PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
28669009-1	2017	The present study conducted in rats defines the requirements for neuroprotective effects of systemically administered AT1 receptor blockers (ARBs) in acute ischaemic stroke.	arbs	141-145	angiotensin II receptor, type 1a	Rattus norvegicus	118-121
29570771-10	2018	Comparative studies investigating eprosartan and other ARBs for the treatment of diseases caused by chronic, agonist-independent, AT1 receptor activation are warranted.	arbs	55-59	angiotensin II receptor type 1	Homo sapiens	130-133
29389354-1	2018	BACKGROUND: Heart failure guidelines recommend up-titration of angiotensin-converting enzyme (ACE) inhibitor/angiotensin receptor blockers (ARBs), beta-blockers, and mineralocorticoid receptor antagonists (MRAs) to doses used in randomized clinical trials, but these recommended doses are often not reached.	arbs	140-144	angiotensin I converting enzyme	Homo sapiens	63-92
28694144-2	2017	These actions mediated by AT1 receptor (AT1R) are well established and led to development of selective AT1R blockers (ARBs).	arbs	118-122	angiotensin II receptor type 1	Homo sapiens	26-38
28694144-2	2017	These actions mediated by AT1 receptor (AT1R) are well established and led to development of selective AT1R blockers (ARBs).	arbs	118-122	angiotensin II receptor type 1	Homo sapiens	40-44
28694144-2	2017	These actions mediated by AT1 receptor (AT1R) are well established and led to development of selective AT1R blockers (ARBs).	arbs	118-122	angiotensin II receptor type 1	Homo sapiens	103-107
29570771-2	2018	The current treatment paradigm for these diseases entails the preferred use of inverse agonist AT1 receptor blockers (ARBs).	arbs	118-122	angiotensin II receptor type 1	Homo sapiens	95-98
29570771-4	2018	Therefore, characterization of robust inverse agonist ARBs for the active state of AT1 receptors is necessary.	arbs	54-58	angiotensin II receptor type 1	Homo sapiens	83-86
29731445-7	2018	Among all Angiotensin II Receptor Antagonists/Blockers (ARBs), Telmisartan, Milfasartan and many others have benzimidazole ring in their structure.	arbs	56-60	angiotensinogen	Homo sapiens	10-24
28669009-12	2017	An effective, long-lasting blockade of brain AT1 receptors after systemic treatment with ARBs without extensive blood pressure reductions is the prerequisite for neuroprotective effects in ischaemic stroke.	arbs	89-93	angiotensin II receptor, type 1a	Rattus norvegicus	45-48
27009027-6	2016	Leukocyte 8-OHdG levels, duration of type 2 diabetes, albuminuria, use of insulin and use of angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs) were independently associated with microangiopathy in patients with type 2 diabetes after adjustment for smoking.	arbs	171-175	angiotensin I converting enzyme	Homo sapiens	93-122
28055971-6	2017	By comparing the Src-induced AR-cistrome and/or transcriptome in LNCaP to those in CRPC and LuCaP35.1 tumors, we identified an 11-gene Src-regulated CRPC signature consisting of AR-dependent, AR binding site (ARBS)-associated genes whose expression is altered by DHT in LNCaP[Src527F] but not in LNCaP cells.	arbs	209-213	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	17-20
28055971-6	2017	By comparing the Src-induced AR-cistrome and/or transcriptome in LNCaP to those in CRPC and LuCaP35.1 tumors, we identified an 11-gene Src-regulated CRPC signature consisting of AR-dependent, AR binding site (ARBS)-associated genes whose expression is altered by DHT in LNCaP[Src527F] but not in LNCaP cells.	arbs	209-213	androgen receptor	Homo sapiens	29-31
28055971-6	2017	By comparing the Src-induced AR-cistrome and/or transcriptome in LNCaP to those in CRPC and LuCaP35.1 tumors, we identified an 11-gene Src-regulated CRPC signature consisting of AR-dependent, AR binding site (ARBS)-associated genes whose expression is altered by DHT in LNCaP[Src527F] but not in LNCaP cells.	arbs	209-213	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	135-138
28055971-6	2017	By comparing the Src-induced AR-cistrome and/or transcriptome in LNCaP to those in CRPC and LuCaP35.1 tumors, we identified an 11-gene Src-regulated CRPC signature consisting of AR-dependent, AR binding site (ARBS)-associated genes whose expression is altered by DHT in LNCaP[Src527F] but not in LNCaP cells.	arbs	209-213	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	276-283
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	49-53	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	8-11
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	49-53	androgen receptor	Homo sapiens	21-23
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	49-53	forkhead box O1	Homo sapiens	67-72
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	49-53	DNA topoisomerase II beta	Homo sapiens	74-79
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	49-53	zinc finger protein 217	Homo sapiens	84-90
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	49-53	DNA topoisomerase II beta	Homo sapiens	122-127
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	49-53	DNA topoisomerase II beta	Homo sapiens	122-127
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	155-159	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	8-11
28329163-11	2017	Conclusion: Patients with HFrEF who were treated with less than 50% of recommended dose of ACE-inhibitors/ARBs and beta-blockers seemed to have a greater risk of death and/or heart failure hospitalization compared with patients reaching >=100%.	arbs	106-110	angiotensin I converting enzyme	Homo sapiens	91-94
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	155-159	androgen receptor	Homo sapiens	21-23
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	155-159	forkhead box O1	Homo sapiens	67-72
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	155-159	DNA topoisomerase II beta	Homo sapiens	74-79
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	155-159	zinc finger protein 217	Homo sapiens	84-90
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	155-159	androgen receptor	Homo sapiens	49-51
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	155-159	DNA topoisomerase II beta	Homo sapiens	122-127
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	155-159	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	169-172
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	155-159	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	169-172
28055971-8	2017	Lastly, Src enhances AR binding to non-canonical ARBS enriched for FOXO1, TOP2B and ZNF217 binding motifs; cooperative AR/TOP2B binding to a non-canonical ARBS was both Src- and DHT-sensitive and correlated with increased levels of Src-induced phosphotyrosyl-TOP2B.	arbs	155-159	DNA topoisomerase II beta	Homo sapiens	122-127
28055971-9	2017	These data suggest that CRPC progression is facilitated via Src-induced sensitization of AR to intracrine androgen levels, resulting in the engagement of canonical and non-canonical ARBS-dependent gene signatures.	arbs	182-186	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	60-63
28055971-9	2017	These data suggest that CRPC progression is facilitated via Src-induced sensitization of AR to intracrine androgen levels, resulting in the engagement of canonical and non-canonical ARBS-dependent gene signatures.	arbs	182-186	androgen receptor	Homo sapiens	89-91
26053493-5	2015	The objective of this retrospective study was to assess the impact of angiotensin-converting enzyme inhibitors (ACEIs) and Ang-II receptor 1 blockers (ARBs) on functional independence, progression-free survival (PFS) and overall survival (OS).	arbs	151-155	angiotensinogen	Homo sapiens	123-129
24304931-1	2014	There are conflicting reports on cancer risk associated with angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs).	arbs	139-143	angiotensin I converting enzyme	Homo sapiens	61-90
26039117-1	2015	The aim of this study is to determine whether renin-angiotensin system blockers (RASBs), which include angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin-2 receptor 1 blockers (ARBs), improve the overall survival (OS) of patients with metastatic non-small cell lung cancer (NSCLC).The medical charts of 117 patients with metastatic NSCLC were retrospectively assessed.	arbs	191-195	renin	Homo sapiens	46-51
24304931-8	2014	Regular use of ACE inhibitors/ARBs was not associated with an increased risk of cancer development and was actually found to decrease overall cancer risk in this study.	arbs	30-34	angiotensin I converting enzyme	Homo sapiens	15-18
22771493-6	2012	From the analysis of chromatin conformation, we conclude that this cooperation results from a chromatin looping over the ATAD2 promoter region between the ARBS and E2F1 binding site in an androgen-dependent manner.	arbs	155-159	ATPase family AAA domain containing 2	Homo sapiens	121-126
23727291-2	2013	Activation of the counter-regulatory Ang-(1-7)-Mas receptor axis may contribute to some of the effects of AT1 receptor blockers (ARBs).	arbs	129-133	angiotensin II receptor, type 1a	Mus musculus	106-109
22771493-6	2012	From the analysis of chromatin conformation, we conclude that this cooperation results from a chromatin looping over the ATAD2 promoter region between the ARBS and E2F1 binding site in an androgen-dependent manner.	arbs	155-159	E2F transcription factor 1	Homo sapiens	164-168
22771493-7	2012	Furthermore, we could show that several genes overexpressed in prostate cancer and potentially involved in several aspects of tumor development have an ARBS and an E2F1 binding site in their regulatory regions and exhibit the same mechanism of regulation by both transcription factors as ATAD2.	arbs	152-156	ATPase family AAA domain containing 2	Homo sapiens	288-293
22548405-7	2012	Moreover, the possible cross-talk between PPAR (peroxisome-proliferator-activated receptor)-gamma and AngII receptor subtypes is an intriguing issue to be addressed in order to understand the roles of RAS in the metabolic syndrome, and interestingly some ARBs (AT(1)-receptor blockers) have been reported to have an AT(1)-receptor-blocking action with a partial PPAR-gamma agonistic effect.	arbs	255-259	peroxisome proliferator activated receptor alpha	Homo sapiens	42-46
22522051-1	2012	The overactivation of the renin-angiotensin-aldosterone system (RAAS) is associated with cardiovascular and renal abnormalities, which can be mitigated by angiotensin converting enzyme inhibitors (ACEIs) and angiotensin-II (Ang-II)-AT(1) receptor blockers (ARBs).	arbs	257-261	renin	Homo sapiens	26-31
22522051-1	2012	The overactivation of the renin-angiotensin-aldosterone system (RAAS) is associated with cardiovascular and renal abnormalities, which can be mitigated by angiotensin converting enzyme inhibitors (ACEIs) and angiotensin-II (Ang-II)-AT(1) receptor blockers (ARBs).	arbs	257-261	angiotensinogen	Homo sapiens	208-222
22548405-7	2012	Moreover, the possible cross-talk between PPAR (peroxisome-proliferator-activated receptor)-gamma and AngII receptor subtypes is an intriguing issue to be addressed in order to understand the roles of RAS in the metabolic syndrome, and interestingly some ARBs (AT(1)-receptor blockers) have been reported to have an AT(1)-receptor-blocking action with a partial PPAR-gamma agonistic effect.	arbs	255-259	peroxisome proliferator activated receptor gamma	Homo sapiens	48-97
22548405-7	2012	Moreover, the possible cross-talk between PPAR (peroxisome-proliferator-activated receptor)-gamma and AngII receptor subtypes is an intriguing issue to be addressed in order to understand the roles of RAS in the metabolic syndrome, and interestingly some ARBs (AT(1)-receptor blockers) have been reported to have an AT(1)-receptor-blocking action with a partial PPAR-gamma agonistic effect.	arbs	255-259	angiotensinogen	Homo sapiens	102-107
22456197-5	2012	We identified a functional AR-binding site (ARBS) including two canonical androgen response elements in the vicinity of TACC2 gene, in which activated hallmarks of histone modification were observed.	arbs	44-48	transforming, acidic coiled-coil containing protein 2	Mus musculus	120-125
21964009-2	2011	The use of evidence-based medications (aspirin, statins, beta-blockers and angiotensin converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBS)) can reduce MACE in these patients.	arbs	153-157	angiotensin I converting enzyme	Homo sapiens	106-109
15596957-1	2005	PURPOSE OF REVIEW: This review summarizes recent clinical trial evidence showing a reduction in the development and recurrence of atrial fibrillation with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor-blocking agents (ARBs).	arbs	244-248	angiotensin I converting enzyme	Homo sapiens	186-189
21915096-4	2011	Besides pioneering the AR pathway, FoxA1 depletion elicited extensive redistribution of AR-binding sites (ARBs) on LNCaP-1F5 cell chromatin that was commensurate with changes in androgen-dependent gene expression signature.	arbs	106-110	forkhead box A1	Homo sapiens	35-40
21915096-5	2011	We identified three distinct classes of ARBs and androgen-responsive genes: (i) independent of FoxA1, (ii) pioneered by FoxA1 and (iii) masked by FoxA1 and functional upon FoxA1 depletion.	arbs	40-44	forkhead box A1	Homo sapiens	95-100
21915096-5	2011	We identified three distinct classes of ARBs and androgen-responsive genes: (i) independent of FoxA1, (ii) pioneered by FoxA1 and (iii) masked by FoxA1 and functional upon FoxA1 depletion.	arbs	40-44	forkhead box A1	Homo sapiens	120-125
21915096-5	2011	We identified three distinct classes of ARBs and androgen-responsive genes: (i) independent of FoxA1, (ii) pioneered by FoxA1 and (iii) masked by FoxA1 and functional upon FoxA1 depletion.	arbs	40-44	forkhead box A1	Homo sapiens	120-125
21915096-5	2011	We identified three distinct classes of ARBs and androgen-responsive genes: (i) independent of FoxA1, (ii) pioneered by FoxA1 and (iii) masked by FoxA1 and functional upon FoxA1 depletion.	arbs	40-44	forkhead box A1	Homo sapiens	120-125
20230346-10	2010	Both ACE inhibitors/ARBs and beta-blockers prescribed on discharge were associated with a lower adjusted hazard ratio (HR) for mortality at 1-year (HR, 0.71; P = 0.003; and HR, 0.68; P = 0.002, respectively).	arbs	20-24	angiotensin I converting enzyme	Homo sapiens	5-8
17268695-1	2007	OBJECTIVE: To investigate the effects of angiotensin converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs) and other anti-hypertensive agents on recombinant human erythropoietin (rHuEPO) in chronic renal failure (CRF) patients.	arbs	119-123	erythropoietin	Homo sapiens	181-195
17268695-8	2007	CONCLUSION: The present data from our population confirms that ACE inhibitors/ARBs interfere with rHuEPO therapy for treatment of anemia in CRF.	arbs	78-82	angiotensin I converting enzyme	Homo sapiens	63-66
17268695-9	2007	The ACE inhibitors/ARBs inhibit erythropoiesis induced by rHuEPO in CRF patients, therefore, simultaneous use of ACE inhibitors/ARBs and rHuEPO should be carried out with caution.	arbs	128-132	angiotensin I converting enzyme	Homo sapiens	4-7
17583183-3	2007	Although previous studies provided some conflicting evidence about the relevance of Ang-(1-7) in the regulation of vascular and renal function, data now demonstrate that Ang-(1-7) contributes to the cardiovascular effects of ACE-inhibitors (ACE-1) and AT1-receptor-blockers (ARBs) both in experimental conditions and in humans.	arbs	275-279	angiopoietin 1	Homo sapiens	170-178
17043228-2	2006	Cortical COX-2 induction by angiotensin-converting enzyme (ACE) inhibitors or AT(1) receptor blockers (ARBs) suggests that angiotensin II may inhibit cortical COX-2 by stimulating the AT(1) receptor pathway.	arbs	103-107	prostaglandin-endoperoxide synthase 2	Mus musculus	9-14
17043228-2	2006	Cortical COX-2 induction by angiotensin-converting enzyme (ACE) inhibitors or AT(1) receptor blockers (ARBs) suggests that angiotensin II may inhibit cortical COX-2 by stimulating the AT(1) receptor pathway.	arbs	103-107	prostaglandin-endoperoxide synthase 2	Mus musculus	159-164
17043228-5	2006	However, we found that angiotensin II infusion further stimulated cortical COX-2 elevation induced by ARBs, suggesting a potential role for an AT(2) receptor-mediated pathway when the AT(1) receptor was inhibited.	arbs	102-106	prostaglandin-endoperoxide synthase 2	Mus musculus	75-80
17043228-5	2006	However, we found that angiotensin II infusion further stimulated cortical COX-2 elevation induced by ARBs, suggesting a potential role for an AT(2) receptor-mediated pathway when the AT(1) receptor was inhibited.	arbs	102-106	angiotensin II receptor, type 2	Mus musculus	143-157
17043228-8	2006	In WT mice ARBs increased cortical COX-2 more than ACE inhibitors, and this stimulation was attenuated by the AT(2) receptor antagonist PD123319.	arbs	11-15	prostaglandin-endoperoxide synthase 2	Mus musculus	35-40
17043228-8	2006	In WT mice ARBs increased cortical COX-2 more than ACE inhibitors, and this stimulation was attenuated by the AT(2) receptor antagonist PD123319.	arbs	11-15	angiotensin II receptor, type 2	Mus musculus	110-124
17043228-9	2006	In the knockout mice ARBs led to significantly less cortical COX-2 elevation, which was not attenuated by PD123319.	arbs	21-25	prostaglandin-endoperoxide synthase 2	Mus musculus	61-66
16180960-6	2005	The angiotensin AT1 receptor blockers (ARBs), which block the effects of angiotensin II, not only lower blood pressure but also provide target-organ protection.	arbs	39-43	angiotensinogen	Homo sapiens	73-87
19665690-5	2009	Plasma, renal, and cardiac levels of CGRP and IGF-I in SHRs were significantly lower than those in normotensive Wistar Kyoto rats (WKYs) (P < 0.01), which increased to levels found in WKYs after the administration of ARBs.	arbs	220-224	calcitonin-related polypeptide alpha	Rattus norvegicus	37-41
19665690-10	2009	Although ARBs reversed decreases in CGRP release and cAMP levels in the presence of Ang II in DRG isolated from WKYs, they increased CGRP release and cAMP levels in the absence of Ang II in DRG isolated from SHRs.	arbs	9-13	calcitonin-related polypeptide alpha	Rattus norvegicus	36-40
19665690-10	2009	Although ARBs reversed decreases in CGRP release and cAMP levels in the presence of Ang II in DRG isolated from WKYs, they increased CGRP release and cAMP levels in the absence of Ang II in DRG isolated from SHRs.	arbs	9-13	cathelicidin antimicrobial peptide	Rattus norvegicus	53-57
19665690-10	2009	Although ARBs reversed decreases in CGRP release and cAMP levels in the presence of Ang II in DRG isolated from WKYs, they increased CGRP release and cAMP levels in the absence of Ang II in DRG isolated from SHRs.	arbs	9-13	angiotensinogen	Rattus norvegicus	84-90
19665690-10	2009	Although ARBs reversed decreases in CGRP release and cAMP levels in the presence of Ang II in DRG isolated from WKYs, they increased CGRP release and cAMP levels in the absence of Ang II in DRG isolated from SHRs.	arbs	9-13	calcitonin-related polypeptide alpha	Rattus norvegicus	133-137
19665690-10	2009	Although ARBs reversed decreases in CGRP release and cAMP levels in the presence of Ang II in DRG isolated from WKYs, they increased CGRP release and cAMP levels in the absence of Ang II in DRG isolated from SHRs.	arbs	9-13	cathelicidin antimicrobial peptide	Rattus norvegicus	150-154
19665690-14	2009	These observations suggest that ARBs might increase CGRP release from sensory neurons by sensitizing VR-1 activation through increases in cAMP levels, which thereby increased the production of IGF-I in SHRs.	arbs	32-36	calcitonin-related polypeptide alpha	Rattus norvegicus	52-56
19665690-14	2009	These observations suggest that ARBs might increase CGRP release from sensory neurons by sensitizing VR-1 activation through increases in cAMP levels, which thereby increased the production of IGF-I in SHRs.	arbs	32-36	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	101-105
19665690-14	2009	These observations suggest that ARBs might increase CGRP release from sensory neurons by sensitizing VR-1 activation through increases in cAMP levels, which thereby increased the production of IGF-I in SHRs.	arbs	32-36	cathelicidin antimicrobial peptide	Rattus norvegicus	138-142
19665690-14	2009	These observations suggest that ARBs might increase CGRP release from sensory neurons by sensitizing VR-1 activation through increases in cAMP levels, which thereby increased the production of IGF-I in SHRs.	arbs	32-36	insulin-like growth factor 1	Rattus norvegicus	193-198
18849338-2	2008	We showed that cardiac ACE2 is elevated following treatment of coronary artery-ligated rats with AT1 receptor blockers (ARBs).	arbs	120-124	angiotensin I converting enzyme 2	Rattus norvegicus	23-27
16007228-4	2005	Hence, compared to angiotensin converting enzyme inhibitors (ACEIs), selective AT1 receptor blockers (ARBs) should provide additional end organ protection via AT2 receptors activation.	arbs	102-106	angiotensin II receptor type 1	Homo sapiens	79-82
16007228-4	2005	Hence, compared to angiotensin converting enzyme inhibitors (ACEIs), selective AT1 receptor blockers (ARBs) should provide additional end organ protection via AT2 receptors activation.	arbs	102-106	angiotensin II receptor type 2	Homo sapiens	159-162
7989349-2	1994	Deletion mapping and DNase I footprinting analysis had previously identified two androgen receptor-binding sites (ARBS) necessary for androgen induction of the probasin gene: ARBS-1, which resembled a glucocorticoid-responsive element, and ARBS-2, which had a unique sequence.	arbs	114-118	deoxyribonuclease 1	Rattus norvegicus	21-28
15311098-8	2004	CONCLUSIONS: The results of this observational study confirm that the rate of BP control can be improved in daily clinical practice by increasing the use of drug combinations, as well as by the first-line prescription of ACE inhibitors and CCBs [and probably angiotensin II receptor inhibitors (ARBs)].	arbs	295-299	angiotensin I converting enzyme	Homo sapiens	221-224
7989349-2	1994	Deletion mapping and DNase I footprinting analysis had previously identified two androgen receptor-binding sites (ARBS) necessary for androgen induction of the probasin gene: ARBS-1, which resembled a glucocorticoid-responsive element, and ARBS-2, which had a unique sequence.	arbs	114-118	probasin	Rattus norvegicus	160-168
7989349-7	1994	Consistent with the higher affinity, ARBS-2 bound AR2 at half the threshold concentration (200 ng) of that required in reciprocal DNase I footprinting experiments with ARBS-1.	arbs	37-41	deoxyribonuclease 1	Rattus norvegicus	130-137
7989349-7	1994	Consistent with the higher affinity, ARBS-2 bound AR2 at half the threshold concentration (200 ng) of that required in reciprocal DNase I footprinting experiments with ARBS-1.	arbs	168-172	deoxyribonuclease 1	Rattus norvegicus	130-137
25981295-4	2015	For example, AGTR1 blockers (ARBs) which are already in clinical use for treating hypertension, merit further investigation as a therapeutic strategy for AGTR1-positive cancer patients and may have the potential to prevent Ang II-AGTR1 signalling mediated cancer pathogenesis and metastases.	arbs	29-33	angiotensin II receptor type 1	Homo sapiens	13-18
25981295-4	2015	For example, AGTR1 blockers (ARBs) which are already in clinical use for treating hypertension, merit further investigation as a therapeutic strategy for AGTR1-positive cancer patients and may have the potential to prevent Ang II-AGTR1 signalling mediated cancer pathogenesis and metastases.	arbs	29-33	angiotensin II receptor type 1	Homo sapiens	154-159
25981295-4	2015	For example, AGTR1 blockers (ARBs) which are already in clinical use for treating hypertension, merit further investigation as a therapeutic strategy for AGTR1-positive cancer patients and may have the potential to prevent Ang II-AGTR1 signalling mediated cancer pathogenesis and metastases.	arbs	29-33	angiotensin II receptor type 1	Homo sapiens	154-159
35365763-5	2022	An integrative genetic analysis identified several AR-target genes associated with CRPC progression including OPRK1, which harbors ARBS and was upregulated upon androgen deprivation.	arbs	131-135	androgen receptor	Homo sapiens	51-53
35365763-5	2022	An integrative genetic analysis identified several AR-target genes associated with CRPC progression including OPRK1, which harbors ARBS and was upregulated upon androgen deprivation.	arbs	131-135	opioid receptor kappa 1	Homo sapiens	110-115
35203711-7	2022	An initial suggestion that the susceptibility to infection and disease severity may be enhanced by angiotensin type-1 receptor blockers (ARBs) and ACE inhibitors (ACEIs) because they increase ACE2 levels, led to the consideration of discontinuing treatments in thousands of patients.	arbs	137-141	angiotensin converting enzyme 2	Homo sapiens	192-196
35203711-8	2022	More recent experimental and clinical data indicate that ACEIs and, particularly, ARBs can be beneficial for COVID-19 outcome, both by reducing inflammatory responses and by triggering mechanisms (such as ADAM17 inhibition) counteracting viral entry.	arbs	82-86	ADAM metallopeptidase domain 17	Homo sapiens	205-211
33219601-8	2021	RESULTS: Multivariate results revealed inverse associations for time to PD diagnosis with exposure to the combination of the combination of angiotensin receptor II blockers (ARBs) and dihydropyridine calcium channel blockers (DHP-CCB) (HR=0.55, p< 0.01) and angiotensin converting enzyme inhibitors (ACEi) and diuretics (HR=0.60, p-value <0.01).	arbs	174-178	angiotensin I converting enzyme	Homo sapiens	258-287
34017843-9	2021	The results of the study strongly suggest that increased ACE2 does not increase risk of COVID-19 and that ACEi and ARBs by blocking excessive AT1R-mediated Ang II activation might favor the increase of ACE2-derived Ang 1-7.	arbs	115-119	angiotensin II receptor type 1	Homo sapiens	142-146
34017843-9	2021	The results of the study strongly suggest that increased ACE2 does not increase risk of COVID-19 and that ACEi and ARBs by blocking excessive AT1R-mediated Ang II activation might favor the increase of ACE2-derived Ang 1-7.	arbs	115-119	angiotensin converting enzyme 2	Homo sapiens	202-206
34017843-9	2021	The results of the study strongly suggest that increased ACE2 does not increase risk of COVID-19 and that ACEi and ARBs by blocking excessive AT1R-mediated Ang II activation might favor the increase of ACE2-derived Ang 1-7.	arbs	115-119	angiopoietin 1	Homo sapiens	215-222
32965603-1	2020	Considerable concern has emerged for the potential harm in the use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor inhibitors (ARBs) in COVID-19 patients, given that ACEIs and ARBs may increase the expression of ACE2 receptors that represent the way for coronavirus 2 to entry into the cell and cause severe acute respiratory syndrome.	arbs	156-160	angiotensin converting enzyme 2	Homo sapiens	241-245
32569491-6	2020	RESULTS: In total, 113 hypertensive Covid-19 patients were included, of them 74 patients were using ACE inh/ARBs.	arbs	108-112	angiotensin I converting enzyme	Homo sapiens	100-103
32569491-8	2020	The frequency of admission to the ICU and endotracheal intubation were significantly higher in patients using ACE inh/ARBs.	arbs	118-122	angiotensin I converting enzyme	Homo sapiens	110-113
32569491-9	2020	In a multivariable analysis, the use of ACE inh/ARBs was an independent predictor of in-hospital mortality (OR: 3.66; 95%CI: 1.11-18.18; p= .032).	arbs	48-52	angiotensin I converting enzyme	Homo sapiens	40-43
32569491-10	2020	Kaplan-Meir curve analysis displayed that patients on ACE inh/ARBs therapy had higher incidence of in-hospital death than those who were not.	arbs	62-66	angiotensin I converting enzyme	Homo sapiens	54-57
32569491-11	2020	CONCLUSION: The present study has found that the use of ACE inh/ARBs therapy might be associated with an increased in-hospital mortality in patients who were diagnosed with Covid-19 pneumonia.	arbs	64-68	angiotensin I converting enzyme	Homo sapiens	56-59
32965603-1	2020	Considerable concern has emerged for the potential harm in the use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor inhibitors (ARBs) in COVID-19 patients, given that ACEIs and ARBs may increase the expression of ACE2 receptors that represent the way for coronavirus 2 to entry into the cell and cause severe acute respiratory syndrome.	arbs	205-209	angiotensin I converting enzyme	Homo sapiens	70-99
32965603-1	2020	Considerable concern has emerged for the potential harm in the use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor inhibitors (ARBs) in COVID-19 patients, given that ACEIs and ARBs may increase the expression of ACE2 receptors that represent the way for coronavirus 2 to entry into the cell and cause severe acute respiratory syndrome.	arbs	205-209	angiotensin converting enzyme 2	Homo sapiens	241-245
32247750-4	2020	Cardiovascular and renal abnormalities are associated with the overactivation of RAS, which can be constrained by angiotensin- converting enzyme inhibitors (ACEIs), angiotensin II (Ang-II) -AT1 receptor blockers (ARBs) and renin inhibitors.	arbs	213-217	angiotensinogen	Homo sapiens	165-179
31545259-9	2019	Our findings indicate that local application of angiotensin converting enzyme inhibitor drugs (ACEIs) and angiotensin receptor blocker drugs (ARBs) can reduce scarring by reducing the expression of collagen I, collagen III, phosphorylated small mothers against decapentaplegic 3 (p-Smad3) and transforming growth factor-beta 1 (TGF-beta1).	arbs	142-146	SMAD family member 3	Mus musculus	282-287
31520575-6	2019	AR binding sites (ARBS) are enriched for FOX, HOX, and GATA motifs in PC cells but not for c-JUN motifs in benign cells.	arbs	18-22	androgen receptor	Homo sapiens	0-2
31545259-9	2019	Our findings indicate that local application of angiotensin converting enzyme inhibitor drugs (ACEIs) and angiotensin receptor blocker drugs (ARBs) can reduce scarring by reducing the expression of collagen I, collagen III, phosphorylated small mothers against decapentaplegic 3 (p-Smad3) and transforming growth factor-beta 1 (TGF-beta1).	arbs	142-146	transforming growth factor, beta 1	Mus musculus	293-326
31545259-9	2019	Our findings indicate that local application of angiotensin converting enzyme inhibitor drugs (ACEIs) and angiotensin receptor blocker drugs (ARBs) can reduce scarring by reducing the expression of collagen I, collagen III, phosphorylated small mothers against decapentaplegic 3 (p-Smad3) and transforming growth factor-beta 1 (TGF-beta1).	arbs	142-146	transforming growth factor, beta 1	Mus musculus	328-337
30191985-5	2019	Angiotensin II increases blood pressure by binding to angiotensin type 1 (AT1 ) receptor, and direct renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors and AT1 receptor blockers (ARBs) are clinically used as antihypertensive agents.	arbs	193-197	angiotensinogen	Homo sapiens	0-14