KLF13: A Potential Drug Target and Biomarker (G51621)

Target Name: KLF13

NCBI ID: G51621

KLF13

KLF13: A Potential Drug Target and Biomarker

Krueppel-like factor 13 (KLF13) is a non-coding RNA molecule that has been identified as a potential drug target and biomarker. KLF13 is a key regulator of gene expression in various organisms, including humans. Its function in cellular processes is not well understood, but it is known to play a role in the regulation of cell adhesion, migration, and invasion.

The KLF13 gene was first identified in the genome using next-generation sequencing techniques. The gene is located on chromosome 6 and has a length of approximately 1,900 base pairs. KLF13 is a member of the KLF gene family, which includes several similar non-coding RNAs that play important roles in cellular processes.

Expression of KLF13 is highly regulated in various organisms, including humans. KLF13 is expressed in many different tissues and cells in the body, including the brain, pancreas, and gastrointestinal tract. It is also expressed in various cell types, including blood cells, nerve cells, and epithelial cells. KLF13 is highly expressed in cancer cells, which makes it an attractive target for drug development.

The function of KLF13 is not well understood, but it is known to play a role in the regulation of cell adhesion, migration, and invasion. KLF13 is involved in the regulation of tight junctions, which are a type of cell-cell adhesion that helps to maintain the integrity of tissues. It is also involved in the regulation of cell migration and invasion, which are critical processes that allow cells to move and migrate to new locations in the body.

In addition to its role in cell adhesion and migration, KLF13 is also involved in the regulation of stem cell proliferation and differentiation. KLF13 has been shown to play a role in the regulation of stem cell self-renewal and the differentiation of stem cells into various cell types.

KLF13 is also a potential biomarker for various diseases, including cancer. Its high expression in cancer cells makes it an attractive target for drug development. Additionally, KLF13 has been shown to be involved in the regulation of various signaling pathways, including the TGF-β pathway. This pathway is involved in the regulation of cell growth, differentiation, and survival, and is a potential target for drug development.

In conclusion, KLF13 is a non-coding RNA molecule that has been identified as a potential drug target and biomarker. Its function in cellular processes is not well understood, but it is known to play a role in the regulation of cell adhesion, migration, and invasion. Its high expression in cancer cells makes it an attractive target for drug development, and its potential as a biomarker for various diseases makes it a valuable tool for the development of new therapies. Further research is needed to fully understand the function of KLF13 and its potential as a drug target and biomarker.

Protein Name: KLF Transcription Factor 13

Functions: Represses transcription by binding to the BTE site, a GC-rich DNA element, in competition with the activator SP1. It also represses transcription by interacting with the corepressor Sin3A and HDAC1. Activates RANTES expression in T-cells

The "KLF13 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 KLF13 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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