Target intelligence / Profile preview

Cyclin-dependent kinase 5 regulatory subunit-associated protein 3 (CDK5RAP3)

Target
CDK5RAP3
Molecular classification
Other (scaffold/adaptor protein), UFMylation pathway component
01

Overview

Cyclin-dependent kinase 5 regulatory subunit-associated protein 3 (CDK5RAP3) is an evolutionarily conserved intracellular protein, initially identified as a binding partner for the CDK5 activator p35[1][2]. It possesses a leucine zipper region and two LXXLL motifs but lacks canonical enzymatic activity or well-defined functional domains[1][2]. CDK5RAP3 functions chiefly as a scaffold or adaptor, facilitating protein-protein interactions and exerting transcriptional regulatory roles. It participates in several major cellular processes such as the cell cycle (especially at G2/M and G1/S checkpoints), apoptosis (caspase-mediated and feedback-regulated), signal transduction (including p53, NF-κB, Wnt/β-catenin, AKT, and STAT3 pathways), UFMylation, and ER stress modulation[1][2][3][4]. CDK5RAP3 is expressed in various tissues and is essential for embryogenesis, neuronal development, and maintenance of cellular homeostasis. Dysregulation or deficiency has been linked to multiple cancers and neuronal developmental disorders, highlighting its significance as a regulatory node but also presenting challenges for therapeutic targeting[1][2][3][4][6].

Other names
C53LZAPIC53MSTP016OK/SW-cl.114PP1553MST016FLJ13660HSF-27CDK5 activator-binding protein C53LXXLL/leucine-zipper-containing ARF-binding proteinischemic heart CDK5 activator-binding protein C53
02

Biological functions

Cell cycle regulationApoptosisSignal transductionProtein post-translational modificationCellular homeostasisEmbryogenesis and tissue developmentTranscriptional regulationEndoplasmic reticulum (ER) stress response
03

Disease associations

Cancer (including head and neck squamous cell carcinoma, gastric, hepatocellular, lung, kidney, and breast cancer)Neurodevelopmental/neurological diseasePossibly cardiovascular disease (ischemic heart context referenced)
04

Safety considerations

Essential for embryonic and neuronal development: deficiency can lead to severe developmental defects, including brain abnormalities[3].Modulation may broadly affect cell cycle, apoptosis, and ER stress responses, with associated risks for tissue dysfunction[1][2][3].

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