CHUK: A Protein Implicated in Neurodegeneration and Inflammation

Target Name: CHUK

NCBI ID: G1147

CHUK

CHUK: A Protein Implicated in Neurodegeneration and Inflammation

CHUK (CHU-Killing Extracellular Kallikrein-Induced Neurodegeneration) is a protein that is expressed in various tissues throughout the body, including the brain. It is a key regulator of inflammation and has been implicated in a number of neurodegenerative diseases, including Alzheimer's and Parkinson's. Despite its importance, little is known about CHUK and its potential as a drug target.

The CHUK gene was first identified in 2004 and has since been shown to encode a protein that is similar to kallikrein, a protein that is involved in the regulation of blood clotting. Kallikrein is a small protein that is composed of two distinct subunits: a monomeric subunit that contains a catalytic active site and a dimeric subunit that contains a carboxylic acid-containing tail. The CHUK protein is similar to kallikrein in that it contains a catalytic active site, but it is not known to have any direct function in the regulation of blood clotting.

One of the defining features of CHUK is its ability to induce neurodegeneration in various tissues. This is achieved through the production of reactive oxygen species (ROS), which can damage cellular components and contribute to the development of neurodegeneration. CHUK has been shown to induce neurodegeneration in a variety of cell types, including neurons, glial cells, and microglia.

The neurodegeneration that is caused by CHUK is characterized by the loss of cellular structure and the dysfunction of cellular processes. This includes the loss of neurotransmitter receptors, the disruption of synaptic plasticity, and the alteration of cellular signaling pathways. The specific cellular components that are affected by CHUK will depend on the cell type and the specific context in which the neurodegeneration is being observed.

One of the challenges in studying CHUK is its ability to cross the blood-brain barrier and its poor stability in the brain. This makes it difficult to study the effects of CHUK on neural function and the development of neurodegenerative diseases. However, recent studies have shown that CHUK is able to cross the blood-brain barrier and that it is expressed in the brains of CHUK-/- mice. These studies suggest that CHUK may have a role in the development and progression of neurodegenerative diseases.

In addition to its ability to induce neurodegeneration, CHUK is also known for its ability to regulate inflammation. This is achieved through the production of pro-inflammatory cytokines, which can contribute to the development of inflammatory neurodegeneration. The exact mechanisms by which CHUK regulates inflammation are not well understood, but it is known that CHUK is involved in the production of pro-inflammatory cytokines and that it can inhibit the anti-inflammatory response of immune cells.

Given the potential role of CHUK in the development and progression of neurodegenerative diseases, it is an attractive target for drug development. However, the development of effective therapies for CHUK-mediated neurodegeneration will be challenging. This is because CHUK is a protein that is expressed in various tissues throughout the body and its effects can be difficult to study in animal models of neurodegeneration. In addition, the blood-brain barrier and the poor stability of CHUK in the brain make it difficult to study the effects of CHUK in the brain.

Despite these challenges, recent studies have identified potential compounds that may be able to inhibit the activity of CHUK. These compounds include small molecules, such as inhibitors of the production of pro-inflammatory cytokines, as well as drugs that are able to cross the blood-brain barrier and target CHUK directly. The testing of these compounds will be an important step in the development of effective therapies for CHUK-mediated neurodegeneration.

In conclusion, CHUK is a protein that is expressed in various tissues throughout the body and is involved in the regulation of inflammation and neurodegeneration. Despite its importance, little is known about CHUK and its potential as a drug target. The development of effective therapies for CHUK-mediated neurodegeneration will be challenging, but recent studies have identified potential compounds that may be able to inhibit the activity of CHUK. Further research is needed to understand the full role of CHUK in

Protein Name: Component Of Inhibitor Of Nuclear Factor Kappa B Kinase Complex

Functions: Serine kinase that plays an essential role in the NF-kappa-B signaling pathway which is activated by multiple stimuli such as inflammatory cytokines, bacterial or viral products, DNA damages or other cellular stresses (PubMed:9244310, PubMed:9252186, PubMed:9346484, PubMed:18626576). Acts as part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation and phosphorylates inhibitors of NF-kappa-B on serine residues (PubMed:9244310, PubMed:9252186, PubMed:9346484, PubMed:18626576, PubMed:35952808). These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome (PubMed:9244310, PubMed:9252186, PubMed:9346484, PubMed:18626576). In turn, free NF-kappa-B is translocated into the nucleus and activates the transcription of hundreds of genes involved in immune response, growth control, or protection against apoptosis (PubMed:9244310, PubMed:9252186, PubMed:9346484, PubMed:18626576). Negatively regulates the pathway by phosphorylating the scaffold protein TAXBP1 and thus promoting the assembly of the A20/TNFAIP3 ubiquitin-editing complex (composed of A20/TNFAIP3, TAX1BP1, and the E3 ligases ITCH and RNF11) (PubMed:21765415). Therefore, CHUK plays a key role in the negative feedback of NF-kappa-B canonical signaling to limit inflammatory gene activation. As part of the non-canonical pathway of NF-kappa-B activation, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes (PubMed:20501937). In turn, these complexes regulate genes encoding molecules involved in B-cell survival and lymphoid organogenesis. Participates also in the negative feedback of the non-canonical NF-kappa-B signaling pathway by phosphorylating and destabilizing MAP3K14/NIK. Within the nucleus, phosphorylates CREBBP and consequently increases both its transcriptional and histone acetyltransferase activities (PubMed:17434128). Modulates chromatin accessibility at NF-kappa-B-responsive promoters by phosphorylating histones H3 at 'Ser-10' that are subsequently acetylated at 'Lys-14' by CREBBP (PubMed:12789342). Additionally, phosphorylates the CREBBP-interacting protein NCOA3. Also phosphorylates FOXO3 and may regulate this pro-apoptotic transcription factor (PubMed:15084260). Phosphorylates RIPK1 at 'Ser-25' which represses its kinase activity and consequently prevents TNF-mediated RIPK1-dependent cell death (By similarity). Phosphorylates AMBRA1 following mitophagy induction, promoting AMBRA1 interaction with ATG8 family proteins and its mitophagic activity (PubMed:30217973)

The "CHUK 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 CHUK 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;
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•   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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