TONSL (IKBR): A Promising Drug Target and Biomarker for the Treatment of Inflammatory Diseases

Target Name: TONSL

NCBI ID: G4796

TONSL (IKBR): A Promising Drug Target and Biomarker for the Treatment of Inflammatory Diseases

Inflammatory diseases, such as rheumatoid arthritis, inflammatory bowel disease, and chronic obstructive pulmonary disease (COPD), affect millions of people worldwide and cause significant morbidity and mortality. Chronic inflammation in these diseases can lead to progressive damage to the affected organs and can result in chronic pain, decreased quality of life, and even early mortality. The identification of potential drug targets and biomarkers for the treatment of inflammatory diseases is crucial for the development of new, more effective therapies. In this article, we will explore TONSL (IKBR), a drug target and biomarker for the treatment of inflammatory diseases.

TONSL (IKBR) as a Drug Target

TONSL (IKBR) is a small molecule inhibitor of the enzyme inhibitor of nuclear factor kappa B (NF-kappa-B), which is a key transcription factor that regulates the expression of genes involved in inflammation and immune responses. TONSL is currently being investigated as a potential drug target for the treatment of inflammatory diseases, including rheumatoid arthritis, inflammatory bowel disease, and COPD.

The NF-kappa-B pathway is involved in the regulation of inflammation, immune responses, and cell survival. It is a well-established pathway that plays a crucial role in the development and maintenance of inflammatory diseases. The NF-kappa-B pathway is activated in response to various stimuli, including cytokines, which result in the production of pro-inflammatory cytokines. These cytokines can cause the recruitment of immune cells to the site of inflammation, leading to the start of an inflammatory response.

TONSL is an inhibitor of the NF-kappa-B pathway, specifically the activity of the enzyme inhibitor of NF-kappa-B (IKB), which is involved in the regulation of NF-kappa-B activity. The inhibition of NF-kappa-B activity by TONSL results in the suppression of pro-inflammatory cytokine production and the termination of the inflammatory response.

TONSL has been shown to be effective in animal models of rheumatoid arthritis, a type of inflammatory arthritis that affects millions of people worldwide. In these models, TONSL was shown to reduce the production of pro-inflammatory cytokines, including cytokines that contribute to the development of joint damage, and to improve the efficacy of anti-inflammatory therapies.

TONSL has also been shown to be effective in animal models of inflammatory bowel disease, a condition that affects millions of people worldwide and can cause significant morbidity and mortality. In these models, TONSL was shown to reduce the production of pro-inflammatory cytokines and to improve the efficacy of anti-inflammatory therapies.

TONSL has also been shown to be effective in animal models of COPD, a condition that affects millions of people worldwide and can cause significant morbidity and mortality. In these models, TONSL was shown to reduce the production of pro-inflammatory cytokines and to improve the efficacy of anti-inflammatory therapies.

TONSL as a Biomarker

In addition to its potential as a drug target, TONSL has also been shown to be a valuable biomarker for the diagnosis and monitoring of inflammatory diseases. The production of pro-inflammatory cytokines is a critical event in the development of inflammatory diseases, and the levels of these cytokines can be used as biomarkers for the diagnosis and monitoring of these diseases.

TONSL has been shown to be effective in the detection of pro-inflammatory cytokines in various biological samples, including blood, urine, and saliva. These samples can be used as

Protein Name: Tonsoku Like, DNA Repair Protein

Functions: Component of the MMS22L-TONSL complex, a complex that promotes homologous recombination-mediated repair of double-strand breaks (DSBs) at stalled or collapsed replication forks (PubMed:21055983, PubMed:21055984, PubMed:21055985, PubMed:21113133, PubMed:26527279, PubMed:27797818, PubMed:29478807, PubMed:27338793, PubMed:30773278). The MMS22L-TONSL complex is required to maintain genome integrity during DNA replication (PubMed:21055983, PubMed:21055984, PubMed:21055985). It mediates the assembly of RAD51 filaments on single-stranded DNA (ssDNA): the MMS22L-TONSL complex is recruited to DSBs following histone replacement by histone chaperones and eviction of the replication protein A complex (RPA/RP-A) from DSBs (PubMed:21055983, PubMed:21055984, PubMed:21055985, PubMed:27797818, PubMed:29478807). Following recruitment to DSBs, the TONSL-MMS22L complex promotes recruitment of RAD51 filaments and subsequent homologous recombination (PubMed:27797818, PubMed:29478807). Within the complex, TONSL acts as histone reader, which recognizes and binds newly synthesized histones following their replacement by histone chaperones (PubMed:29478807, PubMed:27338793). Specifically binds histone H4 lacking methylation at 'Lys-20' (H4K20me0) and histone H3.1 (PubMed:27338793)

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