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Results show negative regulation of HDAC1 (show HDAC1 Proteins) by a Cul3 (show CUL3 Proteins)-REN E3 ubiquitin ligase (show MUL1 Proteins) complex.
REN is upregulated by neurogenic signals (retinoic acid, EGF (show EGF Proteins), and NGF (show NGFB Proteins)) in embryonal stem (ES) cells and neural progenitor cell lines in association with neurotypic differentiation.
REN protein enhances caspase-3 (show CASP3 Proteins) activation and antagonizes the Shh (show SHH Proteins) pathway suggesting that this gene may represent a restraint of Shh (show SHH Proteins) signaling.
Urinary angiotensinogen (show AGT Proteins) and renin excretion are elevated in CKD patients. Both parameters are negatively associated with eGFR (show EGFR Proteins) and these associations are independent of urinary albumin (show ALB Proteins) excretion
Autosomal dominant polycystic kidney disease (ADPKD), uniquely increases urinary angiotensinogen (show AGT Proteins) and renin excretion despite their circulating levels being comparable with those in non-ADPKD chronic kidney disease.
Prospective study of consecutive cardiac disease patients referred for cardiac catheterization has revealed distinct cardiac disease condition-associated differences in the frequencies of elevations in plasma renin, plasma aldosterone concentration, and the aldosterone-renin ratio
Renin-angiotensin system transgenic mouse model suggests that renal injury in preeclampsia may be mediated through local VEGF (show VEGFA Proteins).
Data suggest mild primary aldosteronism (PA), where plasma renin activity is not as suppressed, is susceptible to dietary sodium influences on renin and ARR (show SAG Proteins) (aldosterone to renin ratio). Optimal screening for PA should occur under conditions of high dietary sodium intake (rather than condition of low dietary sodium intake as frequently prescribed for patients with hypertension, which may be a symptom of PA).
This study demonstrates the efficacy of aldosterone/direct renin concentration ratio as a screening test for primary aldosteronism.
The dominant model (CC vs. CT+TT) of rs1894111 polymorphism in the ADRBK1 gene might be associated with low-renin hypertension in Han Chinese.
Data show that the optimum time for beta-adrenoreceptor antagonists (beta-blockers) withdrawal was 2 weeks when using direct renin concentration (DRC (show FECH Proteins)) and 3 weeks for plasma renin activity (PRA (show S100A6 Proteins)).
Active renin was not significantly different between hypertensive patients with and without left ventricular hypertrophy.
The present study provides evidence that the rs1464816 polymorphism in REN is associated with CKD progression in ADPKD.
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.
, BTB/POZ domain-containing protein KCTD11
, retinoic acid, EGF, and NGF upregulated
, renin 1 structural
, angiotensin-forming enzyme
, renin precursor, renal