Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

SP-A (N-19) antibody


Antibody ID


Target Antigen

SP-A (N-19) human, mouse, rat, mouse, rat, human

Proper Citation

(Santa Cruz Biotechnology Cat# sc-7700, RRID:AB_661293)


polyclonal antibody


Discontinued: 2016; validation status unknown check with seller; recommendations: Immunofluorescence; ELISA; Immunoprecipitation; Western Blot; WB, IP, IF, ELISA

Host Organism



Santa Cruz Biotechnology

Cat Num


Publications that use this research resource

Activation of the GLP-1 Receptor by Liraglutide Increases ACE2 Expression, Reversing Right Ventricle Hypertrophy, and Improving the Production of SP-A and SP-B in the Lungs of Type 1 Diabetes Rats.

  • Romaní-Pérez M
  • Endocrinology
  • 2015 Oct 19

Literature context:


Diabetes alters microvascular function in the vascular beds of organs, including the lungs. Cardiovascular complications of pulmonary vascular affectation may be a consequence of the overactivation of the vasoconstrictive and proliferative components of the renin-angiotensin system. We previously reported that pulmonary physiology and surfactant production is improved by the glucagon-like peptide 1 receptor (GLP-1R) agonist liraglutide (LIR) in a rat model of lung hypoplasia. Because we hypothesized that streptozotocin-induced diabetes rats would show deficiencies in lung function, including surfactant proteins, and develop an imbalance of the renin-angiotensin system in the lungs. This effect would in turn be prevented by long-acting agonists of the GLP-1R, such as LIR. The induction of diabetes reduced the surfactant protein A and B in the lungs and caused the vasoconstrictor component of the renin-angiotensin system to predominate, which in turn increased angiotensin II levels, and ultimately being associated with right ventricle hypertrophy. LIR restored surfactant protein levels and reversed the imbalance in the renin-angiotensin system in this type 1 diabetes mellitus rat model. Moreover, LIR provoked a strong increase in angiotensin-converting enzyme 2 expression in the lungs of both diabetic and control rats, and in the circulating angiotensin(1-7) in diabetic animals. These effects prompted complete reversion of right ventricle hypertrophy. The consequences of LIR administration were independent of glycemic control and of glucocorticoids, and they involved NK2 homeobox 1 signaling. This study demonstrates by first time that GLP-1R agonists, such as LIR, might improve the cardiopulmonary complications associated with diabetes.

Funding information:
  • NIDA NIH HHS - R56 DA005084(United States)
  • NINDS NIH HHS - R01 NS034783(United States)