MT1HL1: A Potential Drug Target and Biomarker for Inflammatory Diseases

Target Name: MT1HL1

NCBI ID: G645745

MT1HL1

MT1HL1: A Potential Drug Target and Biomarker for Inflammatory Diseases

Metallothionein (MT) is a protein that plays a crucial role in the regulation of inflammation and immune responses. MT1 is the most abundant isoform ofMT, and it is expressed in various tissues throughout the body, including the liver, spleen, and peripheral blood cells. MT1 functions as a modulator of inflammation, promoting the production of anti-inflammatory cytokines and modulating the activity of immune cells. In this article, we will discuss the potential drug target (MT1HL1) and biomarker for inflammatory diseases, MT1HL1.

Potential Drug Target: MT1HL1

MT1HL1 is a 114-amino acid protein that contains a unique N-terminus and a unique C-terminus. The N-terminus of MT1HL1 contains a conserved region known as the zinc finger domain, which is commonly found in proteins that play a role in metal homeostasis. The C-terminus of MT1HL1 contains a unique farnesylated cysteine residue, which is important for protein stability and functions as a structural modifier.

MT1HL1 has been shown to have a variety of physiological functions, including regulating inflammation, immune responses, and cell signaling. In inflammatory diseases, MT1HL1 has been implicated in the regulation of pro-inflammatory cytokines, such as TNF-伪, IL-1尾, and IL-6. MT1HL1 has also been shown to play a role in the regulation of anti-inflammatory cytokines, such as IL-10 and ITGA-13.

MT1HL1 has been shown to promote the production of pro-inflammatory cytokines by immortalized human keratinocytes. This increase in pro-inflammatory cytokines has been shown to contribute to the development of inflammatory skin diseases, such as psoriasis and acne.

In addition to its role in inflammation, MT1HL1 has also been shown to play a role in the regulation of cellular signaling. MT1HL1 has been shown to function as a negative regulator of the nuclear factor-kappa-B (NF-kappa-B) signaling pathway, which is a well-established regulator of inflammation and immune responses.

MT1HL1 has also been shown to play a role in the regulation of cellular signaling in cancer. For example, MT1HL1 has been shown to function as a negative regulator of the TGF-β signaling pathway, which is a well-established regulator of cancer growth and progression.

Biomarker Potential

MT1HL1 has the potential to serve as a biomarker for a variety of inflammatory diseases, including arthritis, asthma, and cancer. Because MT1HL1 is involved in the regulation of inflammation and immune responses, it has been suggested that it may be a useful biomarker for these diseases.

In addition to its potential as a biomarker, MT1HL1 has also been shown to be a potential therapeutic target for inflammatory diseases. By inhibiting the activity of MT1HL1, it may be possible to reduce the production of pro-inflammatory cytokines and improve the regulation of inflammatory responses. This could have potential therapeutic applications for a variety of inflammatory diseases, including arthritis, asthma, and cancer.

Conclusion

MT1HL1 is a protein that has the potential to serve as a drug target and biomarker for a variety of inflammatory diseases. Its unique N-terminus and C-terminus, as well as its conserved zinc finger domain and farnesylated cysteine residue, give MT1HL1 a unique structure that allows it to function as a regulator of inflammation and immune responses. Further research is needed to fully understand the role of MT1HL1 in

Protein Name: Metallothionein 1H Like 1

Functions: Metallothioneins have a high content of cysteine residues that bind various heavy metals; these proteins are transcriptionally regulated by both heavy metals and glucocorticoids

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•   general information;
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•   expression level;
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•   pharmacochemistry experiments;
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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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