### ARHGAP44 Gene Overview

**Gene Symbol:** ARHGAP44  
**Function:** ARHGAP44 encodes a GTPase-activating protein (GAP) that primarily regulates Rho-type GTPases like CDC42 and RAC1. Its GAP activity promotes the hydrolysis of GTP to GDP, thereby inactivating these GTPases and modulating cellular processes such as dendritic spine morphology and synaptic transmission.

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### 1. Associated Genes
While the provided summaries specifically mention associations with CDC42, RAC1, and SHANK3, other genes and proteins that the ARHGAP44 might interact with based on functional and co-expression studies include:

- **RHOA**: Another member of the Rho GTPase family that may be indirectly influenced by changes in the activity of RAC1 and CDC42 due to ARHGAP44’s GAP functions.
- **GRIA1**: Glutamate receptor implicated indirectly since ARHGAP44 promotes GRIA1 exocytosis.
- **ACTB**: Coding for beta-actin, which is involved in the formation of cellular projections.
- **SHANK Family**: Other members of the SHANK protein family may also show functional interaction in synaptic plasticity, although SHANK3 was highlighted.

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### 2. Aging and Age-Related Diseases
Though there are limited direct studies specifically linking ARHGAP44 to aging or age-related diseases, there are several potential avenues for association:

- **Neurodegeneration**: Given its role in dendritic spine formation and maintenance, ARHGAP44 may play a part in age-related cognitive decline and neurodegenerative diseases where synaptic dysfunction and plasticity are involved, such as Alzheimer's disease.
- **Synaptic Plasticity**: Alterations in ARHGAP44's function may contribute to synaptic alterations observed in aging, which can impact learning and memory processes.
- **Cancer**: Dysregulation of Rho GTPases, including potential downstream effects from ARHGAP44, is associated with tumorigenesis, particularly in age-related cancers.

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### 3. Drug Interactions
As of the most recent data, ARHGAP44 does not have specific drugs directly targeting it, but its involvement in key cellular pathways means it could be impacted indirectly by:

- **Rac1 Inhibitors**: Drugs that inhibit Rac1 could theoretically impact ARHGAP44 function, considering its role as a GAP for RAC1.
- **Rho GTPase Modulators**: Compounds that affect the overall signaling pathways that include Rho GTPases may affect ARHGAP44 activity and consequently dendritic and synaptic dynamics.
  
Research is ongoing, and more specific drug interactions may be elucidated through pharmacogenomics as new drugs are developed targeting related pathways.

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### 4. Pathways and Biological Processes
ARHGAP44 is involved in multiple biological processes and pathways, including but not limited to:

- **Modification of Dendritic Spine**: Critical for maintenance and maturation of synaptic connections.
- **Regulation of Actin Cytoskeleton**: Modulates actin dynamics essential for cellular projections and motility.
- **Synaptic Plasticity**: Implicated in the processes related to long-term potentiation and synaptic changes associated with learning and memory.
- **Cell Projection Organization**: Plays a role in the structural organization of submissions such as filopodia and dendritic spines.
- **Signal Transduction**: Involved in negative regulation of signal transduction pathways mediated by Rho GTPases.
- **Involvement in Endocytosis/Exocytosis**: Coordinates movements of synaptic vesicles and receptors due to its interactions with proteins like SHANK3.

In summary, ARHGAP44 is integral to neuronal function, especially regarding structural dynamics and signaling pathways relevant for synaptic health and neuroplasticity across various stages of life, with potential implications in neurodegenerative conditions associated with aging.