### DYRK3 Gene Overview

The DYRK3 gene (Dual-specificity Tyrosine-regulated Kinase 3) encodes a dual-specificity protein kinase that participates in various cellular processes, particularly in the disassembly of membraneless organelles during mitosis and the regulation of cellular survival under stress.

### 1. Associated Genes
While the summaries primarily mention specific substrates (like SRRM1, PCM1, and AKT1S1), DYRK3 may be linked to other genes indirectly through its role in cellular pathways and regulatory networks. Potentially associated genes could include:

- **AKT1** – As a member of the signaling pathway affected by DYRK3 through AKT1S1.
- **TP53 (p53)** – The pathway affecting apoptosis where DYRK3 phosphorylates SIRT1, thereby inhibiting p53.
- **mTOR (mechanistic target of rapamycin)** – Involved through its relationship with DYRK3 regarding stress granule dissolution and mTORC1 signaling.
- **ZNF207** – As a mitotic regulator that is involved in the context of membraneless organelle disassembly.

### 2. Aging and Age-related Diseases
Current literature highlights several aspects of DYRK3 in the context of aging:

- **Cellular Senescence**: Dysregulation of DYRK3 can potentially contribute to cellular senescence, a hallmark of aging, through its involvement in signaling pathways that regulate cell growth and apoptosis.
- **Cancer** - Given its role in cell survival during stress, DYRK3 may indirectly influence cancer progression, which is often age-related, through its regulation of apoptosis and cell proliferation mechanisms.
- **Neurodegenerative Diseases**: DYRK3 could have implications in neurodegenerative processes due to its modulation of cell survival and the phosphorylation of various substrates that may affect neuronal health and function over time.

### 3. Drug Interactions
While specific drugs targeting DYRK3 have not been extensively characterized, certain drug classes might influence its activity:

- **Kinase Inhibitors**: Drugs that inhibit tyrosine kinases or dual-specificity kinases may modulate DYRK3 activity indirectly.
- **Antioxidants and Cytoprotective Agents**: Given its role in stress responses, compounds that promote cell survival during oxidative stress (e.g., specific neuroprotective agents) may affect DYRK3 functioning.
- **EPO (Erythropoietin)**: Though not a direct drug interaction, its function in erythropoiesis can imply a potential therapeutic dimension in managing conditions related to DYRK3 activity.

### 4. Pathways and Biological Processes
DYRK3 is involved in various biological processes and pathways, including but not limited to:

- **Mitosis**: Plays a crucial role in the disassembly of membraneless organelles such as stress granules, nuclear speckles, and pericentriolar material during cell division.
- **mTOR Signaling Pathway**: Regulates mTORC1 by mediating the dynamics of stress granules, impacting cellular growth and metabolism.
- **Apoptosis**: Inhibits apoptosis through interactions with SIRT1 and p53, thus affecting cell survival under genotoxic stress conditions.
- **Signal Transduction**: Engages in critical signaling cascades that manage cellular responses to stress, thereby influencing the overall cellular homeostasis.

### Conclusion
DYRK3 is a multifaceted dual-specificity kinase with essential roles in mitosis, stress response, and potentially, aging and age-related diseases. Its interactions with various cellular pathways underscore its importance in maintaining normal cellular function and responding to environmental stressors. Further investigation may elucidate more direct associations with drugs or targeted therapies that could improve understanding and management of diseases where DYRK3 is implicated.