CLEC3B

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CLEC3B (C-type lectin domain family 3 member B), also known as tetranectin, is a protein that in humans is encoded by the CLEC3B gene. This protein is a member of the C-type lectin family, characterized by their structural motif that enables calcium-dependent binding to carbohydrates. CLEC3B plays a significant role in various biological processes, including blood coagulation, wound healing, and tumor growth.

Structure[edit | edit source]

CLEC3B is a trimeric protein, meaning it consists of three identical subunits. Each subunit is composed of a C-type lectin domain, which is responsible for its carbohydrate recognition properties. The trimeric structure is crucial for its biological function, as it allows for multivalent binding, enhancing the protein's ability to interact with its ligands.

Function[edit | edit source]

The primary function of CLEC3B is to bind to and promote the aggregation of plasminogen, an important enzyme precursor in the fibrinolysis system, which is responsible for the breakdown of fibrin clots. By binding to plasminogen, CLEC3B facilitates its conversion to plasmin, the active enzyme that degrades fibrin and other components of the extracellular matrix. This activity is essential for normal wound healing and tissue remodeling.

In addition to its role in fibrinolysis, CLEC3B has been implicated in the regulation of tumor growth and metastasis. Studies have shown that CLEC3B can inhibit angiogenesis, the process by which new blood vessels form from pre-existing vessels, which is a critical mechanism through which tumors acquire nutrients and oxygen. By inhibiting angiogenesis, CLEC3B can potentially suppress tumor growth and metastasis.

Clinical Significance[edit | edit source]

Alterations in the expression of CLEC3B have been associated with various diseases. Lower levels of CLEC3B have been observed in patients with certain types of cancer, suggesting its potential role as a tumor suppressor. Conversely, elevated levels of CLEC3B have been reported in conditions associated with excessive fibrinolysis, such as certain bleeding disorders.

Given its involvement in key physiological and pathological processes, CLEC3B is considered a potential therapeutic target. Modulating its activity could lead to new treatments for diseases related to abnormal fibrinolysis, tumor growth, and metastasis.

Genetic Regulation[edit | edit source]

The CLEC3B gene is located on chromosome 3 in humans. Its expression is regulated by various factors, including inflammatory cytokines and growth factors, which can either upregulate or downregulate its production depending on the physiological or pathological context.

See Also[edit | edit source]

References[edit | edit source]


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Contributors: Prab R. Tumpati, MD