PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25520008-7 2015 In salt-sensitive animals, Rac1 activation due to salt loading activates MRs in DCT2, connecting tubules, and collecting ducts. Salts 3-7 Rac family small GTPase 1 Homo sapiens 27-31 25430696-0 2015 The Expression of RAC1 and Mineralocorticoid Pathway-Dependent Genes are Associated With Different Responses to Salt Intake. Salts 112-116 Rac family small GTPase 1 Homo sapiens 18-22 25430696-1 2015 BACKGROUND: Rac1 upregulation has been implicated in salt-sensitive hypertension as a modulator of mineralocorticoid receptor (MR) activity. Salts 53-57 Rac family small GTPase 1 Homo sapiens 12-16 25430696-3 2015 AIM: We evaluated RAC1 expression in relation of high salt intake and association with MR, NGAL, HO-1, and NF-kappaB expression, mineralo- and glucocorticoids levels, and inflammatory parameters. Salts 54-58 Rac family small GTPase 1 Homo sapiens 18-22 25430696-6 2015 RAC1 expression was considered high or low according to the value found in normotensive subjects with low salt intake. Salts 106-110 Rac family small GTPase 1 Homo sapiens 0-4 25430696-13 2015 CONCLUSIONS: RAC1 expression was associated with an increase in MR, NGAL, NF-kappaB, and HO-1 expression, suggesting that RAC1 could be a mediator of cardiovascular damage induced by sodium, and may also useful to identify subjects with different responses to salt intake. Salts 260-264 Rac family small GTPase 1 Homo sapiens 13-17 25430696-13 2015 CONCLUSIONS: RAC1 expression was associated with an increase in MR, NGAL, NF-kappaB, and HO-1 expression, suggesting that RAC1 could be a mediator of cardiovascular damage induced by sodium, and may also useful to identify subjects with different responses to salt intake. Salts 260-264 Rac family small GTPase 1 Homo sapiens 122-126 27004435-5 2016 Salts with less symmetrical substituents tend to maintain the liquid state due to suppression of crystallization; crystallization is completely suppressed in most of the rac-[1]X salts and in some of the [2]X salts, whereas not in [3]X salts. Salts 0-5 Rac family small GTPase 1 Homo sapiens 170-176 25520008-7 2015 In salt-sensitive animals, Rac1 activation due to salt loading activates MRs in DCT2, connecting tubules, and collecting ducts. Salts 50-54 Rac family small GTPase 1 Homo sapiens 27-31 25499230-7 2015 We demonstrated that the Rac1-MR pathway contributes to the ligand-independent aberrant MR activation in salt-sensitive hypertension and renal injury models. Salts 105-109 Rac family small GTPase 1 Homo sapiens 25-29 23377658-0 2013 Role of Rac1 GTPase in salt-sensitive hypertension. Salts 23-27 Rac family small GTPase 1 Homo sapiens 8-12 22713140-6 2012 In the latter, Rac1 activation by salt excess causes MR stimulation. Salts 34-38 Rac family small GTPase 1 Homo sapiens 15-19 8961931-8 1996 The EC50 for Rac1 increased with increasing salt concentrations, whereas that of Rac2 was independent of salt, implicating the involvement of electrostatic forces for the former. Salts 44-48 Rac family small GTPase 1 Homo sapiens 13-17 24578129-5 2014 Furthermore, these studies point to crucial roles for the Rac1-mineralocorticoid receptor-NCC/ENaC and the renal beta-adrenergic stimulant-glucocorticoid receptor-WNK4-NCC pathways in certain rodent models of salt-sensitive hypertension. Salts 209-213 Rac family small GTPase 1 Homo sapiens 58-62 23832326-7 2014 In this review, we have introduced recent findings that suggest the contribution of MR activation to kidney diseases and the role of the Rac1-MR pathway in kidney injury associated with salt-sensitive hypertension and proteinuria. Salts 186-190 Rac family small GTPase 1 Homo sapiens 137-141 23774812-4 2013 High salt intake potentiates these effects, in part by activating the Rho family member Rac1, a regulatory subunit of reduced NADPH oxidase that activates the mineralocorticoid receptor. Salts 5-9 Rac family small GTPase 1 Homo sapiens 88-92 23377658-5 2013 In this review, the roles of Rac1 in the pathogenesis of salt-sensitive hypertension and kidney injury have been summarized. Salts 57-61 Rac family small GTPase 1 Homo sapiens 29-33 23377658-6 2013 RECENT FINDINGS: Genetic engineering studies have highlighted the new aspects of Rac1 and its regulators in salt-sensitive hypertension and cardiac and renal disease. Salts 108-112 Rac family small GTPase 1 Homo sapiens 81-85 23377658-7 2013 New evidence shows the essential roles of Rac1 in salt-evoked paradoxical mineralocorticoid receptor activation observed in salt-sensitive models and in renal tubular Na reabsorption through reduced nicotinamide-adenine dinucleotide phosphate oxidase-mediated oxidative stress or direct regulation of Na transporters. Salts 50-54 Rac family small GTPase 1 Homo sapiens 42-46 23377658-7 2013 New evidence shows the essential roles of Rac1 in salt-evoked paradoxical mineralocorticoid receptor activation observed in salt-sensitive models and in renal tubular Na reabsorption through reduced nicotinamide-adenine dinucleotide phosphate oxidase-mediated oxidative stress or direct regulation of Na transporters. Salts 124-128 Rac family small GTPase 1 Homo sapiens 42-46 23377658-8 2013 SUMMARY: The emerging concept of "ligand-independent aberrant mineralocorticoid receptor activation by Rac1" in the pathogenesis of salt-sensitive hypertension and kidney injury has been reviewed. Salts 132-136 Rac family small GTPase 1 Homo sapiens 103-107 23377658-9 2013 Rac inhibition, in addition to mineralocorticoid receptor blockade and salt restriction, would be a new promising strategy for the treatment of salt-sensitive hypertension. Salts 144-148 Rac family small GTPase 1 Homo sapiens 0-3 22752520-3 2012 Among them, we have identified that rac1, a small GTPase, activates mineralocorticoid receptor in aldosterone-independent fashion and induces salt-sensitive hypertension in several rodent model. Salts 142-146 Rac family small GTPase 1 Homo sapiens 36-40