PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
34130526-2	2021	METHODS: Wistar-Kyoto (WKY) rats and SHRs were administered the UCHL1 inhibitor LDN57444 (20 mug/kg/day) for 4 months.	LDN 57444	80-88	ubiquitin C-terminal hydrolase L1	Rattus norvegicus	64-69
34130526-6	2021	Moreover, SHRs exhibited significantly increased central retinal thickness, inflammation, and reactive oxygen species production compared with WKY rats, and these effects were markedly attenuated by systemic administration of the UCHL1 inhibitor LDN57444.	LDN 57444	246-254	ubiquitin C-terminal hydrolase L1	Rattus norvegicus	230-235
33030206-7	2020	As a conclusion, UCH-L1 inhibitor LDN-57444 suppressed mouse oocyte maturation by improving oxidative stress, attenuating mitochondrial function, curbing spindle body formation and down-regulating ERK1/2 expression, providing a deep insight into the cellular and molecular basis of UCH-L1 during mouse oocyte maturation.	LDN 57444	34-43	mitogen-activated protein kinase 3	Mus musculus	197-203
33745956-4	2021	Systemic administration of the UCHL1 inhibitor LDN57444 significantly ameliorated cardiac fibrosis and improved cardiac function induced by angiotensin II.	LDN 57444	47-55	ubiquitin C-terminal hydrolase L1	Homo sapiens	31-36
33745956-4	2021	Systemic administration of the UCHL1 inhibitor LDN57444 significantly ameliorated cardiac fibrosis and improved cardiac function induced by angiotensin II.	LDN 57444	47-55	angiotensinogen	Homo sapiens	140-154
33745956-5	2021	Also, LDN57444 inhibited CF cell proliferation as well as attenuated collagen I, and CTGF gene expression in the presence of Ang II.	LDN 57444	6-14	cellular communication network factor 2	Homo sapiens	85-89
33030206-5	2020	In the present study, we observed that the introduction of UCH-L1 inhibitor LDN-57444 suppressed first polar body extrusion during mouse oocyte maturation.	LDN 57444	76-85	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	59-65
33030206-6	2020	The inhibition of UCH-L1 by LDN-57444 led to the notable increase of reactive oxygen species (ROS) level, conspicuous reduction of glutathione (GSH) content and mitochondrial membrane potential (MMP), and blockade of spindle body formation.	LDN 57444	28-37	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	18-24
33030206-7	2020	As a conclusion, UCH-L1 inhibitor LDN-57444 suppressed mouse oocyte maturation by improving oxidative stress, attenuating mitochondrial function, curbing spindle body formation and down-regulating ERK1/2 expression, providing a deep insight into the cellular and molecular basis of UCH-L1 during mouse oocyte maturation.	LDN 57444	34-43	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	282-288
33030206-7	2020	As a conclusion, UCH-L1 inhibitor LDN-57444 suppressed mouse oocyte maturation by improving oxidative stress, attenuating mitochondrial function, curbing spindle body formation and down-regulating ERK1/2 expression, providing a deep insight into the cellular and molecular basis of UCH-L1 during mouse oocyte maturation.	LDN 57444	34-43	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	17-23
32541849-4	2020	Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs) were administered the UCHL1 inhibitor LDN-57444 (20 mug/kg/day) from 2 months of age for 4 months.	LDN 57444	105-114	ubiquitin C-terminal hydrolase L1	Rattus norvegicus	89-94
24498857-7	2014	ASBT inhibition by RSV was reversed by proteasome inhibitors (MG-132 and lactacystin) and the ubiquitin inhibitor LDN57444, suggesting involvement of the ubiquitin-proteasome pathway.	LDN 57444	114-122	solute carrier family 10 member 2	Homo sapiens	0-4
32494592-8	2020	Systemic administration of the UCHL1 inhibitor LDN-57444 significantly reversed cardiac hypertrophy and remodeling.	LDN 57444	47-56	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	31-36
29686406-4	2018	Interestingly, through intervening UCHL1 by shRNA knockdown or its inhibitor LDN57444 or overexpression, we found that UCHL1 played a critical role in suppressing cytokines-induced inducible nitric oxide synthase expression in murine MSCs and indoleamine 2,3-dioxygenase expression in human MSCs, thereby restrained their immunosuppressive capacity.	LDN 57444	77-85	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	35-40
29686406-4	2018	Interestingly, through intervening UCHL1 by shRNA knockdown or its inhibitor LDN57444 or overexpression, we found that UCHL1 played a critical role in suppressing cytokines-induced inducible nitric oxide synthase expression in murine MSCs and indoleamine 2,3-dioxygenase expression in human MSCs, thereby restrained their immunosuppressive capacity.	LDN 57444	77-85	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	119-124
31700166-0	2020	Inhibition of UCHL1 by LDN-57444 attenuates Ang II-Induced atrial fibrillation in mice.	LDN 57444	23-26	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	14-19
31700166-0	2020	Inhibition of UCHL1 by LDN-57444 attenuates Ang II-Induced atrial fibrillation in mice.	LDN 57444	23-26	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	44-50
31700166-6	2020	Male wild-type mice were treated with the UCHL1 inhibitor LDN57444 (LDN) at a dose of 40 mug/kg and infused with Ang II (2000 ng/kg/min) for 3 weeks.	LDN 57444	58-66	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	42-47
31700166-6	2020	Male wild-type mice were treated with the UCHL1 inhibitor LDN57444 (LDN) at a dose of 40 mug/kg and infused with Ang II (2000 ng/kg/min) for 3 weeks.	LDN 57444	58-61	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	42-47
31700166-9	2020	Moreover, the administration of LDN significantly reduced Ang II-induced left atrial dilation, fibrosis, inflammatory cell infiltration, and reactive oxygen species (ROS) production.	LDN 57444	32-35	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	58-64
31700166-10	2020	Mechanistically, LDN treatment inhibited the activation of multiple signaling pathways (the AKT, ERK1/2, HIF-1alpha, and TGF-beta/smad2/3 pathways) and the expression of CX43 protein in atrial tissues compared with that in vehicle-treated control mice.	LDN 57444	17-20	thymoma viral proto-oncogene 1	Mus musculus	92-95
31700166-10	2020	Mechanistically, LDN treatment inhibited the activation of multiple signaling pathways (the AKT, ERK1/2, HIF-1alpha, and TGF-beta/smad2/3 pathways) and the expression of CX43 protein in atrial tissues compared with that in vehicle-treated control mice.	LDN 57444	17-20	mitogen-activated protein kinase 3	Mus musculus	97-103
31700166-10	2020	Mechanistically, LDN treatment inhibited the activation of multiple signaling pathways (the AKT, ERK1/2, HIF-1alpha, and TGF-beta/smad2/3 pathways) and the expression of CX43 protein in atrial tissues compared with that in vehicle-treated control mice.	LDN 57444	17-20	hypoxia inducible factor 1, alpha subunit	Mus musculus	105-115
31700166-10	2020	Mechanistically, LDN treatment inhibited the activation of multiple signaling pathways (the AKT, ERK1/2, HIF-1alpha, and TGF-beta/smad2/3 pathways) and the expression of CX43 protein in atrial tissues compared with that in vehicle-treated control mice.	LDN 57444	17-20	transforming growth factor, beta 1	Mus musculus	121-129
31700166-10	2020	Mechanistically, LDN treatment inhibited the activation of multiple signaling pathways (the AKT, ERK1/2, HIF-1alpha, and TGF-beta/smad2/3 pathways) and the expression of CX43 protein in atrial tissues compared with that in vehicle-treated control mice.	LDN 57444	17-20	SMAD family member 2	Mus musculus	130-137
31700166-10	2020	Mechanistically, LDN treatment inhibited the activation of multiple signaling pathways (the AKT, ERK1/2, HIF-1alpha, and TGF-beta/smad2/3 pathways) and the expression of CX43 protein in atrial tissues compared with that in vehicle-treated control mice.	LDN 57444	17-20	gap junction protein, alpha 1	Mus musculus	170-174
31700166-11	2020	Overall, our study identified UCHL1 as a novel regulator that contributes to Ang II-induced AF and suggests that the administration of LDN may represent a potential therapeutic approach for treating hypertensive AF.	LDN 57444	135-138	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	30-35
31700166-11	2020	Overall, our study identified UCHL1 as a novel regulator that contributes to Ang II-induced AF and suggests that the administration of LDN may represent a potential therapeutic approach for treating hypertensive AF.	LDN 57444	135-138	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	77-83
25999815-7	2015	Furthermore, LDN-57444 (LDN), a specific UCH-L1 inhibitor, was used to analyze its effects on cell morphology, microtubule (MT) organization and the proteolytic degradation system.	LDN 57444	13-22	ubiquitin C-terminal hydrolase L1	Rattus norvegicus	41-47
22593014-7	2012	The translocation of GLT-1 from the recycling endosomes to the plasma membrane was blocked by LDN-57444, a specific inhibitor to the deubiquitinating enzyme (DUB) ubiquitin C-terminal hydrolase-L1, but not by an inhibitor of the related DUB ubiquitin C-terminal hydrolase-L3, supporting the existence of specific ubiquitination/deubiquitination cycles that ensure the correct concentrations of GLT-1 at the cell surface.	LDN 57444	94-103	solute carrier family 1 member 2	Homo sapiens	21-26
22593014-7	2012	The translocation of GLT-1 from the recycling endosomes to the plasma membrane was blocked by LDN-57444, a specific inhibitor to the deubiquitinating enzyme (DUB) ubiquitin C-terminal hydrolase-L1, but not by an inhibitor of the related DUB ubiquitin C-terminal hydrolase-L3, supporting the existence of specific ubiquitination/deubiquitination cycles that ensure the correct concentrations of GLT-1 at the cell surface.	LDN 57444	94-103	solute carrier family 1 member 2	Homo sapiens	394-399
20713032-8	2010	Further, inhibition of UCHL1 activity by UCHL1 inhibitor (LDN-57444) increased cellular SMN protein and gems number in the nucleus in NSC34 and SMA skin fibroblasts.	LDN 57444	58-67	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	23-28
20713032-8	2010	Further, inhibition of UCHL1 activity by UCHL1 inhibitor (LDN-57444) increased cellular SMN protein and gems number in the nucleus in NSC34 and SMA skin fibroblasts.	LDN 57444	58-67	ubiquitin carboxy-terminal hydrolase L1	Mus musculus	41-46
20713032-8	2010	Further, inhibition of UCHL1 activity by UCHL1 inhibitor (LDN-57444) increased cellular SMN protein and gems number in the nucleus in NSC34 and SMA skin fibroblasts.	LDN 57444	58-67	survival motor neuron 1	Mus musculus	88-91