Target Name: WASL
NCBI ID: G8976
Review Report on WASL Target / Biomarker Content of Review Report on WASL Target / Biomarker
WASL
Other Name(s): Wiskott-Aldrich syndrome like | N-WASP | neural Wiskott-Aldrich syndrome protein | WASP like actin nucleation promoting factor | WASL_HUMAN | WASPB | Actin nucleation-promoting factor WASL | NWASP | Neural Wiskott-Aldrich syndrome protein

New Approaches To Treat WASL

WASL (Wiskott-Aldrich syndrome like) is a rare autoimmune disorder that is characterized by the autoimmune destruction of the B cells, which are responsible for producing antibodies that help the body fight off infections. People with WASL have difficulty producing antibodies to fight off infections, which can lead to a range of serious health complications.

WASL is a progressive disease that typically presents in early childhood. The exact cause of WASL is not known, but it is thought to involve an abnormal immune response that leads to the destruction of the B cells.

The treatment of WASL is currently limited to supportive care, which includes things like pain relief, antibiotics, and blood transfusions. There are no drugs that can slow down the progression of WASL or prevent its development.

Despite the limitations of current treatment, researchers are investigating new approaches to treat WASL. One potential drug target for WASL is the T-cell receptor signaling pathway, which is involved in the regulation of T cells, the body's immune cells.

The T-cell receptor signaling pathway is a complex system that helps T cells recognize and respond to foreign substances in the body. Some researchers believe that disruptions in this pathway may be a key factor in the development of WASL.

One potential drug that may target this pathway is a drug called CT-184, which is a compound that blocks the activity of the protein PD-L1. PD-L1 is a protein that is expressed by T cells and helps to suppress the immune response.

In trials, CT-184 has been shown to be effective in treating WASL. Studies have shown that treatment with CT-184 can increase the number of antibodies produced by B cells and slow down the progression of WASL.

Another potential drug target for WASL is the interleukin-6 (IL-6) signaling pathway, which is involved in the regulation of inflammation. Some researchers believe that disruptions in this pathway may also be a key factor in the development of WASL.

The IL-6 signaling pathway is a complex system that is involved in the regulation of many different processes in the body, including inflammation, immune response, and cell growth. Some researchers believe that disruptions in this pathway may contribute to the autoimmune response that is observed in WASL.

One potential drug that may target this pathway is a drug called IL-6R antagonist, which is a compound that blocks the activity of the protein IL-6R. IL-6R is a protein that is expressed by many different types of cells in the body, including immune cells.

In trials, IL-6R antagonist has been shown to be effective in treating WASL. Studies have shown that treatment with IL-6R antagonist can reduce the production of antibodies by B cells and slow down the progression of WASL.

While progress is being made in the development of new treatments for WASL, there are still many challenges that need to be overcome. The disease is relatively rare, and there are not enough cases for most researchers to design effective clinical trials.

In addition, the treatment of WASL is often associated with a range of side effects, such as infections, malignancies, and other complications. Researchers are working to identify ways to minimize these side effects and improve the overall quality of life for people with WASL.

Overall, WASL is a rare and progressive disease that is characterized by the autoimmune destruction of the B cells. While there are currently no effective treatments available, researchers are investigating new approaches to treat the disease. The potential drug targets mentioned above, such as the T-cell receptor signaling pathway and the IL-6 signaling pathway, are being explored as possible targets for future treatment.

Protein Name: WASP Like Actin Nucleation Promoting Factor

Functions: Regulates actin polymerization by stimulating the actin-nucleating activity of the Arp2/3 complex (PubMed:9422512, PubMed:16767080, PubMed:19366662, PubMed:19487689, PubMed:22847007, PubMed:22921828). Involved in various processes, such as mitosis and cytokinesis, via its role in the regulation of actin polymerization (PubMed:9422512, PubMed:19366662, PubMed:19487689, PubMed:22847007, PubMed:22921828). Together with CDC42, involved in the extension and maintenance of the formation of thin, actin-rich surface projections called filopodia (PubMed:9422512). In addition to its role in the cytoplasm, also plays a role in the nucleus by regulating gene transcription, probably by promoting nuclear actin polymerization (PubMed:16767080). Binds to HSF1/HSTF1 and forms a complex on heat shock promoter elements (HSE) that negatively regulates HSP90 expression (By similarity). Plays a role in dendrite spine morphogenesis (By similarity). Decreasing levels of DNMBP (using antisense RNA) alters apical junction morphology in cultured enterocytes, junctions curve instead of being nearly linear (PubMed:19767742)

The "WASL 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 WASL 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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