Target Name: BCL9L
NCBI ID: G283149
Review Report on BCL9L Target / Biomarker Content of Review Report on BCL9L Target / Biomarker
BCL9L
Other Name(s): BCL9L variant 2 | B9L | B-cell CLL/lymphoma 9-like protein | BCL9 like | Nuclear co-factor of beta-catenin signalling | B cell CLL/lymphoma 9 like | BCL9-2 | DLNB11 | Protein BCL9-2 | protein BCL9-2 | BCL9 like, transcript variant 2 | B-cell CLL/lymphoma 9-like protein (isoform a) | BCL9-like protein | BCL9L_HUMAN | B-cell lymphoma 9-like protein | nuclear co-factor of beta-catenin signalling

Understanding BCL9L: Potential Drug Target and Biomarker

BCL9L (Bcl-9 long isoform) is a protein that is expressed in various tissues throughout the body, including the brain, lungs, heart, and gastrointestinal tract. It is a member of the Bcl family of proteins, which are known for their ability to form a tight, condensed package around DNA to prevent it from being transcribed into RNA.

In recent years, researchers have been interested in studying BCL9L because of its potential as a drug target or biomarker. BCL9L has been shown to play a role in a variety of biological processes, including cell division, apoptosis (programmed cell death), and inflammation.

One of the reasons for the interest in BCL9L is its ability to interact with multiple protein partners, including other Bcl proteins, p53, and cyclin D1. This makes it a potentially interesting target for drugs that want to inhibit these interactions and disrupt the balance of cell division and apoptosis that BCL9L promotes.

Another potential mechanism by which BCL9L may be targeted by drugs is its role in the regulation of ion channels. BCL9L has been shown to interact with several different ion channels, including the K+ channel. This suggests that BCL9L may play a role in regulating the flow of ions into and out of cells, which could be a potential target for drugs that want to modify ion channels.

In addition to its potential as a drug target, BCL9L is also a potential biomarker for some diseases. For example, BCL9L has been shown to be expressed in the brains of individuals with Alzheimer's disease, and it is also overexpressed in the brains of individuals with neurofibromatosis, a genetic disorder that causes tumors to grow on the brain.

Despite the potential interest in BCL9L as a drug target and biomarker, much more research is needed to fully understand its role in these processes. researchers are currently studying the structure and function of BCL9L to better understand how it works and how it could be targeted by drugs.

In conclusion, BCL9L is a protein that is expressed in various tissues throughout the body that is known for its ability to form a tight, condensed package around DNA. Researchers are increasingly interested in studying BCL9L as a drug target or biomarker due to its potential to disrupt the balance of cell division and apoptosis that it promotes. Further research is needed to fully understand the role of BCL9L in these processes and its potential as a drug.

Protein Name: BCL9 Like

Functions: Transcriptional regulator that acts as an activator. Promotes beta-catenin transcriptional activity. Plays a role in tumorigenesis. Enhances the neoplastic transforming activity of CTNNB1 (By similarity)

The "BCL9L 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 BCL9L 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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