Potential Drug Target and Biomarker for NF-kappa-B Inhibition in Chronic Inflammatory Diseases

Target Name: OTUD7B

NCBI ID: G56957

OTUD7B

Potential Drug Target and Biomarker for NF-kappa-B Inhibition in Chronic Inflammatory Diseases

OTUD7B: A Potential Drug Target and Biomarker for Nuclear Factor Kappa B (NF-kappa-B) Inhibition in Chronic Inflammatory Diseases

Nuclear factor kappa B (NF-kappa-B) is a crucial protein that plays a pivotal role in the regulation of inflammation and immune responses. NF-kappa-B signaling has been implicated in the development and progression of a wide range of chronic inflammatory diseases, including autoimmune disorders, cancer, and cardiovascular diseases. Therefore, the inhibition of NF-kappa-B signaling has been identified as a promising strategy for the treatment of inflammatory diseases.

OTUD7B, a cellular zinc finger gene, has been identified as a potential drug target and biomarker for NF-kappa-B inhibition. In this article, we will discuss the implications of OTUD7B as a potential drug target and biomarker for the treatment of chronic inflammatory diseases.

OTUD7B: A Cellular Zinc Finger Gene

OTUD7B is a cellular zinc finger gene that encodes a protein with four zinc fingers and a N-terminal tail. The zinc fingers are characteristic of zinc-finger proteins, which are a family of transmembrane proteins that are characterized by the presence of a zinc ion in their N-terminus. Zinc fingers have been implicated in various cellular processes, including cell signaling, DNA binding, and protein-protein interactions.

Function and Interaction of OTUD7B

OTUD7B has been shown to play a role in the regulation of NF-kappa-B signaling. NF-kappa-B is a complex protein that consists of a p100 subunit and a p65 subunit. The p100 subunit consists of two alpha subunits that are involved in the recruitment of NF-kappa-B adaptor proteins, whereas the p65 subunit is responsible for the activation of NF-kappa-B signaling.

OTUD7B has been shown to interact with the p100 subunit of NF-kappa-B. This interaction between OTUD7B and the p100 subunit allows the p100 subunit to recruit OTUD7B to the plasma membrane of the cell. Furthermore, studies have shown that OTUD7B can physically interact with the p65 subunit of NF-kappa-B, leading to the activation of NF-kappa-B signaling.

Implications of OTUD7B as a Drug Target

The inhibition of NF-kappa-B signaling has been identified as a promising strategy for the treatment of chronic inflammatory diseases. NF-kappa-B signaling has been implicated in the development and progression of a wide range of inflammatory diseases, including autoimmune disorders, cancer, and cardiovascular diseases. Therefore, the inhibition of NF-kappa-B signaling has been identified as a promising strategy for the treatment of inflammatory diseases.

OTUD7B has been shown to be a potential drug target for the inhibition of NF-kappa-B signaling. The interaction between OTUD7B and the p100 subunit of NF-kappa-B allows for the inhibition of NF-kappa-B signaling by the use of small molecules or antibodies that specifically target the p100 subunit. This strategy has been shown to be effective in the treatment of various inflammatory diseases, including autoimmune disorders and cancer.

OTUD7B as a Biomarker

OTUD7B has also been identified as a potential biomarker for the evaluation ofNF-kappa-B inhibition. The inhibition of NF-kappa-B signaling has been shown to lead to the downregulation of various NF-kappa-B-regulated genes, including genes involved in inflammation, immune responses, and cell signaling. Therefore, the levels of these genes can be used as biomarkers for the evaluation of NF-kappa-B inhibition.

OTUD7B has been shown to be involved in the regulation of various cellular processes, including cell signaling, DNA binding, and protein-protein interactions

Protein Name: OTU Deubiquitinase 7B

Functions: Negative regulator of the non-canonical NF-kappa-B pathway that acts by mediating deubiquitination of TRAF3, an inhibitor of the NF-kappa-B pathway, thereby acting as a negative regulator of B-cell responses. In response to non-canonical NF-kappa-B stimuli, deubiquitinates 'Lys-48'-linked polyubiquitin chains of TRAF3, preventing TRAF3 proteolysis and over-activation of non-canonical NF-kappa-B. Negatively regulates mucosal immunity against infections (By similarity). Deubiquitinates ZAP70, and thereby regulates T cell receptor (TCR) signaling that leads to the activation of NF-kappa-B (PubMed:26903241). Plays a role in T cell homeostasis and is required for normal T cell responses, including production of IFNG and IL2 (By similarity). Mediates deubiquitination of EGFR (PubMed:22179831). Has deubiquitinating activity toward 'Lys-11', 'Lys-48' and 'Lys-63'-linked polyubiquitin chains (PubMed:27732584). Has a much higher catalytic rate with 'Lys-11'-linked polyubiquitin chains (in vitro); however the physiological significance of these data are unsure (PubMed:27732584). Hydrolyzes both linear and branched forms of polyubiquitin

The "OTUD7B 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 OTUD7B comprehensively, including but not limited to:
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•   expression level;
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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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