AXL: The Drug Target of the Future? (G558)

Target Name: AXL

NCBI ID: G558

Content of Review Report on AXL Target / Biomarker

AXL

AXL: The Drug Target of the Future?

AXL, or axl, is a protein that is expressed in various tissues throughout the body, including the brain, heart, lungs, and kidneys. It is a key regulator of cell growth, differentiation, and survival, and has been implicated in numerous diseases, including cancer, neurodegenerative disorders, and chronic obstructive pulmonary disease (COPD). In recent years, researchers have been increasingly interested in using AXL as a drug target or biomarker, with the aim of developing new treatments for a range of diseases. In this article, we will explore the biology of AXL, its functions as a drug target, and the current state of research in this field.

The Biology of AXL

AXL is a member of the TATA gene family, which is known for regulating gene expression and cell growth. It consists of four coding genes, AXL1, AXL2, AXL3, and AXL4, and is expressed in a variety of tissues, including the brain, heart, lungs, and kidneys. AXL is involved in the regulation of cell proliferation, differentiation, and survival, as well as in the development and progression of various diseases.

One of the most well-studied functions of AXL is its role in cancer. Many studies have shown that AXL is highly expressed in various types of cancer, including lung, breast, and ovarian cancer. It has been shown to promote the growth and survival of cancer cells, and to contribute to their invasive and metastatic properties. In addition, AXL has been implicated in the development of neurodegenerative disorders, including Alzheimer's disease and Parkinson's disease.

As a drug target, AXL has the potential to be used to treat a wide range of diseases, including cancer, neurodegenerative disorders, and respiratory diseases. Researchers have been interested in developing compounds that can inhibit the activity of AXL, or that can activate its intracellular signaling pathways, in order to treat these diseases.

The Potential of AXL as a Drug Target

AXL has the potential to be a drug target for a variety of diseases, due to its involvement in multiple cellular processes that are important for disease development. As mentioned above, AXL has been shown to contribute to the growth and survival of cancer cells, and has been implicated in the development of neurodegenerative disorders. Therefore, compounds that can inhibit AXL activity may have a wide range of potential applications in cancer and neurodegenerative diseases.

In addition to its role in cancer and neurodegenerative disorders, AXL is also a potential drug target for respiratory diseases. Studies have shown that AXL is involved in the regulation of cell growth and survival in the lungs, and that it contributes to the development of chronic obstructive pulmonary disease (COPD). Therefore, compounds that can inhibit AXL activity in the lungs may have potential applications in treating COPD and other respiratory diseases.

Current State of Research

Current research on AXL is focused on its potential as a drug target for cancer, neurodegenerative disorders, and respiratory diseases. Researchers have been interested in developing compounds that can inhibit AXL activity, or that can activate its intracellular signaling pathways, in order to treat these diseases.

One approach to developing compounds that can inhibit AXL activity is to use a variety of techniques, including high-throughput screening and drug discovery studies. Researchers have used a variety of compounds, including small molecules, peptides, and antibodies, to test their ability to inhibit AXL activity. Many of these compounds have been shown to be effective in inhibiting AXL activity, and have the potential to be used as drugs.

Another approach to developing compounds that can activate AXL activity is to use gene editing techniques to modify the expression of the AXL gene. Researchers have used CRISPR/Cas9

Protein Name: AXL Receptor Tyrosine Kinase

Functions: Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding growth factor GAS6 and which is thus regulating many physiological processes including cell survival, cell proliferation, migration and differentiation. Ligand binding at the cell surface induces dimerization and autophosphorylation of AXL. Following activation by ligand, AXL binds and induces tyrosine phosphorylation of PI3-kinase subunits PIK3R1, PIK3R2 and PIK3R3; but also GRB2, PLCG1, LCK and PTPN11. Other downstream substrate candidates for AXL are CBL, NCK2, SOCS1 and TNS2. Recruitment of GRB2 and phosphatidylinositol 3 kinase regulatory subunits by AXL leads to the downstream activation of the AKT kinase. GAS6/AXL signaling plays a role in various processes such as endothelial cell survival during acidification by preventing apoptosis, optimal cytokine signaling during human natural killer cell development, hepatic regeneration, gonadotropin-releasing hormone neuron survival and migration, platelet activation, or regulation of thrombotic responses. Also plays an important role in inhibition of Toll-like receptors (TLRs)-mediated innate immune response

The "AXL 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 AXL 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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