FZD4: A Potential Drug Target for Neurological Disorders (G8322)

Target Name: FZD4

NCBI ID: G8322

Other Name(s): FEVR | DG280 | frizzled class receptor 4 | FZD4S | frizzled 4, seven transmembrane spanning receptor | CD344 | Fz4 | frizzled homolog 4 | MGC34390 | FzE4 | frizzled family receptor 4 | WNT receptor frizzled-4 | Frizzled class receptor 4 | EVR1 | Frizzled-4 | Fz-4 | FZD4_HUMAN | hFz4 | GPCR

FZD4: A Potential Drug Target for Neurological Disorders

FZD4 (Feivar) is a drug target (or biomarker) that has been shown to play a crucial role in the development and progression of various neurological disorders, including Alzheimer's disease, Parkinson's disease, and other dementias. FZD4 is a protein that is expressed in the brain and has been shown to be involved in the formation of beta-amyloid plaques, which are a hallmark of Alzheimer's disease.

FZD4 has also been shown to be involved in the regulation of neurotransmitter systems, including dopamine and glutamate. These neurotransmitters are important for the functioning of the brain and have been implicated in the development of various neurological disorders. By regulating these neurotransmitters, FZD4 has been shown to play a role in the treatment of neurological disorders.

FZD4 has also been shown to be involved in the regulation of the immune system. Studies have shown that FZD4 can modulate the immune response and influence the formation of immune complexes, which are important for the development of neurodegenerative disorders.

FZD4 has also been shown to be involved in the regulation of cellular signaling pathways, including the TGF-beta pathway. This pathway is important for the development and maintenance of tissues and has been implicated in the development of various diseases, including cancer.

FZD4 has also been shown to be involved in the regulation of the blood-brain barrier. This barrier is responsible for controlling the movement of substances into and out of the brain and has been shown to be involved in the development of various neurological disorders, including Alzheimer's disease.

In conclusion, FZD4 is a drug target (or biomarker) that has been shown to play a crucial role in the development and progression of various neurological disorders. FZD4 is involved in the formation of beta-amyloid plaques, the regulation of neurotransmitter systems, the immune system, and cellular signaling pathways, and the regulation of the blood-brain barrier. These functions make FZD4 an attractive target for the development of new treatments for neurological disorders.

FZD4 is also a potential biomarker for the diagnosis and monitoring of neurological disorders. By measuring the level of FZD4 in brain tissue, researchers can assess the severity of neurological disorders and monitor the effectiveness of different treatments. This could lead to earlier detection of neurological disorders and the development of more effective treatments.

Overall, FZD4 is a drug target (or biomarker) that has the potential to revolutionize the treatment of neurological disorders. Further research is needed to fully understand the role of FZD4 in the development and progression of neurological disorders and to develop effective treatments.

Protein Name: Frizzled Class Receptor 4

Functions: Receptor for Wnt proteins (PubMed:30135577). Most frizzled receptors are coupled to the beta-catenin (CTNNB1) canonical signaling pathway, which leads to the activation of disheveled proteins, inhibition of GSK-3 kinase, nuclear accumulation of beta-catenin (CTNNB1) and activation of Wnt target genes (PubMed:30135577). Plays a critical role in retinal vascularization by acting as a receptor for Wnt proteins and norrin (NDP) (By similarity). In retina, it can be activated by Wnt protein-binding and also by Wnt-independent signaling via binding of norrin (NDP), promoting in both cases beta-catenin (CTNNB1) accumulation and stimulation of LEF/TCF-mediated transcriptional programs (By similarity). A second signaling pathway involving PKC and calcium fluxes has been seen for some family members, but it is not yet clear if it represents a distinct pathway or if it can be integrated in the canonical pathway, as PKC seems to be required for Wnt-mediated inactivation of GSK-3 kinase. Both pathways seem to involve interactions with G-proteins. May be involved in transduction and intercellular transmission of polarity information during tissue morphogenesis and/or in differentiated tissues

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