DUOXA1 Antibody

Role in Osteoclast Differentiation

• Function: DUOXA1 regulates RANKL-induced reactive oxygen species (ROS) production, essential for osteoclast formation and bone resorption .

• Mechanism: Knockdown of DUOXA1 via siRNA reduces ROS levels and suppresses TRAF6-mediated signaling pathways (MAPKs, Akt, NFATc1), impairing osteoclastogenesis .

• Key Data: Overexpression of DUOXA1 enhances ROS production by 40–60%, correlating with elevated osteoclast activity .

Impact on Myoblast Differentiation

• Study Model: Primary myoblasts and muscle satellite cells .

• Findings:

  • DUOXA1 overexpression increases apoptosis (2× Annexin V+ cells) and reduces myogenin expression by 66%, inhibiting cell fusion .

  • Conversely, DUOXA1 knockdown enhances myoblast fusion by 91% and reduces apoptosis by 45% .

Validation and Quality Control

• Specificity: Antibodies are validated using siRNA knockdown, overexpression models, and peptide blocking . For example, Proteintech’s 26632-1-AP detects DUOXA1 at 29 kDa and 52 kDa in mouse colon and brain tissues .

• Limitations: Some antibodies exhibit cross-reactivity with DUOXA2 or require titration for optimal performance . User reviews note occasional non-specific bands in WB .

Future Directions

Current research focuses on:

• DUOXA1’s role in thyroid dysfunction and cancer progression.

• Therapeutic targeting of DUOXA1-ROS pathways in bone diseases and muscle atrophy.