NUAK2: A Potential Drug Target and Biomarker for Osteoporosis

Target Name: NUAK2

NCBI ID: G81788

NUAK2

NUAK2: A Potential Drug Target and Biomarker for Osteoporosis

Osteoporosis is a condition characterized by the progressive loss of bone mass, leading to a risk of fractures. It is a global health concern, affecting millions of individuals, and its incidence is expected to increase in the coming years due to the aging population. Arthritis is a disease caused by the gradual loss of bone mass, leading to an increased risk of fractures. It is a global health problem that is expected to affect millions of people in the coming years and is expected to increase due to the aging population.

NUAK2 is a kinase that belongs to the Omphalocele kinase 2 family. It plays an important role in a variety of physiological processes, including cell proliferation, survival, and apoptosis. NUAK2 also plays an important role in various cancers, such as liver cancer, breast cancer, and lung cancer. Activation of NUAK2 leads to the phosphorylation of a variety of proteins, and these phosphorylation modifications can affect key biological processes such as cell cycle, proliferation and apoptosis.

In recent years, researchers have discovered that NUAK2 expression levels in bone and connective tissue increase with age. The expression level of NUAK2 is also related to various disease risk factors, such as age, gender, genetic polymorphisms and lifestyle. In addition, the expression level of NUAK2 is also related to the efficacy of various drugs, such as anti-tumor drugs and anti-osteoporosis drugs.

Due to its important role in a variety of diseases, NUAK2 is considered a potential drug target. Activation of NUAK2 is believed to cause a variety of diseases, including cancer, bone diseases, neurological diseases, and metabolic diseases. Therefore, studying the activation mechanism and action targets of NUAK2 has important clinical significance for the development of new treatments and drugs.

The activation mechanism of NUAK2 involves a variety of biological processes, including cell cycle, signaling pathways, proliferation and apoptosis. The activation of NUAK2 requires the participation of a variety of biological molecules, such as phosphorylase, phosphorylation substrates and NUAK2 itself. The occurrence of these biological processes will directly affect the activity and stability of NUAK2.

In recent years, researchers have discovered multiple targets of NUAK2 through high-throughput sequencing and other technologies. These targets include

Protein Name: NUAK Family Kinase 2

Functions: Stress-activated kinase involved in tolerance to glucose starvation. Induces cell-cell detachment by increasing F-actin conversion to G-actin. Expression is induced by CD95 or TNF-alpha, via NF-kappa-B. Protects cells from CD95-mediated apoptosis and is required for the increased motility and invasiveness of CD95-activated tumor cells. Phosphorylates LATS1 and LATS2. Plays a key role in neural tube closure during embryonic development through LATS2 phosphorylation and regulation of the nuclear localization of YAP1 a critical downstream regulatory target in the Hippo signaling pathway (PubMed:32845958)

The "NUAK2 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 NUAK2 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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