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CTS008) and counterstained with hematoxylin (blue). Specific staining was localized to cytoplasm in glomeruli and tubules. View our protocol for Chromogenic IHC Staining of Frozen Tissue Sections." class="big_lightbox" target="_blank">
4277-AS) was serially diluted and captured by Goat Anti-Mouse Renin 1 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF4277) coated on a Clear Polystyrene Microplate (Catalog # DY990). Goat Anti-Mouse Renin 1 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF4277) was biotinylated and incubated with the protein captured on the plate. Detection of the standard curve was achieved by incubating Streptavidin-HRP (Catalog # DY998)" class="big_lightbox" target="_blank">
4277-AS) was serially diluted and captured by Goat Anti-Mouse Renin 1 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF4277) coated on a Clear Polystyrene Microplate (Catalog # DY990). Goat Anti-Mouse Renin 1 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF4277) was biotinylated and incubated with the protein captured on the plate. Detection of the standard curve was achieved by incubating Streptavidin-HRP (Catalog # DY998)" class="big_lightbox" target="_blank">
CTS019) and counterstained with hematoxylin (blue). Lower panel shows a lack of labeling if primary antibodies are omitted and tissue is stained only with secondary antibody followed by incubation with detection reagents. View our protocol for Chromogenic IHC Staining of Paraffin-embedded Tissue Sections." class="big_lightbox" target="_blank">
Renin catalyzes the first step in the activation pathway of angiotensinogen--a cascade that can result in aldosterone release,vasoconstriction, and increase in blood pressure. Renin, an aspartyl protease, cleaves angiotensinogen to form angiotensin I, which is converted to angiotensin II by angiotensin I converting enzyme, an important regulator of blood pressure and electrolyte balance. Transcript variants that encode different protein isoforms and that arise from alternative splicing and the use of alternative promoters have been described, but their full-length nature has not been determined. Mutations in this gene have been shown to cause familial hyperproreninemia.