PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
28245754-2	2017	N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is an active peptide fragment of Tbeta4.	goralatide	39-45	thymosin beta 4, X-linked	Rattus norvegicus	80-86
28075040-3	2018	N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), an endogenous tetrapeptide that is degraded by ACE, has also been shown to ameliorate the pro-fibrotic phenotype displayed in CKD in our recent study.	goralatide	39-46	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	96-99
26403559-2	2015	More recently, the tetrapetide N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP) has emerged as a potent antifibrotic agent and negative regulator of haematopoietic stem cell differentiation which is processed exclusively by ACE.	goralatide	31-55	angiotensin I converting enzyme	Homo sapiens	210-213
29411767-4	2017	In addition, the plasma level of the tetrapeptide N-acetyl-Ser-Asp-Lys-Pro was used as a marker for ACE inhibition.	goralatide	50-74	angiotensin I converting enzyme	Homo sapiens	100-103
26656271-0	2015	The Effects of Angiotensin Converting Enzyme Inhibitors (ACE-I) on Human N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) Levels: A Systematic Review and Meta-Analysis.	goralatide	112-119	angiotensin I converting enzyme	Homo sapiens	57-60
26098610-1	2015	UNLABELLED: Thymosin beta4 (Tbeta4) and its amino-terminal fragment comprising N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) have been reported to act as anti-inflammatory and anti-fibrotic agents in vitro and in vivo.	goralatide	118-125	thymosin, beta 4, X chromosome	Mus musculus	12-26
26350537-1	2015	N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a ubiquitous molecule generated in all mammalian tissues from the N-terminal sequence of thymosin beta4 (Tbeta4) by the action of propyl oligopeptidase.	goralatide	39-46	thymosin beta 4 X-linked	Homo sapiens	140-154
26350537-1	2015	N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a ubiquitous molecule generated in all mammalian tissues from the N-terminal sequence of thymosin beta4 (Tbeta4) by the action of propyl oligopeptidase.	goralatide	39-46	thymosin beta 4 X-linked	Homo sapiens	156-162
26098610-1	2015	UNLABELLED: Thymosin beta4 (Tbeta4) and its amino-terminal fragment comprising N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) have been reported to act as anti-inflammatory and anti-fibrotic agents in vitro and in vivo.	goralatide	118-125	thymosin, beta 4, X chromosome	Mus musculus	28-34
24244481-1	2013	The natural tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (AcSDKP) is generated from the N-terminus of thymosin-beta4 through enzymatic cleavage by prolyl oligopeptidase (POP).	goralatide	25-49	thymosin beta 4 X-linked	Homo sapiens	95-109
26508815-3	2015	Seven days after UUO, there were significant reductions in the expression of both collagen 1 and collagen 3 in kidneys treated with Ac-SDKP or Captopril, and there was a trend towards reductions in collagen IV, alpha-SMA, and MCP-1 versus control.	goralatide	132-139	mast cell protease 1	Mus musculus	226-231
24244481-1	2013	The natural tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (AcSDKP) is generated from the N-terminus of thymosin-beta4 through enzymatic cleavage by prolyl oligopeptidase (POP).	goralatide	25-49	prolyl endopeptidase	Homo sapiens	140-161
24244481-1	2013	The natural tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (AcSDKP) is generated from the N-terminus of thymosin-beta4 through enzymatic cleavage by prolyl oligopeptidase (POP).	goralatide	25-49	prolyl endopeptidase	Homo sapiens	163-166
23327833-2	2013	N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a physiological tetrapeptide hydrolyzed by the angiotensin-converting enzyme (ACE), has antifibrotic effects in the cardiovascular system and in the kidney in experimental models of hypertension, heart failure and renal disease.	goralatide	39-46	angiotensin I converting enzyme	Rattus norvegicus	96-125
23652767-0	2013	N-acetyl-Ser-Asp-Lys-Pro inhibits interleukin-1beta-mediated matrix metalloproteinase activation in cardiac fibroblasts.	goralatide	0-24	interleukin 1 beta	Rattus norvegicus	34-51
23351021-0	2013	Antifibrotic peptide N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP): opportunities for angiotensin-converting enzyme inhibitor design.	goralatide	21-45	angiotensin I converting enzyme	Homo sapiens	75-104
23351021-2	2013	Angiotensin-converting enzyme (ACE), a key protease in the RAS, has a range of substrates, including N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP).	goralatide	101-125	angiotensin I converting enzyme	Homo sapiens	0-29
23351021-2	2013	Angiotensin-converting enzyme (ACE), a key protease in the RAS, has a range of substrates, including N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP).	goralatide	101-125	angiotensin I converting enzyme	Homo sapiens	31-34
23327833-2	2013	N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a physiological tetrapeptide hydrolyzed by the angiotensin-converting enzyme (ACE), has antifibrotic effects in the cardiovascular system and in the kidney in experimental models of hypertension, heart failure and renal disease.	goralatide	39-46	angiotensin I converting enzyme	Rattus norvegicus	127-130
17868792-7	2007	Although similar intensity of RAS blockade can be achieved by either combination therapy or by using high doses of an AT1-receptor antagonist given alone, the ACE inhibitor present in the combination interferes with the bradykinin-nitric oxide pathway and the N-acetyl-Ser-Asp-Lys-Pro metabolism, which both may have additional biological effects.	goralatide	260-284	angiotensin I converting enzyme	Homo sapiens	159-162
22214449-5	2012	ACE is primarily known for its ability to cleave angiotensin-I to the vasoactive octapeptide angiotensin-II, but is also able to cleave a number of other substrates including the vasodilator bradykinin and N-acetyl-seryl-aspartyl-lysyl-proline (acetyl-SDKP), a physiological modulator of hematopoiesis.	goralatide	245-256	angiotensin I converting enzyme	Homo sapiens	0-3
23056909-3	2012	ACE is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angiotensin II (Ang II), but is also able to cleave a number of other substrates including the vasodilator bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a physiological modulator of hematopoiesis.	goralatide	223-247	angiotensin I converting enzyme	Homo sapiens	0-3
23056909-3	2012	ACE is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angiotensin II (Ang II), but is also able to cleave a number of other substrates including the vasodilator bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a physiological modulator of hematopoiesis.	goralatide	223-247	angiotensinogen	Homo sapiens	49-62
23056909-3	2012	ACE is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angiotensin II (Ang II), but is also able to cleave a number of other substrates including the vasodilator bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a physiological modulator of hematopoiesis.	goralatide	223-247	angiotensinogen	Homo sapiens	64-69
23056909-3	2012	ACE is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angiotensin II (Ang II), but is also able to cleave a number of other substrates including the vasodilator bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a physiological modulator of hematopoiesis.	goralatide	223-247	angiotensinogen	Homo sapiens	101-115
23056909-3	2012	ACE is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angiotensin II (Ang II), but is also able to cleave a number of other substrates including the vasodilator bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a physiological modulator of hematopoiesis.	goralatide	223-247	angiotensinogen	Homo sapiens	117-123
23056909-3	2012	ACE is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angiotensin II (Ang II), but is also able to cleave a number of other substrates including the vasodilator bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a physiological modulator of hematopoiesis.	goralatide	249-256	angiotensin I converting enzyme	Homo sapiens	0-3
23056909-3	2012	ACE is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angiotensin II (Ang II), but is also able to cleave a number of other substrates including the vasodilator bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a physiological modulator of hematopoiesis.	goralatide	249-256	angiotensinogen	Homo sapiens	49-62
23056909-3	2012	ACE is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angiotensin II (Ang II), but is also able to cleave a number of other substrates including the vasodilator bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a physiological modulator of hematopoiesis.	goralatide	249-256	angiotensinogen	Homo sapiens	64-69
23056909-3	2012	ACE is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angiotensin II (Ang II), but is also able to cleave a number of other substrates including the vasodilator bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a physiological modulator of hematopoiesis.	goralatide	249-256	angiotensinogen	Homo sapiens	101-115
23056909-3	2012	ACE is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angiotensin II (Ang II), but is also able to cleave a number of other substrates including the vasodilator bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a physiological modulator of hematopoiesis.	goralatide	249-256	angiotensinogen	Homo sapiens	117-123
21133893-1	2011	BACKGROUND AND PURPOSE A serine protease, prolyl oligopeptidase (POP) has been reported to be involved in the release of the pro-angiogenic tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (Ac-SDKP) from its precursor, 43-mer thymosin beta4 (Tbeta4).	goralatide	153-177	prolyl endopeptidase	Homo sapiens	42-63
21133893-1	2011	BACKGROUND AND PURPOSE A serine protease, prolyl oligopeptidase (POP) has been reported to be involved in the release of the pro-angiogenic tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (Ac-SDKP) from its precursor, 43-mer thymosin beta4 (Tbeta4).	goralatide	153-177	prolyl endopeptidase	Homo sapiens	65-68
21133893-1	2011	BACKGROUND AND PURPOSE A serine protease, prolyl oligopeptidase (POP) has been reported to be involved in the release of the pro-angiogenic tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (Ac-SDKP) from its precursor, 43-mer thymosin beta4 (Tbeta4).	goralatide	153-177	thymosin beta 4 X-linked	Homo sapiens	215-229
21133893-1	2011	BACKGROUND AND PURPOSE A serine protease, prolyl oligopeptidase (POP) has been reported to be involved in the release of the pro-angiogenic tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (Ac-SDKP) from its precursor, 43-mer thymosin beta4 (Tbeta4).	goralatide	153-177	thymosin beta 4 X-linked	Homo sapiens	231-237
21052020-12	2011	CONCLUSION: We concluded that Ac-SDKP prevents hypertension-induced inflammatory cell infiltration, collagen deposition, nephrin downregulation and albuminuria, which could lead to renoprotection in hypertensive mice.	goralatide	30-37	nephrosis 1, nephrin	Mus musculus	121-128
18178715-3	2008	N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a tetrapeptide specifically degraded by angiotensin converting enzyme (ACE), reduces inflammation, fibrosis, and TOD induced by HBP.	goralatide	0-24	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	76-105
18178715-3	2008	N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a tetrapeptide specifically degraded by angiotensin converting enzyme (ACE), reduces inflammation, fibrosis, and TOD induced by HBP.	goralatide	0-24	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	107-110
22968858-1	2012	N-Acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) inhibits endothelin-1 (ET-1)-induced activation of p44/42 mitogen-activated protein kinase (p44/42 MAPK) and collagen production in cultured rat cardiac fibroblasts (RCFs).	goralatide	39-46	endothelin 1	Rattus norvegicus	57-69
22968858-1	2012	N-Acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) inhibits endothelin-1 (ET-1)-induced activation of p44/42 mitogen-activated protein kinase (p44/42 MAPK) and collagen production in cultured rat cardiac fibroblasts (RCFs).	goralatide	39-46	endothelin 1	Rattus norvegicus	71-75
22968858-1	2012	N-Acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) inhibits endothelin-1 (ET-1)-induced activation of p44/42 mitogen-activated protein kinase (p44/42 MAPK) and collagen production in cultured rat cardiac fibroblasts (RCFs).	goralatide	39-46	mitogen activated protein kinase 3	Rattus norvegicus	99-102
22968858-1	2012	N-Acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) inhibits endothelin-1 (ET-1)-induced activation of p44/42 mitogen-activated protein kinase (p44/42 MAPK) and collagen production in cultured rat cardiac fibroblasts (RCFs).	goralatide	39-46	mitogen activated protein kinase 3	Rattus norvegicus	140-151
20536450-0	2010	Overexpression of the natural tetrapeptide acetyl-N-ser-asp-lys-pro derived from thymosin beta4 in neoplastic diseases.	goralatide	43-67	thymosin beta 4 X-linked	Homo sapiens	81-95
17083265-0	2006	Therapeutic potential of thymosin-beta4 and its derivative N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) in cardiac healing after infarction.	goralatide	98-105	thymosin beta 4, X-linked	Rattus norvegicus	25-39
16732017-0	2006	Assessment of patients" and physicians" compliance to an ACE inhibitor treatment based on urinary N-acetyl Ser-Asp-Lys-Pro determination in the Noninsulin-Dependent Diabetes, Hypertension, Microalbuminuria, Proteinuria, Cardiovascular Events, and Ramipril (DIABHYCAR) study.	goralatide	98-122	angiotensin I converting enzyme	Homo sapiens	57-60
17083265-2	2006	This article compiles and analyzes the available experimental data regarding the potential therapeutic effects of thymosin-beta4 and its derivative N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) in cardiac healing after myocardial infarction (MI) as well as discussing the possible mechanisms involved.	goralatide	187-194	thymosin beta 4, X-linked	Rattus norvegicus	114-128
15037553-1	2004	N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a ubiquitous tetrapeptide hydrolyzed almost exclusively by angiotensin-converting enzyme (ACE).	goralatide	39-46	angiotensin I converting enzyme	Rattus norvegicus	110-139
16413241-4	2006	The in vivo inhibition of ACE and NEP was monitored by measuring the urinary excretion of N-acetyl-Ser-Asp-Lys-Pro (AcSDKP) and atrial natriuretic peptide (ANP), respectively.	goralatide	90-114	angiotensin I converting enzyme	Homo sapiens	26-29
16413241-4	2006	The in vivo inhibition of ACE and NEP was monitored by measuring the urinary excretion of N-acetyl-Ser-Asp-Lys-Pro (AcSDKP) and atrial natriuretic peptide (ANP), respectively.	goralatide	90-114	membrane metalloendopeptidase	Homo sapiens	34-37
16216963-3	2005	Here, we report a novel mechanism that may explain the cardiac antifibrotic effect of ACE inhibition, involving blockade of the hydrolysis of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP).	goralatide	181-188	angiotensin I converting enzyme	Rattus norvegicus	86-89
15520311-5	2004	To explain these changes, we investigated N-acetyl-Ser-Asp-Lys-Pro (AcSDKP), an alternative substrate that is catabolized exclusively by ACE.	goralatide	42-66	angiotensin I converting enzyme	Rattus norvegicus	137-140
15105290-1	2004	Angiotensin I-converting enzyme (ACE) inhibitors can affect hematopoiesis by several mechanisms including inhibition of angiotensin II formation and increasing plasma concentrations of AcSDKP (acetyl-N-Ser-Asp-Lys-Pro), an ACE substrate and a negative regulator of hematopoiesis.	goralatide	193-217	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	0-31
15105290-1	2004	Angiotensin I-converting enzyme (ACE) inhibitors can affect hematopoiesis by several mechanisms including inhibition of angiotensin II formation and increasing plasma concentrations of AcSDKP (acetyl-N-Ser-Asp-Lys-Pro), an ACE substrate and a negative regulator of hematopoiesis.	goralatide	193-217	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	33-36
15037553-1	2004	N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a ubiquitous tetrapeptide hydrolyzed almost exclusively by angiotensin-converting enzyme (ACE).	goralatide	39-46	angiotensin I converting enzyme	Rattus norvegicus	141-144
14581293-1	2003	N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a natural substrate for the N-terminal active site of angiotensin-converting enzyme (ACE).	goralatide	39-46	angiotensin I converting enzyme	Rattus norvegicus	105-134
15194348-6	2004	We have previously described the presence of N-domain ACE in urine of Wistar (W), Wistar Kyoto (WKY), and spontaneously hypertensive rats (SHR), all of which can hydrolyze the vasodilator peptide Angiotensin 1-7 and also the N-Acetyl-Ser-Asp-Lys-Pro, two peptides described as specific for N-domain ACE.	goralatide	225-249	angiotensin I converting enzyme	Rattus norvegicus	54-57
14581293-1	2003	N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a natural substrate for the N-terminal active site of angiotensin-converting enzyme (ACE).	goralatide	39-46	angiotensin I converting enzyme	Rattus norvegicus	136-139
12093364-2	2002	Mammalian ACE is responsible for the synthesis of angiotensin II and the inactivation of bradykinin and N -acetyl-Ser-Asp-Lys-Pro, but the absence of similar peptide hormones in insects suggests novel functions for Ance.	goralatide	104-129	angiotensin I converting enzyme	Homo sapiens	10-13
10856278-8	2000	The peptides angiotensin-(1-7) and N-acetyl-Ser-Asp-Lys-Pro, described as specific for N-domain ACE, were hydrolyzed by P2 and TP2, which suggests that both enzymes are N-domain ACE.	goralatide	35-59	angiotensin I converting enzyme	Homo sapiens	96-99
12154106-0	2002	N-acetyl-Ser-Asp-Lys-Pro inhibits phosphorylation of Smad2 in cardiac fibroblasts.	goralatide	0-24	SMAD family member 2	Rattus norvegicus	53-58
12154106-1	2002	N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy.	goralatide	0-24	angiotensin I converting enzyme	Rattus norvegicus	85-88
12154106-1	2002	N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy.	goralatide	0-24	angiotensin I converting enzyme	Rattus norvegicus	117-120
11167134-4	2001	Both enzymes have a K(i) of the order of 10(-7) M for the specific inhibitors studied, and are able to hydrolyze luteinizing hormone-releasing hormone and N-acetyl-Ser-Asp-Lys-Pro as described for N-domain ACE.	goralatide	155-179	angiotensin I converting enzyme	Homo sapiens	206-209
10856278-8	2000	The peptides angiotensin-(1-7) and N-acetyl-Ser-Asp-Lys-Pro, described as specific for N-domain ACE, were hydrolyzed by P2 and TP2, which suggests that both enzymes are N-domain ACE.	goralatide	35-59	transition protein 2	Homo sapiens	127-130
10856278-8	2000	The peptides angiotensin-(1-7) and N-acetyl-Ser-Asp-Lys-Pro, described as specific for N-domain ACE, were hydrolyzed by P2 and TP2, which suggests that both enzymes are N-domain ACE.	goralatide	35-59	angiotensin I converting enzyme	Homo sapiens	178-181
10195570-0	1999	In vitro effect of acetyl-N-Ser-Asp-Lys-Pro (AcSDKP) analogs resistant to angiotensin I-converting enzyme on hematopoietic stem cell and progenitor cell proliferation.	goralatide	19-43	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	74-105
10805521-1	2000	N-Acetyl-Ser-Asp-Lys-Pro-OH (AcSDKP-OH), a negative regulator of hematopoietic stem cell proliferation, is shown to be a physiological substrate of angiotensin I-converting enzyme (ACE), a zinc-dipeptidyl carboxypeptidase, involved in cardiovascular homeostasis.	goralatide	0-27	angiotensin I converting enzyme	Homo sapiens	148-179
10805521-1	2000	N-Acetyl-Ser-Asp-Lys-Pro-OH (AcSDKP-OH), a negative regulator of hematopoietic stem cell proliferation, is shown to be a physiological substrate of angiotensin I-converting enzyme (ACE), a zinc-dipeptidyl carboxypeptidase, involved in cardiovascular homeostasis.	goralatide	0-27	angiotensin I converting enzyme	Homo sapiens	181-184
7739760-2	1995	It was previously shown that the N-fragment (1-4) of thymosin beta 4 (Ac-Ser-Asp-Lys-Pro-OH) inhibits in vivo the entry of cell populations into S-phase.	goralatide	70-91	thymosin beta 4 X-linked	Homo sapiens	53-68
7876104-0	1995	The hemoregulatory peptide N-acetyl-Ser-Asp-Lys-Pro is a natural and specific substrate of the N-terminal active site of human angiotensin-converting enzyme.	goralatide	27-51	angiotensin I converting enzyme	Homo sapiens	127-156
9533760-0	1998	Goralatide (AcSDKP), a negative growth regulator, protects the stem cell compartment during chemotherapy, enhancing the myelopoietic response to GM-CSF.	goralatide	0-10	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	145-151
9533760-1	1998	The aim of our study was to investigate the protection afforded to the bone marrow by Goralatide (AcSDKP), an inhibitor of hemopoietic stem cell proliferation, when administered alone or in combination with a growth factor (granulocyte/macrophage colony-stimulating factor [GM-CSF]) during iterative cycles of Ara-C (cytarabine) treatment.	goralatide	86-96	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	274-281
9533760-5	1998	When the cycles of chemotherapy plus Goralatide were followed by GM-CSF, the recovery from leukopenic nadirs was accelerated and the white blood cells and granulocyte levels were markedly increased over those observed in control mice and in mice treated either with Goralatide alone or with GM-CSF alone.	goralatide	37-47	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	65-71
9533760-5	1998	When the cycles of chemotherapy plus Goralatide were followed by GM-CSF, the recovery from leukopenic nadirs was accelerated and the white blood cells and granulocyte levels were markedly increased over those observed in control mice and in mice treated either with Goralatide alone or with GM-CSF alone.	goralatide	37-47	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	291-297
9533760-5	1998	When the cycles of chemotherapy plus Goralatide were followed by GM-CSF, the recovery from leukopenic nadirs was accelerated and the white blood cells and granulocyte levels were markedly increased over those observed in control mice and in mice treated either with Goralatide alone or with GM-CSF alone.	goralatide	266-276	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	65-71
9533760-7	1998	A consistent and significant increase (p < 0.001) in platelet count was also noted in animals given Goralatide in conjunction with Ara-C or Ara-C + GM-CSF.	goralatide	103-113	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	151-157
34347311-1	2021	N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a physiological antifibrotic peptide that is hydrolysed by angiotensin I-converting enzyme (ACE).	goralatide	39-46	angiotensin I converting enzyme	Homo sapiens	110-141
7694679-0	1993	Direct and reversible inhibitory effect of the tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (Seraspenide) on the growth of human CD34+ subpopulations in response to growth factors.	goralatide	60-84	CD34 molecule	Homo sapiens	122-126
7694679-0	1993	Direct and reversible inhibitory effect of the tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (Seraspenide) on the growth of human CD34+ subpopulations in response to growth factors.	goralatide	86-97	CD34 molecule	Homo sapiens	122-126
34921949-0	2022	N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) mitigates the liver fibrosis via WTAP/m6A/Ptch1 axis through Hedgehog pathway.	goralatide	39-45	WT1 associated protein	Rattus norvegicus	80-84
34921949-0	2022	N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) mitigates the liver fibrosis via WTAP/m6A/Ptch1 axis through Hedgehog pathway.	goralatide	39-45	patched 1	Rattus norvegicus	89-94
34347311-1	2021	N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a physiological antifibrotic peptide that is hydrolysed by angiotensin I-converting enzyme (ACE).	goralatide	39-46	angiotensin I converting enzyme	Homo sapiens	143-146
34347311-5	2021	Ac-SDKP-derived analogues that are resistant to ACE degradation may provide a new avenue for fibrosis therapy.	goralatide	0-7	angiotensin I converting enzyme	Homo sapiens	48-51
33007385-7	2020	N-Acetyl-Seryl-Asparyl-Lysyl-Proline (Ac-SDKP), an anti-fibrotic peptide, ameliorated the silica-exposure-induced pathological changes by targeting the RAS system by activating the protective ACE2-Ang-(1-7)-Mas axis and inhibiting the deleterious ACE-Ang II-AT1 axis, thereby exerting a protective effect.	goralatide	38-45	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	192-196
34608942-4	2021	The angiotensin-converting enzyme (ACE) NH2-terminal promotes hematopoiesis by inhibiting the anti-hematopoietic effect of Ac-SDKP.	goralatide	123-130	angiotensin I converting enzyme	Rattus norvegicus	4-33
34608942-4	2021	The angiotensin-converting enzyme (ACE) NH2-terminal promotes hematopoiesis by inhibiting the anti-hematopoietic effect of Ac-SDKP.	goralatide	123-130	angiotensin I converting enzyme	Rattus norvegicus	35-38
34508023-0	2022	Urine N-acetyl-Ser-Asp-Lys-Pro measurement as a versatile biomarker to assess adherence to angiotensin-converting enzyme inhibitors.	goralatide	6-30	angiotensin I converting enzyme	Homo sapiens	91-120
33781839-7	2021	In addition, studies suggest that ACE might mediate at least part of its effect through mechanisms that are independent of the Ang I conversion into Ang II and involve other substrates such as N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP), Ang-(1-7), and bradykinin, among others.	goralatide	232-238	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	34-37
33007385-7	2020	N-Acetyl-Seryl-Asparyl-Lysyl-Proline (Ac-SDKP), an anti-fibrotic peptide, ameliorated the silica-exposure-induced pathological changes by targeting the RAS system by activating the protective ACE2-Ang-(1-7)-Mas axis and inhibiting the deleterious ACE-Ang II-AT1 axis, thereby exerting a protective effect.	goralatide	38-45	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	192-195
33007385-7	2020	N-Acetyl-Seryl-Asparyl-Lysyl-Proline (Ac-SDKP), an anti-fibrotic peptide, ameliorated the silica-exposure-induced pathological changes by targeting the RAS system by activating the protective ACE2-Ang-(1-7)-Mas axis and inhibiting the deleterious ACE-Ang II-AT1 axis, thereby exerting a protective effect.	goralatide	38-45	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	251-257
31877411-2	2020	The present study aimed to determine whether meprin alpha, a master regulator of anti-fibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), is diminished by miR-155-5p in silicotic and control lung macrophages and fibroblasts upon activation.	goralatide	142-149	meprin 1 alpha	Mus musculus	45-57
31877411-2	2020	The present study aimed to determine whether meprin alpha, a master regulator of anti-fibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), is diminished by miR-155-5p in silicotic and control lung macrophages and fibroblasts upon activation.	goralatide	142-149	microRNA 155	Mus musculus	169-176
31589901-8	2020	Our results displayed that Ac-SDKP down regulates caspase-12 and CHOP expression in the hippocampus-resident oligodendrocytes of EAE mice.	goralatide	27-34	caspase 12	Mus musculus	50-60
31940798-2	2020	At the same time, ACE hydrolyzes other substrates such as the vasodilator peptide bradykinin and the anti-inflammatory peptide N-acetyl-SDKP.	goralatide	127-140	angiotensin I converting enzyme	Homo sapiens	18-21
31589901-8	2020	Our results displayed that Ac-SDKP down regulates caspase-12 and CHOP expression in the hippocampus-resident oligodendrocytes of EAE mice.	goralatide	27-34	DNA-damage inducible transcript 3	Mus musculus	65-69
31589901-9	2020	Further, treatment with Ac-SDKP decreased oxidative stress markers and caspase-3 activation in the hippocampus of EAE mice.	goralatide	24-31	caspase 3	Mus musculus	71-80
31889494-1	2020	The two-domain dipeptidylcarboxypeptidase Angiotensin-I-converting enzyme (EC 3.4.15.1; ACE) plays an important physiological role in blood pressure regulation via the renin-angiotensin and kallikrein-kinin systems by converting angiotensin I to the potent vasoconstrictor angiotensin II, and by cleaving a number of other substrates including the vasodilator bradykinin and the anti-inflammatory peptide N-acetyl-SDKP.	goralatide	405-418	angiotensin I converting enzyme	Homo sapiens	88-91
31889494-1	2020	The two-domain dipeptidylcarboxypeptidase Angiotensin-I-converting enzyme (EC 3.4.15.1; ACE) plays an important physiological role in blood pressure regulation via the renin-angiotensin and kallikrein-kinin systems by converting angiotensin I to the potent vasoconstrictor angiotensin II, and by cleaving a number of other substrates including the vasodilator bradykinin and the anti-inflammatory peptide N-acetyl-SDKP.	goralatide	405-418	angiotensinogen	Homo sapiens	229-242
31889494-1	2020	The two-domain dipeptidylcarboxypeptidase Angiotensin-I-converting enzyme (EC 3.4.15.1; ACE) plays an important physiological role in blood pressure regulation via the renin-angiotensin and kallikrein-kinin systems by converting angiotensin I to the potent vasoconstrictor angiotensin II, and by cleaving a number of other substrates including the vasodilator bradykinin and the anti-inflammatory peptide N-acetyl-SDKP.	goralatide	405-418	angiotensinogen	Homo sapiens	273-287
31290182-2	2019	What are the effects of the antifibrotic peptide acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) on the angiotensin-converting enzyme 2 (ACE2)-angiotensin-(1-7)-Mas axis during the occurrence and progression of silicosis?	goralatide	86-93	angiotensin I converting enzyme 2	Rattus norvegicus	102-133
31290182-2	2019	What are the effects of the antifibrotic peptide acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) on the angiotensin-converting enzyme 2 (ACE2)-angiotensin-(1-7)-Mas axis during the occurrence and progression of silicosis?	goralatide	86-93	angiotensin I converting enzyme 2	Rattus norvegicus	135-139
31290182-8	2019	The antifibrotic peptide acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) can be degraded by ACE.	goralatide	62-69	angiotensin I converting enzyme	Rattus norvegicus	90-93
30972974-2	2019	We have previously reported that fibroblast growth factor receptor 1 (FGFR1) is involved in the anti-EndMT effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP).	goralatide	156-162	fibroblast growth factor receptor 1	Homo sapiens	33-68
30972974-2	2019	We have previously reported that fibroblast growth factor receptor 1 (FGFR1) is involved in the anti-EndMT effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP).	goralatide	156-162	fibroblast growth factor receptor 1	Homo sapiens	70-75