Target Name: CLEC5A
NCBI ID: G23601
Review Report on CLEC5A Target / Biomarker Content of Review Report on CLEC5A Target / Biomarker
CLEC5A
Other Name(s): C-type lectin domain family 5 member A | C-type lectin domain containing 5A, transcript variant 1 | CLC5A_HUMAN | MDL1 | MGC138304 | CLECSF5 | CLEC5A variant 1 | C-type lectin domain family 5 member A (isoform 1) | myeloid DAP12-associating lectin-1 | C-type (calcium dependent, carbohydrate-recognition domain) lectin, superfamily member 5 | Myeloid DAP12-associating lectin 1 | MDL-1 | C-type lectin superfamily member 5 | Myeloid DAP12-associating lectin-1 | C-type lectin domain containing 5A

CLEC5A: A promising drug target and biomarker for cancer

Introduction

CLEC5A (C-type lectin domain family 5 member A) is a protein that is expressed in various cell types, including human cancer cells. Its primary function is to recognize and interact with various extracellular matrix (ECM) components, including ECM proteins and carbohydrates . CLEC5A has been shown to be involved in various cellular processes, including cell adhesion, migration, and invasion. As a result, it has been identified as a potential drug target and biomarker for cancer. In this article, we will discuss the biology of CLEC5A, its potential as a drug target, and its potential as a biomarker for cancer.

Biogenesis and localization

CLEC5A is a member of the C-type lectin domain family, which is a conserved group of proteins that are involved in cell adhesion and migration. These proteins typically contain a characteristic C-type lecture domain, which is responsible for their ability to interact with ECM components. CLEC5A is characterized by its approximately 110 amino acid long N-terminal region, which contains a characteristic alpha-helices and a variable region.

CLEC5A is expressed in various cell types, including human cancer cells. It has been shown to be highly expressed in breast cancer tissues and cell lines, with higher levels of expression observed in the breast cancer compared to the surrounding tissue. Additionally, it has been shown to be expressed in other types of cancer, including lung cancer, ovarian cancer, and colorectal cancer.

Function and regulation

CLEC5A is involved in various cellular processes, including cell adhesion, migration, and invasion. It has been shown to play a role in cell-cell adhesion by interacting with the ECM protein E-cadherin. clec5a/E-cadherin interactions have been shown to promote the formation of tight junctions, which are a type of cell-cell adhesion structure that is critical for maintaining tissue structure and function.

In addition to its role in cell-cell adhesion, CLEC5A is also involved in the regulation of cell migration. It has been shown to play a role in the regulation of cell migration by interacting with the ECM protein N-cadherin. N-cadherin is a protein that is involved in cell-cell adhesion, but is often expressed in higher levels in cancer cells compared to normal cells. CLEC5A has been shown to interact with N-cadherin and promote its association with the ECM, which may contribute to the regulation of cell migration.

CLEC5A is also involved in the regulation of cell invasion. In cancer cells, the loss of cell adhesion and the ability to migrate through the ECM is a hallmark feature of the disease. clec5a has been shown to play a role in the regulation of cell invasion. by interacting with the ECM protein vimentin. Vimentin is a protein that is involved in cell-cell adhesion and has been shown to be a potential drug target for cancer. clec5a/vimentin interactions have been shown to promote the formation of invasive extensions in cancer cells.

Potential drug targets and biomarkers

CLEC5A has been identified as a potential drug target for cancer due to its involvement in various cellular processes that are important for cancer growth and progression. clec5a interactions with ECM proteins and carbohydrates have been shown to contribute to the regulation of cell adhesion, migration, and invasion, which are critical processes for cancer growth and progression.

In addition to its potential as a drug target, CLEC5A has also been identified as a potential biomarker for cancer. Its expression is highly correlated with the severity of cancer, as well as the response to anti-cancer drugs. Additionally, clec5a has been shown to be involved in the regulation of cell cycle progression, which is a critical process for cancer growth and progression.

Conclusion

In conclusion, CLEC5A is a protein that is involved in various cellular processes that are important for cancer growth and progression. Its interactions with ECM proteins and carbohydrates have been shown to contribute to the regulation of cell adhesion, migration, and invasion, making it a potential drug target for cancer. Additionally, its high expression in cancer cells and its involvement in cell cycle progression make it a potential biomarker for cancer. Further research is needed to fully understand the role of CLEC5A in cancer biology and its potential as a drug target and biomarker.

Protein Name: C-type Lectin Domain Containing 5A

Functions: Functions as a positive regulator of osteoclastogenesis (By similarity). Cell surface receptor that signals via TYROBP (PubMed:10449773). Regulates inflammatory responses (By similarity)

The "CLEC5A 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 CLEC5A 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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