Target intelligence / Profile preview

Dual specificity protein phosphatase CDC14B (CDC14B)

Target
CDC14B
Molecular classification
Enzyme, Protein tyrosine phosphatase, Serine/threonine phosphatase, Dual specificity phosphatase
01

Overview

Dual specificity protein phosphatase CDC14B (CDC14B) is an enzyme encoded by the CDC14B gene in humans. It belongs to the dual specificity protein tyrosine phosphatase family, with both tyrosine and serine/threonine phosphatase activity. CDC14B is highly homologous to yeast Cdc14 and regulates cell cycle progression, particularly the G2 DNA damage checkpoint and mitotic exit. It acts by dephosphorylating targets such as FZR1/CDH1, enabling activation of the anaphase promoting complex (APC/C), and regulates microtubule organization by stabilizing and bundling microtubules. CDC14B also modulates tumor suppressor protein p53 via site-specific dephosphorylation, affecting its stability and function, and can alter SIRT2 phosphorylation during early anaphase. Disruptions of CDC14B function can lead to cell cycle abnormalities, genomic instability, premature aging, and potentially contribute to disease processes including cancer.

Other names
CDC14 cell division cycle 14 homolog BCDC14B3Cdc14B1Cdc14B2Dual specificity protein phosphatase CDC14B
02

Mechanism of action

Drugs would theoretically act through modulation of phosphatase activity—specifically, inhibition or activation of CDC14B’s dephosphorylation of key substrates such as p53, FZR1/CDH1, SIRT2, and those involved in G2/M checkpoint regulation

03

Biological functions

Cell cycle regulationDNA damage responseCell divisionMicrotubule cytoskeleton organizationCilium assemblyp53 regulation
04

Disease associations

Cancer (regulation of p53 and cell cycle control implicates potential roles in oncogenesis and tumour suppression)Age-related diseases (deletion leads to early-onset aging phenotypes in mice)Other (Potential involvement in neurodegeneration and developmental disorders; limited data)
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Safety considerations

Inhibition or deletion of CDC14B may induce premature aging phenotypes and potentially disrupt cell cycle exit, mitosis, or DNA damage responses, leading to genomic instability or abnormal proliferationTherapeutic targeting could impact normal proliferating tissues.
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Interacting drugs

None specifically approved or in clinical use as direct CDC14B inhibitors or activators are documented in current human therapeutic context
07

Biomarkers

Direct clinical biomarkers for patient selection or efficacy monitoring have not been established. CDC14B expression or mutation status might potentially serve as a research biomarker in cancer or cell cycle-related disorders, pending further validation.

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