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anti-Mouse (Murine) Renin Antikörper:
anti-Rat (Rattus) Renin Antikörper:
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Human Polyclonal Renin Primary Antibody für IF (p), IHC (p) - ABIN715436
Wanka, Staar, Lutze, Peters, Hildebrandt, Beck, Bäumgen, Albers, Krieg, Zimmermann, Sczodrok, Schäfer, Hoffmann, Peters: Anti-necrotic and cardioprotective effects of a cytosolic renin isoform under ischemia-related conditions. in Journal of molecular medicine (Berlin, Germany) 2015
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Cow (Bovine) Polyclonal Renin Primary Antibody für WB - ABIN2776795
Lavoie, Liu, Bianco, Beltz, Johnson, Sigmund: Evidence supporting a functional role for intracellular renin in the brain. in Hypertension 2006
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Human Monoclonal Renin Primary Antibody für ELISA, WB - ABIN562625
Salhan, Husain, Subrati, Goyal, Singh, Rai, Malhotra, Singhal: HIV-induced kidney cell injury: role of ROS-induced downregulated vitamin D receptor. in American journal of physiology. Renal physiology 2012
Results show negative regulation of HDAC1 (zeige HDAC1 Antikörper) by a Cul3 (zeige CUL3 Antikörper)-REN (zeige REN1 Antikörper) E3 ubiquitin ligase (zeige MUL1 Antikörper) complex.
REN is upregulated by neurogenic signals (retinoic acid, EGF, and NGF) in embryonal stem (ES) cells and neural progenitor cell lines in association with neurotypic differentiation.
REN (zeige REN1 Antikörper) protein enhances caspase-3 (zeige CASP3 Antikörper) activation and antagonizes the Shh (zeige SHH Antikörper) pathway suggesting that this gene may represent a restraint of Shh (zeige SHH Antikörper) signaling.
Autosomal dominant polycystic kidney disease (ADPKD), uniquely increases urinary angiotensinogen (zeige AGT Antikörper) 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.
Data suggest mild primary aldosteronism (PA), where plasma renin activity is not as suppressed, is susceptible to dietary sodium influences on renin and ARR (zeige SAG Antikörper) (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 (zeige FECH Antikörper)) and 3 weeks for plasma renin activity (PRA (zeige S100A6 Antikörper)).
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.
Plasma renin and Aldosterone to renin ratio but not aldosterone are independently associated with presence of carotid plaques in coronary artery disease patients.
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