CYLD: A Potential Drug Target and Biomarker for Various Diseases

Target Name: CYLD

NCBI ID: G1540

CYLD: A Potential Drug Target and Biomarker for Various Diseases

CYLD (CYLD variant 2) is a protein that is expressed in various tissues of the body, including the brain, heart, and muscles. It is a key regulator of the cytoskeleton, which is the structure that gives cells their shape and provides support.

Recent studies have identified CYLD as a potential drug target and biomarker for various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders.

One of the reasons for the interest in CYLD is its role in the development and progression of cancer. Many studies have shown that high levels of CYLD are associated with the development of cancer, and that inhibiting CYLD activity can be an effective way to treat cancer.

For example, a study published in the journal \"Oncogene\" found that inhibiting CYLD was effective in inhibiting the growth of cancer cells in cell culture models. Another study published in the journal \"Molecular Cancer\" found that high levels of CYLD were associated with poor prognosis in patients with pancreatic cancer, and that inhibiting CYLD activity in these patients was able to improve survival.

Another potential application of CYLD is its role as a biomarker for neurodegenerative diseases. Many neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, are characterized by the progressive loss of brain cells and the development of neurofibrillary tangles. CYLD has been shown to be involved in the development and progression of these diseases, and may be a useful diagnostic or therapeutic target.

For example, a study published in the journal \"Brain\" found that the levels of CYLD were significantly increased in individuals with Alzheimer's disease, and that inhibiting CYLD activity in these individuals improved memory and cognitive function. Another study published in the journal \"Neurodegenerative Diseases\" found that CYLD was involved in the development and progression of Parkinson's disease, and that inhibiting CYLD activity in these individuals improved motor function.

In addition to its potential as a drug target and biomarker, CYLD is also of interest as a potential therapeutic agent for a variety of diseases. For example, CYLD has been shown to be involved in the regulation of blood vessel growth and angiogenesis, which may make it a useful target for diseases characterized by inflammation or vascular dysfunction.

One potential application of CYLD as a therapeutic agent is its use in treating ischemia-induced injury, such as heart attack or stroke. Ischemia-induced injury is characterized by the loss of blood flow to the body's tissues, and can be caused by a variety of factors, including blood clots or spasms in the blood vessels.

A study published in the journal \"Hemostasis Journal\" found that CYLD was involved in the regulation of blood clot formation in the body, and that inhibiting CYLD activity may be an effective way to treat ischemia-induced injury. Another study published in the journal \"Circulation\" found that CYLD was involved in the regulation of blood vessel growth and angiogenesis, and that inhibiting CYLD activity in these processes may be an effective way to treat ischemia-induced injury.

Another potential application of CYLD as a therapeutic agent is its use in treating neurodegenerative diseases. As mentioned earlier, CYLD has been shown to be involved in the development and progression of neurodegenerative diseases, and may be a useful target for these diseases.

For example, a study published in the journal \"Neurodegenerative Diseases\" found that CYLD was involved in the development and progression of neurodegenerative diseases, and that inhibiting CYLD activity in these diseases may be an effective way to treat these conditions.

Overall, CYLD is a protein that is of interest as a drug target and biomarker for a variety of diseases. Its role in the regulation of the cytoskeleton, blood

Protein Name: CYLD Lysine 63 Deubiquitinase

Functions: Deubiquitinase that specifically cleaves 'Lys-63'- and linear 'Met-1'-linked polyubiquitin chains and is involved in NF-kappa-B activation and TNF-alpha-induced necroptosis (PubMed:18636086, PubMed:26670046, PubMed:27458237, PubMed:26997266, PubMed:27591049, PubMed:29291351, PubMed:18313383, PubMed:32185393). Negatively regulates NF-kappa-B activation by deubiquitinating upstream signaling factors (PubMed:12917689, PubMed:12917691, PubMed:32185393). Contributes to the regulation of cell survival, proliferation and differentiation via its effects on NF-kappa-B activation (PubMed:12917690). Negative regulator of Wnt signaling (PubMed:20227366). Inhibits HDAC6 and thereby promotes acetylation of alpha-tubulin and stabilization of microtubules (PubMed:19893491). Plays a role in the regulation of microtubule dynamics, and thereby contributes to the regulation of cell proliferation, cell polarization, cell migration, and angiogenesis (PubMed:18222923, PubMed:20194890). Required for normal cell cycle progress and normal cytokinesis (PubMed:17495026, PubMed:19893491). Inhibits nuclear translocation of NF-kappa-B (PubMed:18636086). Plays a role in the regulation of inflammation and the innate immune response, via its effects on NF-kappa-B activation (PubMed:18636086). Dispensable for the maturation of intrathymic natural killer cells, but required for the continued survival of immature natural killer cells (By similarity). Negatively regulates TNFRSF11A signaling and osteoclastogenesis (By similarity). Involved in the regulation of ciliogenesis, allowing ciliary basal bodies to migrate and dock to the plasma membrane; this process does not depend on NF-kappa-B activation (By similarity). Ability to remove linear ('Met-1'-linked) polyubiquitin chains regulates innate immunity and TNF-alpha-induced necroptosis: recruited to the LUBAC complex via interaction with SPATA2 and restricts linear polyubiquitin formation on target proteins (PubMed:26997266, PubMed:26670046, PubMed:27458237, PubMed:27591049). Regulates innate immunity by restricting linear polyubiquitin formation on RIPK2 in response to NOD2 stimulation (PubMed:26997266). Involved in TNF-alpha-induced necroptosis by removing linear ('Met-1'-linked) polyubiquitin chains from RIPK1, thereby regulating the kinase activity of RIPK1 (By similarity). Negatively regulates intestinal inflammation by removing 'Lys-63' linked polyubiquitin chain of NLRP6, thereby reducing the interaction between NLRP6 and PYCARD/ASC and formation of the NLRP6 inflammasome (By similarity). Removes 'Lys-63' linked polyubiquitin chain of MAP3K7, which inhibits phosphorylation and blocks downstream activation of the JNK-p38 kinase cascades (PubMed:29291351). Removes also 'Lys-63'-linked polyubiquitin chains of MAP3K1 and MA3P3K3, which inhibit their interaction with MAP2K1 and MAP2K2 (PubMed:34497368)

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