PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
19416205-3	2009	Thus, the objectives of this study were to determine the effects of RLX on the myocardial Wnt/beta-catenin signaling system and MMP expression in the postnatal day 2 (PND 2) porcine heart.	Relaxin	68-71	Wnt family member 4	Homo sapiens	90-93
19319551-4	2009	RESULTS: We demonstrate for the first time an activating effect of RLX for human COX-1 and COX-2 in primary myometrial and decidual cells in vitro.	Relaxin	67-70	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	81-86
19319551-4	2009	RESULTS: We demonstrate for the first time an activating effect of RLX for human COX-1 and COX-2 in primary myometrial and decidual cells in vitro.	Relaxin	67-70	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	91-96
19416205-3	2009	Thus, the objectives of this study were to determine the effects of RLX on the myocardial Wnt/beta-catenin signaling system and MMP expression in the postnatal day 2 (PND 2) porcine heart.	Relaxin	68-71	catenin beta 1	Homo sapiens	94-106
19416205-4	2009	Results showed that myocardial Wnt7a and Wnt4 gene expression at PND 2 decreased following treatment with RLX in vivo from birth, while there was no effect on Wnt5a expression.	Relaxin	106-109	Wnt family member 7A	Homo sapiens	31-36
19416205-4	2009	Results showed that myocardial Wnt7a and Wnt4 gene expression at PND 2 decreased following treatment with RLX in vivo from birth, while there was no effect on Wnt5a expression.	Relaxin	106-109	Wnt family member 4	Homo sapiens	41-45
19416205-5	2009	Immunoreactive myocardial beta-catenin protein was reduced in RLX-treated animals.	Relaxin	62-65	catenin beta 1	Homo sapiens	26-38
19416205-6	2009	Zymographic analysis of medium from RLX-treated heart explants showed an increase in pro-MMP-2 but not pro-MMP-9 activity.	Relaxin	36-39	matrix metallopeptidase 2	Homo sapiens	89-94
19416205-8	2009	Data suggest that the RLX-induced decline in Wnt/beta-catenin expression at PND 2, together with increased MMP-2 activity, may be important for neonatal porcine cardiac remodeling.	Relaxin	22-25	Wnt family member 4	Homo sapiens	45-48
19416205-8	2009	Data suggest that the RLX-induced decline in Wnt/beta-catenin expression at PND 2, together with increased MMP-2 activity, may be important for neonatal porcine cardiac remodeling.	Relaxin	22-25	catenin beta 1	Homo sapiens	49-61
19416205-8	2009	Data suggest that the RLX-induced decline in Wnt/beta-catenin expression at PND 2, together with increased MMP-2 activity, may be important for neonatal porcine cardiac remodeling.	Relaxin	22-25	matrix metallopeptidase 2	Homo sapiens	107-112
19416208-7	2009	Significant reductions of phosphorylated SMAD2, mesangial cell proliferation, and alpha-smooth muscle actin expression were observed in rats treated with RLX.	Relaxin	154-157	SMAD family member 2	Rattus norvegicus	41-46
19416208-7	2009	Significant reductions of phosphorylated SMAD2, mesangial cell proliferation, and alpha-smooth muscle actin expression were observed in rats treated with RLX.	Relaxin	154-157	actin gamma 2, smooth muscle	Rattus norvegicus	82-107
19416222-5	2009	Relaxin or insulin-like peptide 3 treatment suppressed transforming growth factor beta-induced phosphorylation of SMAD2 in rat leiomyoma ELT-3 cells in vitro, suggesting a possible involvement of relaxins in the etiology of leiomyoma.	Relaxin	196-204	distal membrane arm assembly component 2 like	Rattus norvegicus	75-86
19416222-5	2009	Relaxin or insulin-like peptide 3 treatment suppressed transforming growth factor beta-induced phosphorylation of SMAD2 in rat leiomyoma ELT-3 cells in vitro, suggesting a possible involvement of relaxins in the etiology of leiomyoma.	Relaxin	196-204	SMAD family member 2	Rattus norvegicus	114-119
16484357-3	2006	We first corroborated our earlier work by showing that pro- and active forms of MMP-2 were increased in small renal arteries from pregnant compared with virgin rats and Rlx-treated compared with vehicle-treated nonpregnant rats.	Relaxin	169-172	matrix metallopeptidase 2	Rattus norvegicus	80-85
18562087-7	2008	These data suggest that during early pregnancy IGF-I, RLX and PGE(2) can affect VEGF expression in the endometrium and therefore may support uterine and embryo development, implantation and pregnancy.	Relaxin	54-57	vascular endothelial growth factor A	Homo sapiens	80-84
17289798-11	2007	Incubation with RLX (90 min) reduced THP-1 expression of the NF-kappaB inhibitor protein, IkappaB-alpha.	Relaxin	16-19	NFKB inhibitor alpha	Homo sapiens	90-103
17289798-14	2007	In conclusion, these data suggest that RLX-induced tissue remodeling through increasing MMP-9 expression is dependent on NF-kappaB activation.	Relaxin	39-42	matrix metallopeptidase 9	Homo sapiens	88-93
18304981-9	2008	Pretreatment with ICI increased VEGF in both tissues and increased RLX-induced cervical VEGF.	Relaxin	67-70	vascular endothelial growth factor A	Homo sapiens	88-92
18304981-13	2008	Effects of RLX on uterine and cervical ERalpha and VEGF expression may be important for neonatal reproductive tract development.	Relaxin	11-14	estrogen receptor 1	Homo sapiens	39-46
18304981-13	2008	Effects of RLX on uterine and cervical ERalpha and VEGF expression may be important for neonatal reproductive tract development.	Relaxin	11-14	vascular endothelial growth factor A	Homo sapiens	51-55
17055075-3	2007	The purpose of this study was to evaluate a possible effect of RLX on OTR regulation in human uterine smooth muscle cells.	Relaxin	63-66	oxytocin receptor	Homo sapiens	70-73
17055075-8	2007	CONCLUSION: We report for the first time an effect of RLX on OTR regulation in human uterine myometrial cells.	Relaxin	54-57	oxytocin receptor	Homo sapiens	61-64
16847443-9	2006	As a result, RLX led to a reduction of ileal cell apoptosis (caspase 3, terminal deoxynucleotidyltransferase-mediated UTP end labeling).	Relaxin	13-16	caspase 3	Rattus norvegicus	61-70
16847443-9	2006	As a result, RLX led to a reduction of ileal cell apoptosis (caspase 3, terminal deoxynucleotidyltransferase-mediated UTP end labeling).	Relaxin	13-16	DNA nucleotidylexotransferase	Rattus norvegicus	72-108
16484357-8	2006	MMP-2 mRNA as measured by real-time PCR was increased in small renal arteries from pregnant and Rlx-treated nonpregnant rats compared with their respective controls.	Relaxin	96-99	matrix metallopeptidase 2	Rattus norvegicus	0-5
16604479-10	2006	CONCLUSION: The effect of RLX on BMD in postmenopausal women with osteoporosis is regulated by the polymorphisms of Fok I of VDR gene and Pvu II of ESR1 gene.	Relaxin	26-29	vitamin D receptor	Homo sapiens	125-128
16484357-10	2006	Thus increases in MMP-2 mRNA and protein expression are major factors contributing to increased MMP-2 activity in small arteries from pregnant and Rlx-treated nonpregnant rats.	Relaxin	147-150	matrix metallopeptidase 2	Rattus norvegicus	18-23
16484357-10	2006	Thus increases in MMP-2 mRNA and protein expression are major factors contributing to increased MMP-2 activity in small arteries from pregnant and Rlx-treated nonpregnant rats.	Relaxin	147-150	matrix metallopeptidase 2	Rattus norvegicus	96-101
16604479-10	2006	CONCLUSION: The effect of RLX on BMD in postmenopausal women with osteoporosis is regulated by the polymorphisms of Fok I of VDR gene and Pvu II of ESR1 gene.	Relaxin	26-29	estrogen receptor 1	Homo sapiens	148-152
15722441-6	2005	In addition, RLX increased the phosphorylation of CRE binding protein (CREB to p-CREB) and p-CREB resided in the nucleus, indicating that RLX activates the protein kinase (PKA) system in decidual cells.	Relaxin	13-16	cAMP responsive element binding protein 1	Homo sapiens	71-75
15784719-2	2005	We investigated the effects of relaxin (RLX) and prostaglandin E(2) (PGE(2)) on IL-11 secretion by human endometrial stromal cells (HESC) and during cAMP or medroxyprogesterone acetate (P)-induced decidualization.	Relaxin	40-43	interleukin 11	Homo sapiens	80-85
15784719-4	2005	RLX, cAMP, or PGE(2) increased IL-11 mRNA and IL-11 secretion, with maximal response to RLX and cAMP.	Relaxin	0-3	interleukin 11	Homo sapiens	31-36
15784719-4	2005	RLX, cAMP, or PGE(2) increased IL-11 mRNA and IL-11 secretion, with maximal response to RLX and cAMP.	Relaxin	0-3	interleukin 11	Homo sapiens	46-51
15784719-5	2005	Addition of the cAMP/protein kinase A inhibitor Rp-adenosine-3,5-cyclic-monophosphorothioate to either RLX- or PGE(2)-treated cells decreased IL-11 secretion.	Relaxin	103-106	interleukin 11	Homo sapiens	142-147
15784719-7	2005	Cotreatment of HESC with RLX, PGE(2), or cAMP and estrogen plus P down-regulated IL-11 mRNA and IL-11 secretion at 24 h, before secretion of prolactin (decidualization marker).	Relaxin	25-28	interleukin 11	Homo sapiens	81-86
15784719-7	2005	Cotreatment of HESC with RLX, PGE(2), or cAMP and estrogen plus P down-regulated IL-11 mRNA and IL-11 secretion at 24 h, before secretion of prolactin (decidualization marker).	Relaxin	25-28	interleukin 11	Homo sapiens	96-101
15784719-8	2005	Addition of W147AIL-11 (IL-11 signaling inhibitor) reduced prolactin secretion stimulated by RLX or PGE(2) and estrogen plus P. This is the first demonstration that cAMP-decidualized HESC secrete IL-11 and that IL-11 mRNA and IL-11 secretion are regulated by RLX and PGE(2), partly via a cAMP/protein kinase A-dependent pathway.	Relaxin	93-96	interleukin 11	Homo sapiens	17-22
15784719-8	2005	Addition of W147AIL-11 (IL-11 signaling inhibitor) reduced prolactin secretion stimulated by RLX or PGE(2) and estrogen plus P. This is the first demonstration that cAMP-decidualized HESC secrete IL-11 and that IL-11 mRNA and IL-11 secretion are regulated by RLX and PGE(2), partly via a cAMP/protein kinase A-dependent pathway.	Relaxin	93-96	interleukin 11	Homo sapiens	24-29
15784719-8	2005	Addition of W147AIL-11 (IL-11 signaling inhibitor) reduced prolactin secretion stimulated by RLX or PGE(2) and estrogen plus P. This is the first demonstration that cAMP-decidualized HESC secrete IL-11 and that IL-11 mRNA and IL-11 secretion are regulated by RLX and PGE(2), partly via a cAMP/protein kinase A-dependent pathway.	Relaxin	93-96	interleukin 11	Homo sapiens	24-29
15784719-8	2005	Addition of W147AIL-11 (IL-11 signaling inhibitor) reduced prolactin secretion stimulated by RLX or PGE(2) and estrogen plus P. This is the first demonstration that cAMP-decidualized HESC secrete IL-11 and that IL-11 mRNA and IL-11 secretion are regulated by RLX and PGE(2), partly via a cAMP/protein kinase A-dependent pathway.	Relaxin	93-96	interleukin 11	Homo sapiens	24-29
15722441-6	2005	In addition, RLX increased the phosphorylation of CRE binding protein (CREB to p-CREB) and p-CREB resided in the nucleus, indicating that RLX activates the protein kinase (PKA) system in decidual cells.	Relaxin	13-16	cAMP responsive element binding protein 1	Homo sapiens	81-85
15722441-6	2005	In addition, RLX increased the phosphorylation of CRE binding protein (CREB to p-CREB) and p-CREB resided in the nucleus, indicating that RLX activates the protein kinase (PKA) system in decidual cells.	Relaxin	13-16	cAMP responsive element binding protein 1	Homo sapiens	81-85
15722441-7	2005	Gel shift assay showed that nuclear extracts prepared from RLX treated decidual cells increased the binding to the CRE site of the IGFBP-1 promoter.	Relaxin	59-62	insulin like growth factor binding protein 1	Homo sapiens	131-138
15722441-9	2005	RLX enhanced IGFBP-1 promoter activity was inhibited by cAMP dependent PKA inhibitor, H-89.	Relaxin	0-3	insulin like growth factor binding protein 1	Homo sapiens	13-20
11641245-5	2001	Furthermore, RLX modulates effects of angiotensin II, another crucial mediator.	Relaxin	13-16	angiotensinogen	Homo sapiens	38-52
15155604-2	2004	The effect of RLX on insulin-like growth factor binding protein-1 (IGFBP-1) production was determined to evaluate the biological function of RLX/receptor in human endometrial cells.	Relaxin	14-17	insulin like growth factor binding protein 1	Homo sapiens	21-65
15155604-2	2004	The effect of RLX on insulin-like growth factor binding protein-1 (IGFBP-1) production was determined to evaluate the biological function of RLX/receptor in human endometrial cells.	Relaxin	14-17	insulin like growth factor binding protein 1	Homo sapiens	67-74
15155604-8	2004	In stromal cells, MPA alone caused a slight increase (2-4-fold) of the production rate of IGFBP-1 whereas MPA plus RLX synergistically increased (>40-fold) the IGFBP-1 production.	Relaxin	115-118	insulin like growth factor binding protein 1	Homo sapiens	163-170
15155604-11	2004	CONCLUSION: The present study showed that in undifferentiated endometrial stromal cells, progestin increases the RLX receptor content to enhance the effect of RLX on the target gene (IGFBP-1).	Relaxin	113-116	insulin like growth factor binding protein 1	Homo sapiens	183-190
15026539-6	2004	This effect of RLX appears to be mediated by activation of NOS II transcription factor NF-kappaB, since it was abolished by the NF-kappaB inhibitors curcumin-95 and dexamethasone.	Relaxin	15-18	nuclear factor kappa B subunit 1	Homo sapiens	87-96
15026539-6	2004	This effect of RLX appears to be mediated by activation of NOS II transcription factor NF-kappaB, since it was abolished by the NF-kappaB inhibitors curcumin-95 and dexamethasone.	Relaxin	15-18	nuclear factor kappa B subunit 1	Homo sapiens	128-137
12522118-2	2003	RLX inhibits the stimulation of endothelin-1, the most potent vasoconstrictor in heart failure.	Relaxin	0-3	endothelin 1	Homo sapiens	32-44
12522118-5	2003	Therefore, we investigated RLX-induced regulation of ET(B) in human umbilical vein endothelial, epithelial (HeLa), and vascular smooth muscle cells.	Relaxin	27-30	endothelin receptor type B	Homo sapiens	53-58
12522118-9	2003	In NF-kappaB-luciferase reporter assays, we demonstrated complete inhibition of RLX-induced NF-kappaB activation in cells transfected with dominant-negative Raf-1, MEK-1, or ERK-1/2 constructs, whereas dominant-negative Ras had no effect.	Relaxin	80-83	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	157-162
12522118-9	2003	In NF-kappaB-luciferase reporter assays, we demonstrated complete inhibition of RLX-induced NF-kappaB activation in cells transfected with dominant-negative Raf-1, MEK-1, or ERK-1/2 constructs, whereas dominant-negative Ras had no effect.	Relaxin	80-83	mitogen-activated protein kinase kinase 1	Homo sapiens	164-169
12522118-9	2003	In NF-kappaB-luciferase reporter assays, we demonstrated complete inhibition of RLX-induced NF-kappaB activation in cells transfected with dominant-negative Raf-1, MEK-1, or ERK-1/2 constructs, whereas dominant-negative Ras had no effect.	Relaxin	80-83	mitogen-activated protein kinase 3	Homo sapiens	174-181
12522118-11	2003	RLX pretreatment augmented the dilator effect of the ET(B) agonist endothelin-3 by 100+/-8% and 133+/-13%.	Relaxin	0-3	endothelin receptor type B	Homo sapiens	53-58
12522118-11	2003	RLX pretreatment augmented the dilator effect of the ET(B) agonist endothelin-3 by 100+/-8% and 133+/-13%.	Relaxin	0-3	endothelin 3	Homo sapiens	67-79
12522118-12	2003	In conclusion, RLX stimulates endothelial and epithelial ET(B) via a Ras-independent Raf-1-MEK-1-ERK-1/2 pathway that activates NF-kappaB.	Relaxin	15-18	endothelin receptor type B	Homo sapiens	57-62
12522118-12	2003	In conclusion, RLX stimulates endothelial and epithelial ET(B) via a Ras-independent Raf-1-MEK-1-ERK-1/2 pathway that activates NF-kappaB.	Relaxin	15-18	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	85-90
12522118-12	2003	In conclusion, RLX stimulates endothelial and epithelial ET(B) via a Ras-independent Raf-1-MEK-1-ERK-1/2 pathway that activates NF-kappaB.	Relaxin	15-18	mitogen-activated protein kinase kinase 1	Homo sapiens	91-96
12522118-12	2003	In conclusion, RLX stimulates endothelial and epithelial ET(B) via a Ras-independent Raf-1-MEK-1-ERK-1/2 pathway that activates NF-kappaB.	Relaxin	15-18	mitogen-activated protein kinase 1	Homo sapiens	97-104
14593002-7	2003	Moreover, a neutralizing antibody specific for MMP-2 completely abrogated the reduced myogenic reactivity of small renal arteries from relaxin-treated nonpregnant and midterm pregnant rats.	Relaxin	135-142	matrix metallopeptidase 2	Rattus norvegicus	47-52
14593002-9	2003	Using gelatin zymography, we showed increased pro and active MMP-2 activity in small renal arteries from relaxin-treated nonpregnant and midterm pregnant rats relative to the control animals.	Relaxin	105-112	matrix metallopeptidase 2	Rattus norvegicus	61-66
12373075-13	2003	In this group, Rlx treatment was accompanied by a decrease in serum creatinine (Veh 1.01 +/- 0.03 vs. Rlx 0.81 +/- 0.05 mg/dl, p = 0.02) and an increase in GFR (Veh 0.90 +/- 0.14 vs. Rlx 1.33 +/- 0.11 ml/min, p = 0.03).	Relaxin	15-18	mitochondrial ribosomal protein L19	Homo sapiens	183-188
12349956-3	2002	RLX reduced dose-dependently the expression of the activation marker CD63, the release of histamine and the rise of intracellular Ca2+ levels which triggers granule release by stimulated basophils.	Relaxin	0-3	CD63 molecule	Homo sapiens	69-73
9275049-2	1997	Although we have evidence of a role for insulin-like growth factor I (IGF-I) in mediating relaxin-induced growth of porcine granulosa cells in vitro, the mechanism of action by which relaxin enhances uterine growth has not been identified.	Relaxin	90-97	insulin like growth factor 1	Sus scrofa	40-68
10021461-7	1999	In contrast, the renal vasoconstrictory response to angiotensin II was attenuated by the RLX treatment.	Relaxin	89-92	angiotensinogen	Rattus norvegicus	52-66
10021461-10	1999	In conclusion, the renal and osmoregulatory effects of chronic RLX administration to conscious rats resemble the physiological changes of pregnancy in several respects: (a) marked increases in ERPF and GFR with a mediatory role for nitric oxide; (b) attenuation of the renal circulatory response to angiotensin II; and (c) reduction in plasma osmolality.	Relaxin	63-66	angiotensinogen	Rattus norvegicus	299-313
9622136-7	1998	RLX stimulated the expression of immunoreactive inducible NO synthase and increased significantly and in a concentration-related fashion inducible NO synthase activity, NO generation, and intracellular cGMP levels.	Relaxin	0-3	nitric oxide synthase 2	Bos taurus	48-69
9622136-7	1998	RLX stimulated the expression of immunoreactive inducible NO synthase and increased significantly and in a concentration-related fashion inducible NO synthase activity, NO generation, and intracellular cGMP levels.	Relaxin	0-3	nitric oxide synthase 2	Bos taurus	137-158
9275049-2	1997	Although we have evidence of a role for insulin-like growth factor I (IGF-I) in mediating relaxin-induced growth of porcine granulosa cells in vitro, the mechanism of action by which relaxin enhances uterine growth has not been identified.	Relaxin	90-97	insulin like growth factor 1	Sus scrofa	70-75
1547722-6	1992	Exposure of luteal cell-containing monolayers to basic FGF resulted in a significant reduction (P less than 0.05) in the rate of RLX-induced plaque formation, evidence of an inhibitory effect of basic FGF on the rate of basal RLX secretion.	Relaxin	129-132	fibroblast growth factor 2	Ovis aries	49-58
8150531-5	1994	The findings obtained show that RLX, when applied at micromolar concentrations, or even at nanomolar concentrations for long exposure times, suppresses proliferation, stimulates differentiation, and enhances expression of the surface molecule E-cadherin.	Relaxin	32-35	cadherin 1	Homo sapiens	243-253
35594150-4	2022	Focused structure-activity relationship studies of the hit compound resulted in RLX-33 (33) that was able to inhibit relaxin-3 activity in a battery of functional assays.	Relaxin	80-83	relaxin 3	Rattus norvegicus	117-126
1708779-10	1991	Cultures in which RLX alone induced high IGFBP-1 high production were obtained from endometrium during the progesterone-dominated luteal phase.	Relaxin	18-21	insulin like growth factor binding protein 1	Homo sapiens	41-48
3008478-8	1986	The addition of Rlx treatment reversed an inhibiting effect of oestrogen alone on both uterine and cervical collagenase and proteoglycanase activities, at the same time as completely obliterating the stimulating effect of oestrogen on uterine and cervical beta-glucuronidase activity.	Relaxin	16-19	glucuronidase, beta	Rattus norvegicus	256-274
7263848-2	1981	In previous experiments we observed that the inhibition of spontaneous uterine contractions produced by decidual RLX was masked or absent if the samples were contaminated with PRL.	Relaxin	113-116	prolactin	Homo sapiens	176-179
33142814-11	2020	In ESCs stimulated with RLX-2, p38 MAPK phosphorylation was significantly suppressed.	Relaxin	24-27	mitogen-activated protein kinase 14	Mus musculus	31-39
33894403-7	2021	Furthermore, NP-RLX ameliorated the chronic AAD-induced AI, pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha), chemokines (CCL2, CCL11) and the pro-fibrotic TGF-beta1/IL-1beta axis on AWR and resulting AHR, as well as human myofibroblast-induced collagen gel contraction, to a similar extent as unconjugated RLX.	Relaxin	16-19	interleukin 1 alpha	Homo sapiens	88-96
33894403-7	2021	Furthermore, NP-RLX ameliorated the chronic AAD-induced AI, pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha), chemokines (CCL2, CCL11) and the pro-fibrotic TGF-beta1/IL-1beta axis on AWR and resulting AHR, as well as human myofibroblast-induced collagen gel contraction, to a similar extent as unconjugated RLX.	Relaxin	16-19	interleukin 6	Homo sapiens	98-102
33894403-7	2021	Furthermore, NP-RLX ameliorated the chronic AAD-induced AI, pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha), chemokines (CCL2, CCL11) and the pro-fibrotic TGF-beta1/IL-1beta axis on AWR and resulting AHR, as well as human myofibroblast-induced collagen gel contraction, to a similar extent as unconjugated RLX.	Relaxin	16-19	tumor necrosis factor	Homo sapiens	104-113
33894403-7	2021	Furthermore, NP-RLX ameliorated the chronic AAD-induced AI, pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha), chemokines (CCL2, CCL11) and the pro-fibrotic TGF-beta1/IL-1beta axis on AWR and resulting AHR, as well as human myofibroblast-induced collagen gel contraction, to a similar extent as unconjugated RLX.	Relaxin	16-19	C-C motif chemokine ligand 2	Homo sapiens	128-132
33894403-7	2021	Furthermore, NP-RLX ameliorated the chronic AAD-induced AI, pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha), chemokines (CCL2, CCL11) and the pro-fibrotic TGF-beta1/IL-1beta axis on AWR and resulting AHR, as well as human myofibroblast-induced collagen gel contraction, to a similar extent as unconjugated RLX.	Relaxin	16-19	C-C motif chemokine ligand 11	Homo sapiens	134-139
33894403-7	2021	Furthermore, NP-RLX ameliorated the chronic AAD-induced AI, pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha), chemokines (CCL2, CCL11) and the pro-fibrotic TGF-beta1/IL-1beta axis on AWR and resulting AHR, as well as human myofibroblast-induced collagen gel contraction, to a similar extent as unconjugated RLX.	Relaxin	16-19	transforming growth factor beta 1	Homo sapiens	162-171
33894403-7	2021	Furthermore, NP-RLX ameliorated the chronic AAD-induced AI, pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha), chemokines (CCL2, CCL11) and the pro-fibrotic TGF-beta1/IL-1beta axis on AWR and resulting AHR, as well as human myofibroblast-induced collagen gel contraction, to a similar extent as unconjugated RLX.	Relaxin	16-19	interleukin 1 alpha	Homo sapiens	172-180
32825567-2	2020	Serelaxin (RLX) designates the pharmaceutical form of the human natural hormone relaxin-2 that has been shown to markedly reduce tissue and cell damage induced by hypoxia and reoxygenation (HR).	Relaxin	11-14	relaxin 2	Homo sapiens	80-89
29046312-8	2018	With both acute and chronic RLX, efferent arteriolar resistance vessels relaxed to a greater extent than afferent arteriolar resistance vessels, thus producing falls in PGC.	Relaxin	28-31	progastricsin	Rattus norvegicus	169-172
32297670-9	2020	These findings demonstrated that RLX can indirectly activate AT2 R-dependent phosphatase activity in HCMFs by signaling through RXFP1-AT2 R crosstalk, which have important therapeutic implications for its anti-fibrotic actions.	Relaxin	33-36	relaxin family peptide receptor 1	Homo sapiens	128-133
32297670-9	2020	These findings demonstrated that RLX can indirectly activate AT2 R-dependent phosphatase activity in HCMFs by signaling through RXFP1-AT2 R crosstalk, which have important therapeutic implications for its anti-fibrotic actions.	Relaxin	33-36	angiotensin II receptor type 2	Homo sapiens	134-139
32297670-9	2020	These findings demonstrated that RLX can indirectly activate AT2 R-dependent phosphatase activity in HCMFs by signaling through RXFP1-AT2 R crosstalk, which have important therapeutic implications for its anti-fibrotic actions.	Relaxin	33-36	angiotensin II receptor type 2	Homo sapiens	61-66
32494202-5	2020	Results: In the first part, the expression of MMP-9 was increased in groups treated by RLX compared with NS group, especially three days after RLX infusion (p=0.001).	Relaxin	87-90	matrix metalloproteinase-9	Oryctolagus cuniculus	46-51
32494202-5	2020	Results: In the first part, the expression of MMP-9 was increased in groups treated by RLX compared with NS group, especially three days after RLX infusion (p=0.001).	Relaxin	143-146	matrix metalloproteinase-9	Oryctolagus cuniculus	46-51
30592984-5	2019	This review summarises known signalling pathways induced by acute versus chronic treatment with relaxin across a range of cell types, it describes RXFP1 crosstalk with other receptors, signalling pathways activated by other ligands targeting RXFP1, and it also outlines physiological relevance of RXFP1 signalling outputs.	Relaxin	96-103	relaxin family peptide receptor 1	Homo sapiens	242-247
30592984-5	2019	This review summarises known signalling pathways induced by acute versus chronic treatment with relaxin across a range of cell types, it describes RXFP1 crosstalk with other receptors, signalling pathways activated by other ligands targeting RXFP1, and it also outlines physiological relevance of RXFP1 signalling outputs.	Relaxin	96-103	relaxin family peptide receptor 1	Homo sapiens	242-247
29180109-2	2018	This study demonstrates the involvement of ADAM10 and PI3K/Akt signaling in mediating RLX-induced Notch-1 activation.	Relaxin	86-89	ADAM metallopeptidase domain 10	Homo sapiens	43-49
29180109-2	2018	This study demonstrates the involvement of ADAM10 and PI3K/Akt signaling in mediating RLX-induced Notch-1 activation.	Relaxin	86-89	AKT serine/threonine kinase 1	Homo sapiens	59-62
26915460-2	2016	This study investigates whether serelaxin (RLX, recombinant human relaxin-2) endowed with promising therapeutic properties in CVD, can be credited of a protective effect against cigarette smoke (CS)-induced vascular damage and dysfunction.	Relaxin	43-46	relaxin 2	Homo sapiens	66-75
28540295-16	2017	However, with preadministration of PI3K/Akt pathway inhibitor LY294002, the effect of RLX was blocked.	Relaxin	86-89	AKT serine/threonine kinase 1	Homo sapiens	40-43
29399073-5	2018	Furthermore, RLX significantly suppressed the formation of reactive oxygen species and malondialdehyde, and enhanced the activity of SOD.	Relaxin	13-16	superoxide dismutase 2	Rattus norvegicus	133-136
29399073-7	2018	However, the Notch inhibitor DAPT almost abolished the protective effects of RLX.	Relaxin	77-80	notch receptor 1	Rattus norvegicus	13-18
29399073-8	2018	These results suggested that RLX protected cardiomyocytes from HG-induced hypertrophy and apoptosis partly through a Notch1-dependent pathway, which may be associated with reducing oxidative stress.	Relaxin	29-32	notch receptor 1	Rattus norvegicus	117-123
28386751-9	2017	RLX restored expression of phosphorylated Akt which found to be decreased in the AA-I only treated cells.	Relaxin	0-3	AKT serine/threonine kinase 1	Homo sapiens	42-45
28386751-10	2017	RLX co-treatment led to a decrease in the Bax/Bcl-2 ratio as well as the cleaved form of caspase-3 compared to the AA-I only treated cells.	Relaxin	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	42-45
28386751-10	2017	RLX co-treatment led to a decrease in the Bax/Bcl-2 ratio as well as the cleaved form of caspase-3 compared to the AA-I only treated cells.	Relaxin	0-3	BCL2 apoptosis regulator	Homo sapiens	46-51
28386751-10	2017	RLX co-treatment led to a decrease in the Bax/Bcl-2 ratio as well as the cleaved form of caspase-3 compared to the AA-I only treated cells.	Relaxin	0-3	caspase 3	Homo sapiens	89-98
28386751-11	2017	This anti-apoptotic effect of RLX was attenuated by co-administration of the Akt inhibitor LY294002.	Relaxin	30-33	AKT serine/threonine kinase 1	Homo sapiens	77-80
27629886-9	2016	Total circulating nitrate-nitrite improved and placental PPET-1 and TNF-alpha were significantly decreased with the higher dose of RLX.	Relaxin	131-134	endothelin 1	Rattus norvegicus	57-63
27629886-9	2016	Total circulating nitrate-nitrite improved and placental PPET-1 and TNF-alpha were significantly decreased with the higher dose of RLX.	Relaxin	131-134	tumor necrosis factor	Rattus norvegicus	68-77
27629886-10	2016	Renal cortex PPET-1 was reduced with both doses of RLX.	Relaxin	51-54	endothelin 1	Rattus norvegicus	13-19
27048661-9	2016	In fact, treatment of CS-exposed animals with RLX reduced the inflammatory recruitment of leukocytes, accompanied by a significant reduction of the release of proinflammatory cytokines (tumor necrosis factor alpha and interleukin-1beta).	Relaxin	46-49	tumor necrosis factor	Homo sapiens	186-213
27048661-9	2016	In fact, treatment of CS-exposed animals with RLX reduced the inflammatory recruitment of leukocytes, accompanied by a significant reduction of the release of proinflammatory cytokines (tumor necrosis factor alpha and interleukin-1beta).	Relaxin	46-49	interleukin 1 beta	Homo sapiens	218-235
26769058-9	2016	Expression of lysyl oxidase homolog 2, which contributes to collagen cross-linking and is up-regulated by TAA treatment, was significantly decreased by week 3 in the TAA + RLX group.	Relaxin	172-175	lysyl oxidase-like 2	Rattus norvegicus	14-37
27065874-5	2016	At the highest concentration tested, both RLX and DEA/NO promoted MMP-2 and MMP-9 levels by 25-33%, while inhibiting pSmad2 and alpha-SMA expression by up to 50% (all p < 0.05 vs. untreated and vehicle-treated cells).	Relaxin	42-45	matrix metallopeptidase 2	Homo sapiens	66-71
27065874-5	2016	At the highest concentration tested, both RLX and DEA/NO promoted MMP-2 and MMP-9 levels by 25-33%, while inhibiting pSmad2 and alpha-SMA expression by up to 50% (all p < 0.05 vs. untreated and vehicle-treated cells).	Relaxin	42-45	matrix metallopeptidase 9	Homo sapiens	76-81
27065874-8	2016	CONCLUSION: These findings confirmed that RLX mediates its TGF-beta1-inhibitory and gelatinase-promoting effects via a NO-sGC-cGMP-dependent pathway, which was additively augmented by co-administration of DEA/NO.	Relaxin	42-45	transforming growth factor beta 1	Homo sapiens	59-68
25303828-0	2014	Cell specific apoptosis by RLX is mediated by NFkappaB in human colon carcinoma HCT-116 cells.	Relaxin	27-30	nuclear factor kappa B subunit 1	Homo sapiens	46-54
26316699-5	2015	Transforming growth factor beta (TGF-beta) was used to induce EndMT in human umbilical vein endothelial cells, which were pretreated with RLX, 200 ng mL(-1), then with the inhibitor of Notch.	Relaxin	138-141	transforming growth factor beta 1	Homo sapiens	0-31
26316699-5	2015	Transforming growth factor beta (TGF-beta) was used to induce EndMT in human umbilical vein endothelial cells, which were pretreated with RLX, 200 ng mL(-1), then with the inhibitor of Notch.	Relaxin	138-141	transforming growth factor beta 1	Homo sapiens	33-41
26316699-10	2015	In vitro, RLX decreased the mobility of human umbilical vein endothelial cells induced by TGF-beta, increased the expression of endothelial CD31, and decreased vimentin content.	Relaxin	10-13	transforming growth factor beta 1	Homo sapiens	90-98
26316699-10	2015	In vitro, RLX decreased the mobility of human umbilical vein endothelial cells induced by TGF-beta, increased the expression of endothelial CD31, and decreased vimentin content.	Relaxin	10-13	platelet and endothelial cell adhesion molecule 1	Homo sapiens	140-144
26316699-10	2015	In vitro, RLX decreased the mobility of human umbilical vein endothelial cells induced by TGF-beta, increased the expression of endothelial CD31, and decreased vimentin content.	Relaxin	10-13	vimentin	Homo sapiens	160-168
25415609-5	2015	According to the literature, RLX promoted MMP-2 and MMP-9 expression/release.	Relaxin	29-32	matrix metallopeptidase 2	Homo sapiens	42-47
25415609-5	2015	According to the literature, RLX promoted MMP-2 and MMP-9 expression/release.	Relaxin	29-32	matrix metallopeptidase 9	Homo sapiens	52-57
26400184-4	2015	Low-dose intracarotid artery infusion of RLX (155 pmol ml(-1) h(-1); 1.5 h) had minor transient effects on AP and activated neurons [increased Fos-immunoreactivity (IR)] in the SFO and in spinally projecting (19 +- 2%) and arginine-vasopressin (AVP)-IR (21 +- 5%) cells in the paraventricular nucleus of the hypothalamus of NP, but not pregnant (P), rats.	Relaxin	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
25786395-12	2015	Here, we have shown, for the first time, that RLX (100 ng ml(-1) ) significantly reduced both voltage- and Ca(2+) -dependent delayed-rectifier and inward-rectifying K(+) currents that are typically increased in myofibroblasts compared with proto-myofibroblasts, suggesting that this hormone can antagonize the biophysical effects of transforming growth factor-beta1 in inducing myofibroblast differentiation.	Relaxin	46-49	transforming growth factor beta 1	Homo sapiens	333-365
25403022-13	2014	Overexpression of Bax, interleukin-6 and tumor necrosis factor-alpha observed in the kidneys of the CDDP group was reduced in the CDDP+RLX group.	Relaxin	135-138	BCL2 associated X, apoptosis regulator	Rattus norvegicus	18-21
25403022-13	2014	Overexpression of Bax, interleukin-6 and tumor necrosis factor-alpha observed in the kidneys of the CDDP group was reduced in the CDDP+RLX group.	Relaxin	135-138	interleukin 6	Rattus norvegicus	23-68
23343143-7	2013	Increased MMP-2 levels in RLX-treated rats demonstrated that the hormone was administered and active in this model.	Relaxin	26-29	matrix metallopeptidase 2	Rattus norvegicus	10-15
23973652-6	2013	Our data suggest that RLX may inhibit TGF-beta1-mediated fibrosis during the process of silicosis, providing evidence for the protective effect of RLX on silica-induced pulmonary fibrosis.	Relaxin	22-25	transforming growth factor beta 1	Homo sapiens	38-47
23946288-12	2013	Overexpression of caspase-3 observed in the IR kidneys was reduced in the IR-RLX group.	Relaxin	77-80	caspase 3	Rattus norvegicus	18-27
23043266-11	2012	CONCLUSIONS: The decreased cellular expression of RLX-2 receptor RXFP1 in scleroderma skin might represent a pro-fibrotic factor and contribute to the substantial inefficacy of RLX treatment in SSc, as reported in the literature.	Relaxin	50-53	relaxin family peptide receptor 1	Homo sapiens	65-70
23748429-9	2013	Independent of antifibrotic actions, RLX (0.1 micromol/L) increased Na+ current density, INa ( 2-fold in 48 hours) in human cardiomyocytes derived from inducible pluripotent stem cells (n=18/18; P<0.01).	Relaxin	37-40	internexin neuronal intermediate filament protein alpha	Homo sapiens	89-92
23543443-3	2013	RLX was also found to enhance in-vitro invasiveness of breast cancer cell lines by induction of matrix metalloproteinases (MMPs) expression.	Relaxin	0-3	matrix metallopeptidase 2	Homo sapiens	123-127
23207895-8	2012	V cells treated with RLX displayed a similar response to that observed in P cells, suggesting that RLX can modulate the reactivity of the MCs to Ang II.	Relaxin	21-24	angiotensinogen	Rattus norvegicus	145-151
22086971-5	2012	RESULTS: The short-term RLX treatment significantly attenuated the high-salt diet-induced rise in BP in DS rats with increasing neuronal NOS and endothelial NOS protein in kidneys.	Relaxin	24-27	nitric oxide synthase 3	Rattus norvegicus	145-160
22086971-7	2012	The long-term treatment of DS rats with RLX for 6 weeks significantly reduced systolic BP, lessened glomerular and tubulointerstitial changes and reduced TGF-beta signaling compared to saline-treated controls.	Relaxin	40-43	transforming growth factor, beta 1	Rattus norvegicus	154-162
23207895-8	2012	V cells treated with RLX displayed a similar response to that observed in P cells, suggesting that RLX can modulate the reactivity of the MCs to Ang II.	Relaxin	99-102	angiotensinogen	Rattus norvegicus	145-151
23207895-10	2012	CONCLUSION: Results suggest that RLX is a mediator of the refractoriness of the MCs to Ang II during pregnancy.	Relaxin	33-36	angiotensinogen	Rattus norvegicus	87-93
22092841-9	2011	CD31-positive vessels and VEGF protein expression were significantly greater in the RLX group.	Relaxin	84-87	platelet and endothelial cell adhesion molecule 1	Rattus norvegicus	0-4
22092841-9	2011	CD31-positive vessels and VEGF protein expression were significantly greater in the RLX group.	Relaxin	84-87	vascular endothelial growth factor A	Rattus norvegicus	26-30
22092841-10	2011	Thus, administration of RLX-expressing adenovirus into elevated skin flaps increased VEGF expression, the number of capillaries, and blood flow to the flap, thereby improving skin flap survival.	Relaxin	24-27	vascular endothelial growth factor A	Rattus norvegicus	85-89
21317299-8	2011	Supplemental RLX increased (P<0.05) uterine ESR1 protein and mRNA in nursed gilts, as well as VEGFA protein in nursed and VEGFA mRNA in both nursed and replacer-fed gilts.	Relaxin	13-16	estrogen receptor 1	Homo sapiens	47-51