New England Biolabs Canada

Product Pathways - Protein Stability

SENP1 (D16D7) Rabbit mAb #11929

Item# Description List Price Web Price Qty
11929S SENP1 (D16D7) Rabbit mAb - 100 µl $383.00
*On-line ordering is for Canadian customers only. Web pricing is applicable only to orders placed online at
Application Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W Human Endogenous 76 Rabbit IgG

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting


Specificity / Sensitivity

SENP1 (D16D7) Rabbit mAb recognizes endogenous levels of total SENP1 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gln175 of human SENP1 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from 293, A-204, and PANC-1 cells using SENP1 (D16D7) Rabbit mAb.


SENP1 is a member of the sentrin/SUMO-specific protease (SENP) family. SENP1 localizes to the nucleoplasm and catalyzes the release of SUMO1, SUMO2, and SUMO3 monomers from sumoylated substrates (1,2). SENP1 has been reported to be responsible for intracellular SUMO homeostasis in the control of normal cellular function (2). The removal of sumoylation by SENP1 from many important target proteins, such as HDAC1, HIF-1α, Stat5, p300, Elk-1, and SirT1, leads to the regulation of the related biological pathways (3-8). SENP1-induced desumoylation of HIF-1α stabilizes the target during hypoxia (5), activating downstream VEGF expression and angiogenesis (9). SENP1 desumoylates Stat5 and contributes to Stat5 acetylation and subsequent signaling during normal lymphocyte development (6). Under stress conditions, SENP1 interacts with and inactivates SirT1 by desumoylation, protecting cells from apoptosis (8). SENP1 has been reported to target the progesterone and androgen receptors, either directly or indirectly through HDAC1, thereby upregulating their transcriptional function and potentially affecting receptor-related cancer progression (3,10-13).

  1. Cheng, J. et al. (2006) Neoplasia 8, 667-76.
  2. Bawa-Khalfe, T. and Yeh, E.T. (2010) Genes Cancer 1, 748-752.
  3. Cheng, J. et al. (2004) Mol Cell Biol 24, 6021-8.
  4. Cheng, J. et al. (2005) J Biol Chem 280, 14492-8.
  5. Cheng, J. et al. (2007) Cell 131, 584-95.
  6. Van Nguyen, T. et al. (2012) Mol Cell 45, 210-21.
  7. Witty, J. et al. (2010) Biochem J 428, 247-54.
  8. Yang, Y. et al. (2007) Nat Cell Biol 9, 1253-62.
  9. Xu, Y. et al. (2010) J Biol Chem 285, 36682-8.
  10. Kaikkonen, S. et al. (2009) Mol Endocrinol 23, 292-307.
  11. Abdel-Hafiz, H.A. and Horwitz, K.B. (2012) BMC Mol Biol 13, 10.
  12. Wang, Q. et al. (2012) Oncogene , .
  13. Knutson, T.P. et al. (2012) Breast Cancer Res 14, R95.

Application References

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