Target intelligence / Profile preview

Cell division cycle 5-like protein (CDC5L)

Target
CDC5L
Molecular classification
Transcription factor, Pre-mRNA splicing factor, Component of multiprotein spliceosome complex
01

Overview

Cell division cycle 5-like protein (CDC5L) is a conserved nuclear protein encoded by the CDC5L gene in humans and homologous to the yeast CDC5 gene product[1][2][6]. CDC5L acts as a positive regulator of the G2/M cell cycle transition and is an essential component of a non-snRNA spliceosome complex critical for the second catalytic step of pre-mRNA splicing[1][2][4]. It participates in regulating mitotic and meiotic progression, modulating expression and splicing efficiency of mitosis- and DNA repair-associated genes[3][5][6]. CDC5L is involved in DNA damage response by interacting with ATR and facilitating S-phase checkpoint activation[5]. Dysregulation or depletion arrests mitosis, disrupts kinetochore-microtubule attachment, activates the spindle assembly checkpoint, and leads to mitotic catastrophe or DNA damage[3][6]. Clinical research implicates CDC5L in several human cancers, suggesting a cancer-promoting role when overexpressed or mutated[6]. No clinically approved drugs target CDC5L directly to date, but its essential function in splicing and the cell cycle makes it a potential anti-mitotic therapeutic target[3].

Other names
Cdc5-like proteinKIAA0432PCDC5RPhCDC5CEF1Pombe cdc5-related proteindJ319D22.1CDC5L proteinCDC5L complex component
02

Mechanism of action

Not established for direct drugs; mechanistically, depletion or dysfunction impairs G2/M progression, mitotic spindle checkpoint, and genomic stability

03

Biological functions

Cell cycle regulation (particularly G2/M progression)Pre-mRNA splicing (second catalytic step)DNA damage response and checkpoint regulationMeiotic and mitotic progression
04

Disease associations

CancerGenomic instabilityPossible role in cell proliferative disorders
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Safety considerations

Targeting CDC5L could disrupt essential mRNA splicing and cell cycle progression in normal tissues, raising risk for cytotoxicity and developmental defects
06

Interacting drugs

None reported or clinically validated
07

Biomarkers

Overexpression or altered expression may serve as a marker in certain cancers (colorectal, prostate, gliomas, bladder, hepatocellular carcinoma)

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