CDC14B
Cell division cycle 14B (CDC14B) is a protein-coding gene involved in cell cycle regulation. It plays a crucial role in the control of cell division and cell cycle progression. CDC14B is a member of the CDC14 phosphatase family, which is known for its phosphatase activity in cell cycle regulation.
Function[edit | edit source]
CDC14B functions as a dual-specificity phosphatase, meaning it can dephosphorylate both phosphotyrosine and phosphoserine/threonine residues on its substrate proteins. This dephosphorylation activity allows CDC14B to regulate key cell cycle events, such as mitotic exit and cytokinesis. By dephosphorylating specific target proteins, CDC14B helps coordinate the orderly progression of the cell cycle.
Structure[edit | edit source]
The CDC14B protein consists of several conserved domains, including a phosphatase domain responsible for its enzymatic activity. It also contains regulatory domains that control its subcellular localization and activity during different phases of the cell cycle. The structure of CDC14B allows it to interact with various binding partners and substrates to carry out its functions in cell cycle regulation.
Regulation[edit | edit source]
The activity of CDC14B is tightly regulated to ensure proper cell cycle progression. It is subject to post-translational modifications, such as phosphorylation and ubiquitination, which can affect its stability and activity. Additionally, CDC14B localization within the cell is dynamically regulated, with changes in localization playing a role in its function during different stages of the cell cycle.
Role in Disease[edit | edit source]
Mutations or dysregulation of CDC14B have been associated with various diseases, including cancer. Aberrant expression of CDC14B can disrupt normal cell cycle control, leading to uncontrolled cell proliferation and tumor formation. Understanding the role of CDC14B in disease pathogenesis may provide insights for developing targeted therapies for conditions involving cell cycle dysregulation.
References[edit | edit source]
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