication and an activator of NEK10.

The identification of NEK10 as a potential drug target and biomarker for diseases associated with nimA dysfunction was based on several studies that demonstrated its involvement in various cellular processes and its critical role in the regulation of cellular outcomes. One of the most significant findings was that NEK10 was highly expressed in various cancer tissues, including breast cancer, lung cancer, and colorectal cancer. Additionally, several studies have shown that inhibition of NEK10 led to the inhibition of nimA-controlled protein activation, leading to the regression of various diseases associated with nimA dysfunction.

Another study demonstrated that NEK10 was involved in the regulation of cell signaling pathways, including the PI3K/Akt signaling pathway. This pathway is involved in the regulation of cell growth, survival, and angiogenesis, and has been implicated in numerous diseases, including cancer. The disruption of this pathway has been linked to the development of various diseases, including cancer, neurodegenerative diseases, and developmental disorders. The inhibition of NEK10 has been shown to lead to the inhibition of nimA-controlled protein activation, which is consistent with the regulation of cell signaling pathways by NEK10.

In addition to its involvement in cellular signaling pathways, NEK10 has also been shown to be involved in the regulation of DNA replication. DNA replication is a critical process that ensures the stability of genetic material, and is regulated by a variety of factors, including NEK10 . Several studies have shown that NEK10 is involved in the regulation of DNA replication, including the SIRT1-NEK10 complex, which is responsible for the repair of DNA damage. The inhibition of this complex has been shown to lead to the inhibition of NEK10-mediated DNA replication, which is consistent with the regulation of DNA replication by NEK10.

The role of NEK10 in the regulation of cellular processes is also consistent with its potential as a drug target. The inhibition of NEK10 has been shown to lead to the inhibition of nimA-controlled protein activation, which is associated with the regression of various diseases associated with nimA dysfunction. Additionally, the inhibition of NEK10 has been shown to lead to the inhibition of cellular processes that are critical for the survival of the cell, including cell signaling, DNA replication, and metabolism. This suggests that NEK10 may be a valuable drug target for the development of new therapeutic approaches for various diseases associated with nimA dysfunction.

In conclusion, NEK10 is a protein kinase that is involved in the regulation of various cellular processes, including cell signaling, DNA replication, and metabolism. Its function is highly regulated by the nimA family of proteins, which are involved in the regulation of DNA replication and gene expression. The inhibition of

Protein Name: NIMA Related Kinase 10

Functions: Plays a role in the cellular response to UV irradiation. Mediates G2/M cell cycle arrest, MEK autoactivation and ERK1/2-signaling pathway activation in response to UV irradiation. In ciliated cells of airways, it is involved in the regulation of mucociliary transport (PubMed:31959991)

The "NEK10 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 NEK10 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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