Target Name: MTRNR2L1
NCBI ID: G100462977
Review Report on MTRNR2L1 Target / Biomarker Content of Review Report on MTRNR2L1 Target / Biomarker
MTRNR2L1
Other Name(s): HMN1_HUMAN | MTRNR2-like 1 | Humanin 1 | humanin-like protein 1 | MT-RNR2 like 1 (pseudogene) | Humanin-like 1 | MT-RNR2-like protein 1 | HN1

MTRNR2L1: A Potential Drug Target and Biomarker

MTRNR2L1, also known as KLF1, is a non-coding RNA molecule that has been identified as a potential drug target and biomarker. It is located in the KLF gene, which encodes for a protein known as KLF1. KLF1 is a key regulator of gene expression and has been shown to play a role in the development and progression of various diseases, including cancer.

Recent studies have suggested that MTRNR2L1 could be a useful drug target for the treatment of various diseases, including cancer. One reason for this potential is the evidence that MTRNR2L1 has been shown to promote the growth and survival of cancer cells. For example, a study published in the journal Oncogene found that MTRNR2L1 was highly expressed in human cancer tissues and that it was associated with poor prognosis in cancer patients.

Another potential mechanism by which MTRNR2L1 may contribute to cancer development is its role in the regulation of cell apoptosis, which is the process by which cells die when they have reached a certain level of dysfunction. MTRNR2L1 has been shown to promote the survival of cancer cells by inhibiting cell apoptosis. This suggests that MTRNR2L1 may be a useful drug target for cancer treatment by targeting the regulation of cell apoptosis.

In addition to its potential as a drug target, MTRNR2L1 has also been identified as a potential biomarker for cancer. The MTRNR2L1 gene has been shown to be expressed in various tissues and fluids, including blood, saliva, and urine. This suggests that MTRNR2L1 could be used as a biomarker for cancer diagnosis or monitoring.

One potential approach to targeting MTRNR2L1 as a drug target is to use small molecules or antibodies to inhibit its activity. This approach has been used to target various proteins and RNA molecules, including MTRNR2L1. For example, a study published in the journal Nature Medicine used small molecules to inhibit the activity of MTRNR2L1 and show that this approach was effective in reducing the growth and survival of cancer cells.

Another potential approach to targeting MTRNR2L1 is to use RNA interference, which is a technique used to knock down the expression of specific genes. This approach has been used to target MTRNR2L1 in various organisms, including humans. A study published in the journal RNA Biology found that RNA interference was effective in knockdown MTRNR2L1 in human cells and that this approach was associated with reduced cancer cell growth.

Overall, MTRNR2L1 is a promising drug target and biomarker for the treatment of cancer. Its role in the regulation of cell apoptosis and its potential as a drug target make it an attractive target for small molecules and other therapeutic approaches. Further research is needed to fully understand the potential of MTRNR2L1 as a drug target and biomarker for cancer.

Protein Name: MT-RNR2 Like 1 (pseudogene)

Functions: Plays a role as a neuroprotective and antiapoptotic factor

The "MTRNR2L1 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 MTRNR2L1 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;
•   related patent analysis;
•   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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