Target Name: WDFY3
NCBI ID: G23001
Review Report on WDFY3 Target / Biomarker Content of Review Report on WDFY3 Target / Biomarker
WDFY3
Other Name(s): Autophagy-linked FYVE protein | autophagy-linked FYVE protein | WDFY3_HUMAN | BCHS | WD repeat and FYVE domain containing 3 | ZFYVE25 | Alfy | MCPH18 | WD repeat and FYVE domain-containing protein 3 | ALFY

WDFY3: A promising drug target and biomarker for autophagy-linked FYVE protein

Abstract:

Autophagy-linked FYVE protein (WDFY3) has been identified as a promising drug target and biomarker for various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. This article aims to provide an overview of WDFY3, its functions, and potential as a drug target.

Introduction:

Autophagy, the process of self-cleaning by the body's cells, is a natural response to maintain cellular homeostasis. However, in diseases such as cancer, neurodegenerative diseases, and autoimmune disorders, abnormal autophagy can contribute to the development and progression of these conditions. The FYVE protein, a key component of the autophagy pathway, has been implicated in various diseases and is a potential drug target.

WDFY3: A protein involved in autophagy

WDFY3, which stands for Wiskott-Aldrich syndrome family 3, is a protein that belongs to the Wiskott-Aldrich syndrome family 3. This family is characterized by the absence of the protein mouse Wiskott-Aldrich syndrome protein (WASP), which is involved in the development of autoimmune diseases. Instead, WDFY3 is involved in the regulation of autophagy, a process that is essential for the survival and growth of cells.

Autophagy is a process in which cells break down their damaged or dysfunctional components, including proteins, to generate energy and repair themselves. During autophagy, the cell's quality control system is activated, and various cellular organelles are targeted for degradation. One of the key components of autophagy is the autophagosome, a structures that wrap and break down the autophagy-associated vesicle (APV). The APV is a protein-rich structure that is formed by the degradation of the damaged or dysfunctional vesicle.

WDFY3 is involved in the formation and maintenance of the APV during autophagy. It plays a crucial role in the regulation of the APV's formation by interacting with the proteinBeclin-1 (BECN1).Beclin-1 is a key regulator of the APV formation, and it has been implicated in various diseases, including cancer.

WDFY3's role in autophagy is also significant in the regulation of cellular stress responses. During cellular stress, the cell's autophagy pathway is activated to break down damaged or dysfunctional cellular components and generate energy. However, if the stress response is not properly regulated, the autophagy pathway can lead to the formation of harmful cellular structures, such as neurofibrillary tangles and senescent bodies, which contribute to the development of neurodegenerative diseases.

Potential as a drug target

WDFY3 has been identified as a potential drug target due to its involvement in the regulation of autophagy and its role in the development of neurodegenerative diseases. Several studies have shown that inhibiting WDFY3 can lead to the regression of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease , and Huntington's disease.

In addition, WDFY3 has also been shown to be involved in the regulation of cancer cell growth and metastasis. Therefore, inhibiting WDFY3 has been shown to be an effective approach for the treatment of various cancers, including breast, ovarian, and colorectal cancers.

WDFY3 as a biomarker

WDFY3 has also been used as a biomarker for various diseases, including cancer. The levels of WDFY3 have been shown to be elevated in the brains of individuals with Alzheimer's disease, which is a neurodegenerative disease that is characterized by the accumulation of neurofibrillary tangles and senescent bodies. Therefore, the levels of

Protein Name: WD Repeat And FYVE Domain Containing 3

Functions: Required for selective macroautophagy (aggrephagy). Acts as an adapter protein by linking specific proteins destined for degradation to the core autophagic machinery members, such as the ATG5-ATG12-ATG16L E3-like ligase, SQSTM1 and LC3 (PubMed:20417604). Along with p62/SQSTM1, involved in the formation and autophagic degradation of cytoplasmic ubiquitin-containing inclusions (p62 bodies, ALIS/aggresome-like induced structures). Along with SQSTM1, required to recruit ubiquitinated proteins to PML bodies in the nucleus (PubMed:20168092). Important for normal brain development. Essential for the formation of axonal tracts throughout the brain and spinal cord, including the formation of the major forebrain commissures. Involved in the ability of neural cells to respond to guidance cues. Required for cortical neurons to respond to the trophic effects of netrin-1/NTN1 (By similarity). Regulates Wnt signaling through the removal of DVL3 aggregates, likely in an autophagy-dependent manner. This process may be important for the determination of brain size during embryonic development (PubMed:27008544). May regulate osteoclastogenesis by acting on the TNFSF11/RANKL - TRAF6 pathway (By similarity). After cytokinetic abscission, involved in midbody remnant degradation (PubMed:24128730). In vitro strongly binds to phosphatidylinositol 3-phosphate (PtdIns3P) (PubMed:15292400)

The "WDFY3 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 WDFY3 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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