RPL10A Recombinant Monoclonal Antibody

RPL10A, also known as 60S ribosomal protein L10a or NEDD6, serves as an essential component of the large ribosomal subunit where it plays a fundamental role in protein synthesis. Originally identified as a developmentally regulated gene in neural precursor cells, RPL10A has gained significant research attention for its involvement in ribosome biogenesis, translational regulation, and emerging connections to cellular proliferation pathways. Understanding RPL10A expression and localization provides valuable insights into ribosomal function across both normal physiology and disease states.

This recombinant monoclonal antibody, clone 17A6, offers the reproducibility and consistency that rigorous research demands. Generated against a synthetic peptide derived from human RPL10A, the antibody is produced using recombinant technology, ensuring sequence-defined specificity and eliminating the lot-to-lot variability often encountered with traditional hybridoma-derived reagents. This consistency proves particularly valuable for longitudinal studies or multi-site collaborations where experimental reproducibility is paramount.

Extensive validation demonstrates reliable performance across multiple experimental platforms. Western blot analysis detects a band at approximately 26 kDa across diverse human cell lines including HeLa, COLO-205, HT-29, MCF-7, Jurkat, and U-937, as well as mouse liver tissue, confirming cross-species reactivity. The slight difference from the predicted 25 kDa molecular weight likely reflects post-translational modifications. Immunohistochemistry staining has been validated in human gastric cancer and small intestine tissues, while immunofluorescence successfully localizes RPL10A in HepG2 cells. Flow cytometry applications have been demonstrated using Jurkat cells.

This versatile antibody supports investigations into ribosome biology, translational control mechanisms, cancer research, and developmental studies where RPL10A dysregulation may contribute to disease pathogenesis.