CLEC3B: A Potential Drug Target for Cancer (G7123)

Target Name: CLEC3B

NCBI ID: G7123

CLEC3B

CLEC3B: A Potential Drug Target for Cancer

clec3b, also known as TETN-HUMAN, is a protein that is expressed in the human placenta and has been shown to play a role in the development and maintenance of cancer. The protein is derived from the TETN gene, which encodes for the tumor suppressor protein TERT-1. TERT-1 is known to function as a negative regulator of the cell cycle, helping to prevent the uncontrolled growth and division that can occur in cancer cells.

Recent studies have shown that clec3b is involved in the regulation of several key cellular processes, including cell growth, apoptosis (programmed cell death), and angiogenesis (the formation of new blood vessels). It has also been shown to play a role in the development of several types of cancer, including breast, ovarian, and prostate cancer.

One of the key functions of clec3b is its role in regulating the cell cycle. The cell cycle is the process by which a cell grows and replicates its genetic material. clec3b is known to help ensure that the cell cycle is properly regulated, and that cells do not enter an uncontrolled state of growth. This helps to prevent the development of cancer.

In addition to its role in cell cycling, clec3b is also involved in the regulation of apoptosis. Apoptosis is the process by which a cell undergoes programmed cell death, which is a natural and essential part of the cell cycle. When a cell is no longer needed or is damaged beyond repair, it can undergo apoptosis, which helps to remove damaged or dysfunctional cells from the body. clec3b has been shown to help regulate theApoptosis, by activating or inhibiting the different cell cycle checkpoints.

CLEC3B also plays a role in the regulation of angiogenesis, the process by which new blood vessels are formed in the body. Angiogenesis is a critical process for the development and maintenance of tissues, including blood vessels. clec3b has been shown to be involved in the regulation of angiogenesis, by activating or inhibiting the different angiogenic factors.

Clec3b has also been shown to be involved in the regulation of cellular signaling pathways. clec3b has been shown to be involved in the regulation of several signaling pathways, including the PI3K/Akt signaling pathway, the TGF-β signaling pathway, and the Wnt signaling pathway. These signaling pathways are important for the development and maintenance of cancer, and clec3b has been shown to play a role in their regulation.

Clec3b is also involved in the regulation of cellular adhesion. Adhesion is the process by which cells stick together to form tissues and organs. clec3b has been shown to be involved in the regulation of cellular adhesion, by activating or inhibiting the different adhesion molecules.

In conclusion, clec3b is a protein that is expressed in the human placenta and has been shown to play a role in the development and maintenance of cancer. The protein is derived from the TETN gene, which encodes for the tumor suppressor protein TERT-1. TERT-1 is known to function as a negative regulator of the cell cycle, helping to prevent the uncontrolled growth and division that can occur in cancer cells. clec3b is involved in the regulation of cell cycling, apoptosis, angiogenesis, cellular signaling pathways and cellular adhesion. Therefore, clec3b may be a potential drug target or biomarker for the treatment of cancer.

Protein Name: C-type Lectin Domain Family 3 Member B

Functions: Tetranectin binds to plasminogen and to isolated kringle 4. May be involved in the packaging of molecules destined for exocytosis. Plays a role in retinal function (PubMed:35331648)

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•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
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•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
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•   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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