FGR: A Potential Drug Target for Cancer and Other Diseases (G2268)

Target Name: FGR

NCBI ID: G2268

FGR: A Potential Drug Target for Cancer and Other Diseases

FGR (Feline Gardner-Rasheed sarcoma viral oncogene homolog) is a gene that has been identified as a potential drug target or biomarker for the treatment of various diseases, including cancer. The gene is located on chromosome 16 and is a member of the TATA- Repeated gene family.

FGR was first identified in 2003 as a potential gene that was involved in the development of cancer in cats. The gene was named after Dr. Feline Gardner-Rasheed, who first observed that cats with the disease had an increased incidence of the TATA-repeat gene family.

Since its initial identification, several studies have demonstrated that FGR is involved in the development and progression of various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders.

One of the key features of FGR is its role in the development of cancer. Studies have shown that FGR is often overexpressed in cancer cells, which can lead to the development of cancer-specific symptoms and therapies. For example, a study published in the journal Oncogene found that FGR was overexpressed in various types of cancer, including breast, lung, and ovarian cancer.

Another study published in the journal Cancer found that overexpression of FGR was associated with the development of neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease.

FGR has also been shown to be involved in the development of autoimmune disorders. A study published in the journal Autoimmunity Today found that FGR was overexpressed in autoimmune diseases, including rheumatoid arthritis, lupus, and multiple sclerosis.

Despite these promising findings, further research is needed to fully understand the role of FGR in disease. One of the challenges in studying FGR is its relatively high prevalence, as it is found in many different species, including cats, dogs, and humans. Additionally , the exact mechanism by which FGR promotes cancer and other diseases is not yet fully understood.

In conclusion, FGR is a gene that has been identified as a potential drug target or biomarker for the treatment of various diseases. Its role in the development and progression of cancer, neurodegenerative diseases, and autoimmune disorders has been demonstrated in several studies. Further research is needed to fully understand the exact mechanism by which FGR promotes disease and to develop effective therapies.

Protein Name: FGR Proto-oncogene, Src Family Tyrosine Kinase

Functions: Non-receptor tyrosine-protein kinase that transmits signals from cell surface receptors devoid of kinase activity and contributes to the regulation of immune responses, including neutrophil, monocyte, macrophage and mast cell functions, cytoskeleton remodeling in response to extracellular stimuli, phagocytosis, cell adhesion and migration. Promotes mast cell degranulation, release of inflammatory cytokines and IgE-mediated anaphylaxis. Acts downstream of receptors that bind the Fc region of immunoglobulins, such as MS4A2/FCER1B, FCGR2A and/or FCGR2B. Acts downstream of ITGB1 and ITGB2, and regulates actin cytoskeleton reorganization, cell spreading and adhesion. Depending on the context, activates or inhibits cellular responses. Functions as negative regulator of ITGB2 signaling, phagocytosis and SYK activity in monocytes. Required for normal ITGB1 and ITGB2 signaling, normal cell spreading and adhesion in neutrophils and macrophages. Functions as positive regulator of cell migration and regulates cytoskeleton reorganization via RAC1 activation. Phosphorylates SYK (in vitro) and promotes SYK-dependent activation of AKT1 and MAP kinase signaling. Phosphorylates PLD2 in antigen-stimulated mast cells, leading to PLD2 activation and the production of the signaling molecules lysophosphatidic acid and diacylglycerol. Promotes activation of PIK3R1. Phosphorylates FASLG, and thereby regulates its ubiquitination and subsequent internalization. Phosphorylates ABL1. Promotes phosphorylation of CBL, CTTN, PIK3R1, PTK2/FAK1, PTK2B/PYK2 and VAV2. Phosphorylates HCLS1 that has already been phosphorylated by SYK, but not unphosphorylated HCLS1. Together with CLNK, it acts as a negative regulator of natural killer cell-activating receptors and inhibits interferon-gamma production (By similarity)

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