gene

CDK16

Entity Detail — Knowledge Graph Node

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This page aggregates everything SciDEX knows about CDK16: its mechanistic relationships (Knowledge Graph edges), hypotheses targeting it, analyses mentioning it, and supporting scientific papers. The interactive graph below shows its immediate neighbors. All content is AI-synthesized from peer-reviewed literature.

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Summary

Page for CDK16 — Cyclin-Dependent Kinase 16 (PCTAIRE-1)

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🧬 Gene Info

Gene Symbol	CDK16
Full Name	Cyclin-Dependent Kinase 16 (PCTAIRE-1)
Aliases	PCTAIRE-1
Function	CDK16/PCTAIRE-1 is a unique member of the CDK family characterized by its testis-specific cyclin binding and predominantly neuronal expression pattern.
Primary Expression	substantia nigra 5
Ensembl ID	ENSG00000103150
GeneCards	CDK16
Human Protein Atlas	CDK16
Kinase Domain	Canonical serine/threonine kinase domain
PSTAIRE-like Motif	Cyclin-binding motif in the cyclin-binding domain
Unique C-terminal Region	Specific to PCTAIRE subfamily
Dopaminergic neuron vulnerability	CDK16 is highly expressed in dopaminergic neurons of the substantia nigra, the neurons most vulnerable in Parkinson's disease
Single-cell analysis	Confirmed CDK16 expression in dopaminergic neuron populations
Synaptic dysfunction	Regulates synaptic vesicle cycling, dysfunction contributes to dopaminergic synaptic deficits
Alpha-synuclein connection	May phosphorylate proteins involved in alpha-synuclein processing[@suzuki2020]
Associated Diseases	neurodegeneration
Databases	GeneCards UniProt NCBI Gene HPA STRING

Wiki Pages (3)

Knowledge base pages for this entity

Canonical Page

Pathway Diagram

graph TD
    CDK16["CDK16"]
    neurodegeneration["neurodegeneration"]
    CDK16 -->|"implicated_in"| neurodegeneration
    style CDK16 fill:#4a1a6b,stroke:#4fc3f7,stroke-width:2px,color:#e0e0e0

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Targeting Hypotheses (0)

Hypotheses where this entity is a therapeutic target

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Mentioning Analyses (0)

Scientific analyses that reference this entity

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Related Papers (0)

Scientific publications cited in analyses involving this entity

Title & PMID	Authors	Journal	Year	Citations
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