Rab10 regulates vesicular transport, receptor trafficking, and cellular signaling through GTPase activity. Key functions include:
TLR4 signaling modulation: Rab10 promotes TLR4 transport from the Golgi to the plasma membrane, amplifying LPS-induced inflammatory responses (e.g., TNF-α, IL-6) and exacerbating acute respiratory distress syndrome (ARDS) in vivo .
Neuronal trafficking: Facilitates retrograde transport of TrkB receptors in hippocampal neurons, critical for BDNF signaling and axonogenesis .
Cancer progression: Overexpression in breast cancer (BC) and hepatocellular carcinoma (HCC) correlates with poor prognosis, HER2 status, and proliferation via oncogenic pathways .
LRRK2 phosphorylation: Phosphorylation at Thr-73 by LRRK2 regulates ciliogenesis, lysosomal stability, and Parkinson’s disease-related pathways .
Rab-10 antibodies are widely used in:
LRRK2-Rab10 interaction: Phospho-specific antibodies (e.g., MJFF-pRAB10) confirmed Rab10 phosphorylation at Thr-73 in Parkinson’s models, linking it to disrupted vesicular trafficking .
Neuronal trafficking defects: Knockdown of Rab10 in hippocampal neurons impaired TrkB receptor retrograde transport, reducing BDNF signaling .
Breast cancer: RAB10 upregulation in BC tissues correlated with HER2 positivity and immune infiltration (CIBERSORT analysis) .
HCC progression: shRNA-mediated Rab10 knockdown in HepG2 cells reduced proliferation and survival via apoptosis pathways .
TLR4-mediated ARDS: Rab10 overexpression in macrophages increased LPS-induced lung injury, highlighting its role as a therapeutic target .
Rab10 antibodies have identified its involvement in: