PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33522686-13	2021	CONCLUSION: Verbascoside mitigated the cell proliferation and aggressiveness of prostate cancer via downregulation of TGF-beta-associated EMT progression through HMGB1/RAGE suppression.	acteoside	12-24	high mobility group box 1	Homo sapiens	162-167
34054222-8	2021	EGCG also shows protective effects against 1) cytokine storm-associated acute lung injury/acute respiratory distress syndrome, 2) thrombosis via suppressing tissue factors and activating platelets, 3) sepsis by inactivating redox-sensitive HMGB1, and 4) lung fibrosis through augmenting Nrf2 and suppressing NF-kappaB.	epigallocatechin gallate	0-4	high mobility group box 1	Homo sapiens	240-245
3405231-2	1988	One of the satellite binding proteins (SBP1) purified by column chromatography using DEAE-, phospho- and DNA-cellulose steps interacted also with adenovirus 5 replication enhancer (ARE), another protein (SBP2) was separated during phosphocellulose chromatography from ARE-binding protein.	2-diethylaminoethanol	85-89	high mobility group box 1	Homo sapiens	39-43
5164097-2	1971	These are a simple synthesis of the substrate precursor HMG-3-(14)C anhydride and a double-label ((14)C and (3)H) method for determining the amount of mevalonate-3-(14)C that is formed from the substrate.	Mevalonic Acid	151-161	high mobility group box 1	Homo sapiens	56-61
34007314-3	2021	In the present study, the exact molecular mechanism underlying HMGB1-mediated drug resistance in MM was explored using three chemotherapy-resistant MM cells (RPMI8226/ADR, RPMI8226/BOR and RPMI8226/DEX) that were successfully established.	rpmi8226	158-166	high mobility group box 1	Homo sapiens	63-68
34007314-3	2021	In the present study, the exact molecular mechanism underlying HMGB1-mediated drug resistance in MM was explored using three chemotherapy-resistant MM cells (RPMI8226/ADR, RPMI8226/BOR and RPMI8226/DEX) that were successfully established.	rpmi8226	172-180	high mobility group box 1	Homo sapiens	63-68
34007314-3	2021	In the present study, the exact molecular mechanism underlying HMGB1-mediated drug resistance in MM was explored using three chemotherapy-resistant MM cells (RPMI8226/ADR, RPMI8226/BOR and RPMI8226/DEX) that were successfully established.	Boron	181-184	high mobility group box 1	Homo sapiens	63-68
34007314-3	2021	In the present study, the exact molecular mechanism underlying HMGB1-mediated drug resistance in MM was explored using three chemotherapy-resistant MM cells (RPMI8226/ADR, RPMI8226/BOR and RPMI8226/DEX) that were successfully established.	rpmi8226	172-180	high mobility group box 1	Homo sapiens	63-68
34007314-3	2021	In the present study, the exact molecular mechanism underlying HMGB1-mediated drug resistance in MM was explored using three chemotherapy-resistant MM cells (RPMI8226/ADR, RPMI8226/BOR and RPMI8226/DEX) that were successfully established.	Dextromethorphan	198-201	high mobility group box 1	Homo sapiens	63-68
34007314-4	2021	Reverse transcription-quantitative polymerase chain reaction revealed that the three chemotherapy-resistant MM cells exhibited a higher release of HMGB1 compared with the parental RPMI8226 cells.	rpmi8226	180-188	high mobility group box 1	Homo sapiens	147-152
33986864-10	2021	HMGB1 knockdown increased nicotinamide adenine nucleotide phosphate oxidase-mediated ROS production and induced DNA damage via the MAPK signaling pathway, which may promote apoptosis and radiosensitivity after radiation in TE-1 cells.	Niacinamide	26-38	high mobility group box 1	Homo sapiens	0-5
33986864-10	2021	HMGB1 knockdown increased nicotinamide adenine nucleotide phosphate oxidase-mediated ROS production and induced DNA damage via the MAPK signaling pathway, which may promote apoptosis and radiosensitivity after radiation in TE-1 cells.	Reactive Oxygen Species	85-88	high mobility group box 1	Homo sapiens	0-5
33716257-4	2021	Ethanol consumption leads to the activation of neuroimmune signaling in the central nervous system through many subtypes of Toll-like receptors (TLRs), as well as release of their endogenous agonists (high-mobility group protein B1 (HMGB1), S100 protein, heat shock proteins (HSPs), and extracellular matrix degradation proteins).	Ethanol	0-7	high mobility group box 1	Homo sapiens	201-231
34054124-10	2021	CONCLUSIONS This study demonstrated that the rs1360485 SNP of the HMGB1 gene is associated with susceptibility of NEC in neonates, and the rs1360485 genotypes TC and CC may affect HMGB1 expression and are associated with the survival prognosis of neonates with NEC.	Technetium	159-161	high mobility group box 1	Homo sapiens	66-71
34054124-10	2021	CONCLUSIONS This study demonstrated that the rs1360485 SNP of the HMGB1 gene is associated with susceptibility of NEC in neonates, and the rs1360485 genotypes TC and CC may affect HMGB1 expression and are associated with the survival prognosis of neonates with NEC.	Technetium	159-161	high mobility group box 1	Homo sapiens	180-185
34024230-9	2022	Knockdown of HMGB1 expression rescued LMP, restored the degradative capacity of autophagy, decreased the expression of inflammatory factors and VEGF (vascular endothelial growth factor), and protected against apoptosis in RPE cells in the early stages of DR.	(2~{s},3~{r},4~{s})-2-[(2~{s},3~{r})-1,3-Bis(Oxidanyl)-1-Oxidanylidene-Butan-2-Yl]-4-[(3~{s},5~{s})-5-(Dimethylcarbamoyl)pyrrolidin-3-Yl]sulfanyl-3-Methyl-3,4-Dihydro-2~{h}-Pyrrole-5-Carboxylic Acid	38-41	high mobility group box 1	Homo sapiens	13-18
33716257-4	2021	Ethanol consumption leads to the activation of neuroimmune signaling in the central nervous system through many subtypes of Toll-like receptors (TLRs), as well as release of their endogenous agonists (high-mobility group protein B1 (HMGB1), S100 protein, heat shock proteins (HSPs), and extracellular matrix degradation proteins).	Ethanol	0-7	high mobility group box 1	Homo sapiens	233-238
33621742-0	2021	Corrigendum to "Paclitaxel alleviates the sepsis-induced acute kidney injury via lnc-MALAT1/miR-370-3p/HMGB1 axis" [Life Sci.	Paclitaxel	16-26	high mobility group box 1	Homo sapiens	103-108
33975537-0	2021	Therapeutic administration of etoposide coincides with reduced systemic HMGB1 levels in macrophage activation syndrome.	Etoposide	30-39	high mobility group box 1	Homo sapiens	72-77
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Sulfhydryl Compounds	109-114	high mobility group box 1	Homo sapiens	22-27
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Sulfhydryl Compounds	109-114	high mobility group box 1	Homo sapiens	98-103
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Sulfhydryl Compounds	109-114	high mobility group box 1	Homo sapiens	98-103
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Sulfhydryl Compounds	109-114	high mobility group box 1	Homo sapiens	98-103
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Disulfides	188-197	high mobility group box 1	Homo sapiens	22-27
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Disulfides	188-197	high mobility group box 1	Homo sapiens	98-103
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Disulfides	188-197	high mobility group box 1	Homo sapiens	98-103
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Disulfides	188-197	high mobility group box 1	Homo sapiens	98-103
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Alkanesulfonates	348-357	high mobility group box 1	Homo sapiens	22-27
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Alkanesulfonates	348-357	high mobility group box 1	Homo sapiens	98-103
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Alkanesulfonates	348-357	high mobility group box 1	Homo sapiens	98-103
33107103-4	2021	Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form.	Alkanesulfonates	348-357	high mobility group box 1	Homo sapiens	98-103
33107103-6	2021	Antagonists such as ethyl pyruvate inhibit HMGB1 by interfering with its cytoplasmic exportation, while others such as glycyrrhizin directly bind to HMGB1 and render it unavailable for its receptors.	ethyl pyruvate	20-34	high mobility group box 1	Homo sapiens	43-48
33107103-6	2021	Antagonists such as ethyl pyruvate inhibit HMGB1 by interfering with its cytoplasmic exportation, while others such as glycyrrhizin directly bind to HMGB1 and render it unavailable for its receptors.	Glycyrrhizic Acid	119-131	high mobility group box 1	Homo sapiens	149-154
33864964-0	2021	HMGB1 expression in leukocytes as a biomarker of cellular damage induced by [99mTc]Tc-HMPAO-labelling procedure: A quality control study.	Technetium Tc 99m Exametazime	83-91	high mobility group box 1	Homo sapiens	0-5
33864964-11	2021	CONCLUSIONS: The evaluation of HMGB1 levels in WBC-CE from each subject after radiolabelling with [99mTc]Tc-HMPAO did not show significant changes compared to the cold cellular sample.	Technetium Tc 99m Exametazime	105-113	high mobility group box 1	Homo sapiens	31-36
33946401-0	2021	Meta-Analysis of Methamphetamine Modulation on Amyloid Precursor Protein through HMGB1 in Alzheimer"s Disease.	Methamphetamine	17-32	high mobility group box 1	Homo sapiens	81-86
33965862-6	2021	Furthermore, the HMGB1/p62/LC3II/LC3I and p53/SSAT/beta-catenin pathways were mainly involved in the inhibition of 13b-induced HCC metastasis by targeting polyamine transporters (PTs) overexpressed in HCC.	CHEMBL3741121	115-118	high mobility group box 1	Homo sapiens	17-22
33946401-6	2021	Simulated METH exposure increased APP expression through HMGB1 at a confidence of p < 0.00001 (Z-score = 7.64, two-tailed).	Methamphetamine	10-14	high mobility group box 1	Homo sapiens	57-62
33946401-9	2021	Our analyses suggest the involvement of HMGB1 signaling pathway in METH-induced modulation of APP as a potential casual factor of AD.	Methamphetamine	67-71	high mobility group box 1	Homo sapiens	40-45
33871066-0	2021	Clinical application of heparin in the treatment of severe acute pancreatitis -- new discovery of the HMGB1 pathway.	Heparin	24-31	high mobility group box 1	Homo sapiens	102-107
33903607-6	2021	Histological examination of the HMGB-1 treated group showed a vast area covered by lamellar and woven bone surrounding the beta-TCP granule remnants.	beta-tricalcium phosphate	123-131	high mobility group box 1	Homo sapiens	32-38
33903887-0	2021	[Dexmedetomidine alleviates hepatic ischemia-reperfusion injury by regulating MALAT1/miR-126-5p/HMGB1 axis].	Dexmedetomidine	1-16	high mobility group box 1	Homo sapiens	96-101
33903887-11	2021	The results suggest that Dex protects hepatocytes from HIRI via regulating MALAT1/miR-126-5p/HMGB1 axis.	Dexmedetomidine	25-28	high mobility group box 1	Homo sapiens	93-98
33617946-11	2021	CONCLUSION: G-Rg1 had a protective effect against LPS- and D-gal-induced ALF both in vitro and in vivo, which might be related to inhibited HMGB1-mediated TLR4-NF-kappaB Pathway.	g-rg1	12-17	high mobility group box 1	Homo sapiens	140-145
33854044-3	2021	Using a phenotypic screening strategy with recombinant HMGB1 and peritoneal macrophages, we discovered that FeTPPS, a small molecule selectively inhibits HMGB1-mediated caspase-11 activation.	fetpps	108-114	high mobility group box 1	Homo sapiens	55-60
33854044-3	2021	Using a phenotypic screening strategy with recombinant HMGB1 and peritoneal macrophages, we discovered that FeTPPS, a small molecule selectively inhibits HMGB1-mediated caspase-11 activation.	fetpps	108-114	high mobility group box 1	Homo sapiens	154-159
33854044-5	2021	Treatment of FeTPPS significantly attenuates HMGB1- and caspase-11-mediated immune responses, organ damage, and lethality in endotoxemia and bacterial sepsis.	fetpps	13-19	high mobility group box 1	Homo sapiens	45-50
33836651-13	2021	Compared with the C group, the levels of HMGB1, TNF-alpha, and IL-6 were significantly decreased 1 and 3 days after surgery in the QLB group (P < 0.05).	N-Octyl(oxyethylene)(3)ethanol	131-134	high mobility group box 1	Homo sapiens	41-46
33618227-1	2021	To screen for specific transcription factors (TFs) that induce expression of the HMGB1 promoter in response to stimulation by Ang-II.	ang-ii	126-132	high mobility group box 1	Homo sapiens	81-86
33618227-5	2021	However, compared with NC, invasion and migration by HMGB1 siRNA HCC cells stimulated by Ang-II were not altered; the expression of E-cadherin and vimentin was also unaltered.	ang-ii	89-95	high mobility group box 1	Homo sapiens	53-58
33496921-8	2021	Moreover, the inhibitory effect of circ_0081146 knockdown on the progression of GC cells were reversed by silencing miR-144 or HMGB1 overexpression.	circ_0081146	35-47	high mobility group box 1	Homo sapiens	127-132
33453094-0	2021	HMGB1 is a key factor for tamoxifen resistance and has the potential to predict the efficacy of CDK4/6 inhibitors in breast cancer.	Tamoxifen	26-35	high mobility group box 1	Homo sapiens	0-5
33453094-9	2021	Moreover, we demonstrated that HMGB1 promoted tamoxifen resistance by combining with Toll-like receptor 4 (TLR4) and activating nuclear factor kappa B (NF-kappaB) pathway.	Tamoxifen	46-55	high mobility group box 1	Homo sapiens	31-36
33453094-10	2021	CDK4/6 inhibitors could down-regulate the expression of HMGB1 and suppress TLR4-NF-kappaB pathway, in turn reverse tamoxifen resistance.	Tamoxifen	115-124	high mobility group box 1	Homo sapiens	56-61
33453094-11	2021	These results illuminated the critical role of HMGB1 in the process of tamoxifen resistance, explained the mechanism of CDK4/6 inhibitors reversing tamoxifen resistance, and suggested the feasibility of HMGB1 serving as a potential biomarker for screening sensitive patients of CDK4/6 inhibitors.	Tamoxifen	71-80	high mobility group box 1	Homo sapiens	47-52
33166075-4	2021	Animal and human studies have found cigarette smoke exposure upregulates RAGE expression, suggesting that the HMGB1-RAGE pathway might be involved in maternal nicotine-induced lung injury.	Nicotine	159-167	high mobility group box 1	Homo sapiens	110-115
33660567-5	2021	Treatment with PF-43 prevented the downregulation of the epithelial barrier by HMGB1 and inflammatory cytokines in 2D culture.	pf-43	15-20	high mobility group box 1	Homo sapiens	79-84
33660567-6	2021	Treatment with PF-43 prevented the epithelial hyperpermeability induced by HMGB1 and inflammatory cytokines in 2.5D culture.	pf-43	15-20	high mobility group box 1	Homo sapiens	75-80
33660567-7	2021	In 2.5D culture, treatment with PF-43 inhibited the decreases of angulin-1/LSR, TRIC, pJNK, pAMPK and pMAPK induced by HMGB1 and the inflammatory cytokines.	pf-43	32-37	high mobility group box 1	Homo sapiens	119-124
33617946-0	2021	Gensenoside Rg1 protects against lipopolysaccharide- and d-galactose-induced acute liver failure via suppressing HMGB1-mediated TLR4-NF-kappaB pathway.	Galactose	57-68	high mobility group box 1	Homo sapiens	113-118
33617946-11	2021	CONCLUSION: G-Rg1 had a protective effect against LPS- and D-gal-induced ALF both in vitro and in vivo, which might be related to inhibited HMGB1-mediated TLR4-NF-kappaB Pathway.	Galactose	59-64	high mobility group box 1	Homo sapiens	140-145
33691128-3	2021	propose that heparin provides protection during gram-negative sepsis by dampening harmful CASP11-dependent signaling through inhibition of HMGB1- and heparanase-mediated cytosolic delivery of LPS.	Heparin	13-20	high mobility group box 1	Homo sapiens	139-144
33841665-6	2021	RESULTS: Ectopic HESCs showed markedly decreased cell viability with the increased release of HMGB-1 following treatment with H2O2.	Hydrogen Peroxide	126-130	high mobility group box 1	Homo sapiens	94-100
33461096-0	2021	Reactive oxygen species induce Cys106-mediated anti-parallel HMGB1 dimerization that protects against DNA damage.	Oxygen	9-15	high mobility group box 1	Homo sapiens	61-66
33461096-3	2021	As a redox-sensitive protein, HMGB1 contains three cysteine residues: Cys23, Cys45, and Cys106.	Cysteine	51-59	high mobility group box 1	Homo sapiens	30-35
33461096-5	2021	HMGB1 dimerization was positively modulated by CuCl2 and H2O2.	cupric chloride	47-52	high mobility group box 1	Homo sapiens	0-5
33461096-5	2021	HMGB1 dimerization was positively modulated by CuCl2 and H2O2.	Hydrogen Peroxide	57-61	high mobility group box 1	Homo sapiens	0-5
33461096-7	2021	Treatment of HEK293T cells with CuCl2 and H2O2 enhanced the oxidative self-dimerization of HMGB1, whereas this dimerization was inhibited in mutant HMGB1C106A cells.	cupric chloride	32-37	high mobility group box 1	Homo sapiens	91-96
33461096-7	2021	Treatment of HEK293T cells with CuCl2 and H2O2 enhanced the oxidative self-dimerization of HMGB1, whereas this dimerization was inhibited in mutant HMGB1C106A cells.	cupric chloride	32-37	high mobility group box 1	Homo sapiens	148-153
33461096-7	2021	Treatment of HEK293T cells with CuCl2 and H2O2 enhanced the oxidative self-dimerization of HMGB1, whereas this dimerization was inhibited in mutant HMGB1C106A cells.	Hydrogen Peroxide	42-46	high mobility group box 1	Homo sapiens	91-96
33729484-0	2021	miR-92d-3p suppresses the progression of diabetic nephropathy renal fibrosis by inhibiting the C3/HMGB1/TGF-beta1 pathway.	mir-92d-3p	0-10	high mobility group box 1	Homo sapiens	98-103
33729484-9	2021	miR-92d-3p inhibited inflammatory factor production by C3 in the HK-2 cells and the activation of the C3/HMGB1/TGF-beta1 pathway and EMT by C3 and TGF-beta1.	mir-92d-3p	0-10	high mobility group box 1	Homo sapiens	105-110
33729484-10	2021	miR-92d-3p suppressed the progression of DN renal fibrosis by inhibiting the activation of the C3/HMGB1/TGF-beta1 pathway and EMT.	mir-92d-3p	0-10	high mobility group box 1	Homo sapiens	98-103
33731757-0	2021	Disulfide HMGB1 acts via TLR2/4 receptors to reduce the numbers of oligodendrocyte progenitor cells after traumatic injury in vitro.	Disulfides	0-9	high mobility group box 1	Homo sapiens	10-15
33561388-5	2021	Heparin or a chemically modified form of heparin without anticoagulant function inhibited the alarmin HMGB1-lipopolysaccharide (LPS) interaction and prevented the macrophage glycocalyx degradation by heparanase.	Heparin	0-7	high mobility group box 1	Homo sapiens	102-107
33561388-5	2021	Heparin or a chemically modified form of heparin without anticoagulant function inhibited the alarmin HMGB1-lipopolysaccharide (LPS) interaction and prevented the macrophage glycocalyx degradation by heparanase.	Heparin	41-48	high mobility group box 1	Homo sapiens	102-107
33658363-5	2021	Further characterizing HMGB1 as a sialic acid-binding lectin, we found that optimal binding takes place at normal blood pH and is markedly reduced when pH is adjusted with lactic acid to levels found in sepsis.	N-Acetylneuraminic Acid	34-45	high mobility group box 1	Homo sapiens	23-28
33500702-0	2021	miR-142-3p reduces the viability of human cervical cancer cells by negatively regulating the cytoplasmic localization of HMGB1.	mir-142-3p	0-10	high mobility group box 1	Homo sapiens	121-126
33658363-5	2021	Further characterizing HMGB1 as a sialic acid-binding lectin, we found that optimal binding takes place at normal blood pH and is markedly reduced when pH is adjusted with lactic acid to levels found in sepsis.	Lactic Acid	172-183	high mobility group box 1	Homo sapiens	23-28
33658363-6	2021	Glycan array studies confirmed the binding of HMGB1 to sialylated glycan sequences typically found on plasma glycoproteins, with binding again being dependent on zinc and normal blood pH.	Polysaccharides	0-6	high mobility group box 1	Homo sapiens	46-51
33658363-6	2021	Glycan array studies confirmed the binding of HMGB1 to sialylated glycan sequences typically found on plasma glycoproteins, with binding again being dependent on zinc and normal blood pH.	Polysaccharides	66-72	high mobility group box 1	Homo sapiens	46-51
33314408-0	2021	H19/miR-107 / HMGB1 axis sensitizes laryngeal squamous cell carcinoma to cisplatin by suppressing autophagy in vitro and in vivo.	Cisplatin	73-82	high mobility group box 1	Homo sapiens	14-19
33500702-9	2021	Transfection with a miR-142-3p inhibitor increased cytoplasmic HMGB1 expression in HeLa cells, as shown by western blot analysis, while transfection with miR-142-3p mimics decreased the cytoplasmic expression of HMGB1 in HeLa cells.	mir-142-3p	20-30	high mobility group box 1	Homo sapiens	63-68
33500702-9	2021	Transfection with a miR-142-3p inhibitor increased cytoplasmic HMGB1 expression in HeLa cells, as shown by western blot analysis, while transfection with miR-142-3p mimics decreased the cytoplasmic expression of HMGB1 in HeLa cells.	mir-142-3p	20-30	high mobility group box 1	Homo sapiens	212-217
33500702-9	2021	Transfection with a miR-142-3p inhibitor increased cytoplasmic HMGB1 expression in HeLa cells, as shown by western blot analysis, while transfection with miR-142-3p mimics decreased the cytoplasmic expression of HMGB1 in HeLa cells.	mir-142-3p	154-164	high mobility group box 1	Homo sapiens	212-217
33500702-10	2021	Therefore, miR-142-3p negatively regulated HMGB1 levels in cervical cancer cells.	mir-142-3p	11-21	high mobility group box 1	Homo sapiens	43-48
33500702-11	2021	These findings indicated that miR-142-3p inhibited the proliferation of human cervical cancer cells, at least in part, by negatively regulating the cytoplasmic localization of HMGB1.	mir-142-3p	30-40	high mobility group box 1	Homo sapiens	176-181
32426849-0	2021	Disulfide-HMGB1 Drives Ischemia-Reperfusion Injury in Human Liver Transplantation.	Disulfides	0-9	high mobility group box 1	Homo sapiens	10-15
32426849-4	2021	Portal blood immediately following allograft reperfusion (liver flush, LF) had increased total HMGB1, but only LF from patients with histopathological IRI had increased disulfide-HMGB1 and induced TLR4-dependent TNFalpha production by macrophages.	Disulfides	169-178	high mobility group box 1	Homo sapiens	179-184
32426849-5	2021	Disulfide HMGB1 levels increased concomitantly with IRI severity.	Disulfides	0-9	high mobility group box 1	Homo sapiens	10-15
32426849-6	2021	IRI+ pre-reperfusion biopsies contained macrophages with hyperacetylated, lysosomal disulfide-HMGB1 that increased post-reperfusion at sites of injury, paralleling increased histone acetyltransferase GTF3C4 and decreased histone deacetylase HDAC5 expression.	Disulfides	84-93	high mobility group box 1	Homo sapiens	94-99
32426849-7	2021	Purified disulfide-HMGB1 or IRI+ blood stimulated further production of disulfide-HMGB1 and increased pro-inflammatory molecule and cytokine expression in macrophages via a positive feedback loop.	Disulfides	9-18	high mobility group box 1	Homo sapiens	19-24
32426849-7	2021	Purified disulfide-HMGB1 or IRI+ blood stimulated further production of disulfide-HMGB1 and increased pro-inflammatory molecule and cytokine expression in macrophages via a positive feedback loop.	Disulfides	9-18	high mobility group box 1	Homo sapiens	82-87
32426849-7	2021	Purified disulfide-HMGB1 or IRI+ blood stimulated further production of disulfide-HMGB1 and increased pro-inflammatory molecule and cytokine expression in macrophages via a positive feedback loop.	Disulfides	72-81	high mobility group box 1	Homo sapiens	19-24
32426849-7	2021	Purified disulfide-HMGB1 or IRI+ blood stimulated further production of disulfide-HMGB1 and increased pro-inflammatory molecule and cytokine expression in macrophages via a positive feedback loop.	Disulfides	72-81	high mobility group box 1	Homo sapiens	82-87
32426849-8	2021	CONCLUSIONS: These data identify disulfide-HMGB1 as a mechanistic biomarker of, and therapeutic target for, minimizing sterile inflammation during human liver IRI.	Disulfides	33-42	high mobility group box 1	Homo sapiens	43-48
33741691-4	2021	This nuclear retention of HMGB1 may also be a mediator of the anti-inflammatory effect of melatonin therapy in COVID-19-complementing melatonin"s suppression of nuclear factor kappa B activity and upregulation of nuclear factor erythroid 2-related factor 2.	Melatonin	90-99	high mobility group box 1	Homo sapiens	26-31
33741691-4	2021	This nuclear retention of HMGB1 may also be a mediator of the anti-inflammatory effect of melatonin therapy in COVID-19-complementing melatonin"s suppression of nuclear factor kappa B activity and upregulation of nuclear factor erythroid 2-related factor 2.	Melatonin	134-143	high mobility group box 1	Homo sapiens	26-31
33732708-7	2021	The higher cell viability observed in the HMGB1 knocked-down group after stimulation with H2O2 indicated the possible negative effect of HMGB1 on cellular lifespan.	Hydrogen Peroxide	90-94	high mobility group box 1	Homo sapiens	42-47
33565572-0	2021	HMGB1 regulates ferroptosis through Nrf2 pathway in mesangial cells in response to high glucose.	Glucose	88-95	high mobility group box 1	Homo sapiens	0-5
33565572-2	2021	The present study explored the role of high-mobility group box-1 (HMGB1) on the regulation of ferroptosis in mesangial cells in response to high glucose.	Glucose	145-152	high mobility group box 1	Homo sapiens	39-64
33565572-2	2021	The present study explored the role of high-mobility group box-1 (HMGB1) on the regulation of ferroptosis in mesangial cells in response to high glucose.	Glucose	145-152	high mobility group box 1	Homo sapiens	66-71
33565572-5	2021	Suppression of HMGB1 restored cellular proliferation, prevented ROS and LDH generation, decreased ACSL4, PTGS2, and NOX1, and increased GPX4 levels in mesangial cells.	Reactive Oxygen Species	64-67	high mobility group box 1	Homo sapiens	15-20
33565572-6	2021	Furthermore, nuclear factor E2-related factor 2 (Nrf2) was decreased in DN patients and high glucose mediated translocation of HMGB1 in mesangial cells.	Glucose	93-100	high mobility group box 1	Homo sapiens	127-132
33565572-7	2021	Knockdown of HMGB1 suppressed high glucose-induced activation of TLR4/NF-kappaB axis and promoted Nrf2 expression as well as its downstream targets including HO-1, NQO-1, GCLC and GCLM.	Glucose	35-42	high mobility group box 1	Homo sapiens	13-18
33565572-8	2021	Collectively, these findings suggest that HMGB1 regulates glucose-induced ferroptosis via Nrf2 pathway in mesangial cells.	Glucose	58-65	high mobility group box 1	Homo sapiens	42-47
33716687-6	2021	Galantamine treatment also recovered the AIE-increased expression of the proinflammatory receptors TLR4 and RAGE, the endogenous TLR4/RAGE agonist HMGB1, and the transcription activation marker pNF-kappaB p65.	Galantamine	0-11	high mobility group box 1	Homo sapiens	147-152
33716687-10	2021	Together, these data suggest that AIE induces HMGB1-TLR4/RAGE-pNF-kappaB p65 signals, causing the loss of cholinergic phenotype (i.e., ChAT, TrkA, and p75NTR) through epigenetic histone transcription silencing that result in the loss of the BFCN phenotype that can be prevented and restored by galantamine.	Galantamine	294-305	high mobility group box 1	Homo sapiens	46-51
33732708-7	2021	The higher cell viability observed in the HMGB1 knocked-down group after stimulation with H2O2 indicated the possible negative effect of HMGB1 on cellular lifespan.	Hydrogen Peroxide	90-94	high mobility group box 1	Homo sapiens	137-142
33509758-0	2021	[Dihydromyricetin inhibits proliferation and migration of gastric cancer cells through regulating Akt/STAT3 signaling pathways and HMGB1 expression].	dihydromyricetin	1-17	high mobility group box 1	Homo sapiens	131-136
33624300-6	2021	We observed increased ACE2 expression with both HMGB1 and hyperglycemia treatment in A549 as well as H441 cells, which were blunted by TCBN treatment.	triciribine	135-139	high mobility group box 1	Homo sapiens	48-53
33611821-7	2021	Depletion of microglia prior to ethanol treatment prevented pro-inflammatory activity of EtOH-MVs, as did incubation of EtOH-MVs with the HMGB1 inhibitor glycyrrhizin.	Ethanol	120-124	high mobility group box 1	Homo sapiens	138-143
33611821-7	2021	Depletion of microglia prior to ethanol treatment prevented pro-inflammatory activity of EtOH-MVs, as did incubation of EtOH-MVs with the HMGB1 inhibitor glycyrrhizin.	Glycyrrhizic Acid	154-166	high mobility group box 1	Homo sapiens	138-143
33611821-8	2021	Ethanol caused HMGB1 secretion from cultured BV2 microglia in MVs through activation of PI3 kinase.	Ethanol	0-7	high mobility group box 1	Homo sapiens	15-20
33664952-4	2021	Vitamin D played a role in inhibiting HMGB1 secretion in the animal study.	Vitamin D	0-9	high mobility group box 1	Homo sapiens	38-43
33664952-11	2021	Conclusions: Strong negative correlation between VDR and HMGB1 in different immunodeficiency statuses suggesting an important role of vitamin D in inflammation control in HIV infection.	Vitamin D	134-143	high mobility group box 1	Homo sapiens	57-62
32374414-4	2021	Endothelial thrombomodulin (TM) and recombinant human soluble TM, TMalpha, dramatically promote thrombin-dependent degradation of HMGB1, and systemic administration of TMalpha prevents and reverses various HMGB1-dependent pathological pain.	tmalpha	66-73	high mobility group box 1	Homo sapiens	130-135
32666385-0	2021	Involvement of HMGB1 in vemurafenib resistance in thyroid cancer cells harboring BRAF (V600E) mutation by regulating excessive autophagy.	Vemurafenib	24-35	high mobility group box 1	Homo sapiens	15-20
32666385-3	2021	Here, we sought to elucidate the function of high mobility group box 1 (HMGB1) in vemurafenib resistance in thyroid cancer harboring BRAF mutation.	Vemurafenib	82-93	high mobility group box 1	Homo sapiens	45-70
32666385-3	2021	Here, we sought to elucidate the function of high mobility group box 1 (HMGB1) in vemurafenib resistance in thyroid cancer harboring BRAF mutation.	Vemurafenib	82-93	high mobility group box 1	Homo sapiens	72-77
32666385-5	2021	Then, BCPAP cells were transfected with recombinant HMGB1 plasmids, and vemurafenib-resistant BCPAP-R cells were treated with si-HMGB1.	Vemurafenib	72-83	high mobility group box 1	Homo sapiens	129-134
32666385-6	2021	The efficacy of HMGB1 on vemurafenib resistance was evaluated by detecting cell viability, apoptosis, and caspase-3 activity.	Vemurafenib	25-36	high mobility group box 1	Homo sapiens	16-21
32666385-8	2021	RESULTS: Lower expression of HMGB1 was observed in BRAF-mutant BCPAP cells that had high sensitivity to vemurafenib.	Vemurafenib	104-115	high mobility group box 1	Homo sapiens	29-34
32666385-9	2021	Overexpression of HMGB1 attenuated BCPAP cell sensitivity to vemurafenib by increasing cell viability and decreasing cell apoptosis and caspase-3 activity.	Vemurafenib	61-72	high mobility group box 1	Homo sapiens	18-23
32666385-10	2021	Intriguingly, higher expression of HMGB1 was confirmed in vemurafenib-resistant BCPAP-R cells.	Vemurafenib	58-69	high mobility group box 1	Homo sapiens	35-40
32666385-11	2021	Moreover, knockdown of HMGB1 sensitized BCPAP-R cells to vemurafenib resistance.	Vemurafenib	57-68	high mobility group box 1	Homo sapiens	23-28
32666385-13	2021	Importantly, targeting HMGB1 suppressed vemurafenib-induced autophagy.	Vemurafenib	40-51	high mobility group box 1	Homo sapiens	23-28
32666385-15	2021	CONCLUSIONS: These findings highlight that HMGB1-mediated autophagy may account for vemurafenib resistance in thyroid cancer harboring BRAF mutation, implying a promising approach to overcome vemurafenib resistance in vemurafenib-mutant thyroid carcinomas.	Vemurafenib	84-95	high mobility group box 1	Homo sapiens	43-48
32666385-15	2021	CONCLUSIONS: These findings highlight that HMGB1-mediated autophagy may account for vemurafenib resistance in thyroid cancer harboring BRAF mutation, implying a promising approach to overcome vemurafenib resistance in vemurafenib-mutant thyroid carcinomas.	Vemurafenib	192-203	high mobility group box 1	Homo sapiens	43-48
32666385-15	2021	CONCLUSIONS: These findings highlight that HMGB1-mediated autophagy may account for vemurafenib resistance in thyroid cancer harboring BRAF mutation, implying a promising approach to overcome vemurafenib resistance in vemurafenib-mutant thyroid carcinomas.	Vemurafenib	192-203	high mobility group box 1	Homo sapiens	43-48
33614649-0	2021	Temozolomide Treatment Induces HMGB1 to Promote the Formation of Glioma Stem Cells via the TLR2/NEAT1/Wnt Pathway in Glioblastoma.	Temozolomide	0-12	high mobility group box 1	Homo sapiens	31-36
33614649-4	2021	Our study showed that TMZ treatment promoted GSCs formation by glioma cells; TMZ treatment of biopsy-derived glioblastoma multiforme cells upregulated HMGB1; HMGB1 altered gene expression profile of glioma cells with respect to mRNA, lncRNA and miRNA.	Temozolomide	22-25	high mobility group box 1	Homo sapiens	158-163
33614649-4	2021	Our study showed that TMZ treatment promoted GSCs formation by glioma cells; TMZ treatment of biopsy-derived glioblastoma multiforme cells upregulated HMGB1; HMGB1 altered gene expression profile of glioma cells with respect to mRNA, lncRNA and miRNA.	Temozolomide	77-80	high mobility group box 1	Homo sapiens	151-156
33614649-4	2021	Our study showed that TMZ treatment promoted GSCs formation by glioma cells; TMZ treatment of biopsy-derived glioblastoma multiforme cells upregulated HMGB1; HMGB1 altered gene expression profile of glioma cells with respect to mRNA, lncRNA and miRNA.	Temozolomide	77-80	high mobility group box 1	Homo sapiens	158-163
33614649-5	2021	Furthermore, our results showed that TMZ-induced HMGB1 increased the formation of GSCs and when HMGB1 was downregulated, TMZ-mediated GSCs formation was attenuated.	Temozolomide	37-40	high mobility group box 1	Homo sapiens	49-54
33614649-5	2021	Furthermore, our results showed that TMZ-induced HMGB1 increased the formation of GSCs and when HMGB1 was downregulated, TMZ-mediated GSCs formation was attenuated.	Temozolomide	37-40	high mobility group box 1	Homo sapiens	96-101
33614649-5	2021	Furthermore, our results showed that TMZ-induced HMGB1 increased the formation of GSCs and when HMGB1 was downregulated, TMZ-mediated GSCs formation was attenuated.	Temozolomide	121-124	high mobility group box 1	Homo sapiens	49-54
33614649-5	2021	Furthermore, our results showed that TMZ-induced HMGB1 increased the formation of GSCs and when HMGB1 was downregulated, TMZ-mediated GSCs formation was attenuated.	Temozolomide	121-124	high mobility group box 1	Homo sapiens	96-101
33614649-8	2021	In conclusion, TMZ treatment upregulates HMGB1, which promotes the formation of GSCs via the TLR2/NEAT1/Wnt pathway.	Temozolomide	15-18	high mobility group box 1	Homo sapiens	41-46
33614649-9	2021	Blocking HMGB1-mediated GSCs formation could serve as a potential therapeutic target for preventing TMZ resistance in GBM patients.	Temozolomide	100-103	high mobility group box 1	Homo sapiens	9-14
33308900-0	2021	Astragaloside IV antagonizes M2 phenotype macrophage polarization-evoked ovarian cancer cell malignant progression by suppressing the HMGB1-TLR4 axis.	astragaloside	0-13	high mobility group box 1	Homo sapiens	134-139
33308900-7	2021	During this process, administration with astragaloside IV restrained the high expression of high-mobility group box1 (HMGB1) and TLR4 in macrophages co-cultured with ovarian cancer cells, concomitant with decreases in release of M2 marker TGF-beta, MMP-9 and IL-10.	astragaloside	41-54	high mobility group box 1	Homo sapiens	92-116
33308900-7	2021	During this process, administration with astragaloside IV restrained the high expression of high-mobility group box1 (HMGB1) and TLR4 in macrophages co-cultured with ovarian cancer cells, concomitant with decreases in release of M2 marker TGF-beta, MMP-9 and IL-10.	astragaloside	41-54	high mobility group box 1	Homo sapiens	118-123
33308900-9	2021	Noticeably, exogenous HMGB1 overturned the inhibitory efficacy of astragaloside IV against macrophage M2 polarization-evoked malignant potential in ovarian cancer cells.	astragaloside	66-79	high mobility group box 1	Homo sapiens	22-27
33308900-10	2021	Together, these findings suggest that astragaloside IV may protect against M2 macrophages-evoked malignancy in ovarian cancer cells by suppressing the HMGB1-TLR4 signaling.	astragaloside	38-51	high mobility group box 1	Homo sapiens	151-156
33053467-0	2021	Amorphous silica nanoparticles induce inflammation via activation of NLRP3 inflammasome and HMGB1/TLR4/MYD88/NF-kb signaling pathway in HUVEC cells.	Silicon Dioxide	10-16	high mobility group box 1	Homo sapiens	92-97
33053467-5	2021	In addition, SiO2 NPs were found to promote the translocation and release of high-mobility group box 1 (HMGB1) from nucleus to cytoplasm, which was demonstrated to be regulated by ROS and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome.	Reactive Oxygen Species	180-183	high mobility group box 1	Homo sapiens	77-102
33053467-5	2021	In addition, SiO2 NPs were found to promote the translocation and release of high-mobility group box 1 (HMGB1) from nucleus to cytoplasm, which was demonstrated to be regulated by ROS and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome.	Reactive Oxygen Species	180-183	high mobility group box 1	Homo sapiens	104-109
33559243-7	2021	Treatment of cholangiocytes with ethyl pyruvate suppressed the release of HMGB1.	ethyl pyruvate	33-47	high mobility group box 1	Homo sapiens	74-79
33655086-8	2021	Second, curcumin protects from lethal pneumonia and ARDS via targeting NF-kappaB, inflammasome, IL-6 trans signal, and HMGB1 pathways.	Curcumin	8-16	high mobility group box 1	Homo sapiens	119-124
33535837-8	2021	Furthermore, upregulation of high mobility group box protein 1 (HMGB1) protein levels and downregulation of miR-129-5p levels were observed in vivo and in vitro following sufentanil treatment.	Sufentanil	171-181	high mobility group box 1	Homo sapiens	29-62
33535837-8	2021	Furthermore, upregulation of high mobility group box protein 1 (HMGB1) protein levels and downregulation of miR-129-5p levels were observed in vivo and in vitro following sufentanil treatment.	Sufentanil	171-181	high mobility group box 1	Homo sapiens	64-69
33535837-11	2021	CONCLUSION: Sufentanil regulated the miR-129-5p/HMGB1 axis to enhance IkappaB-alpha expression, suggesting that sufentanil represents a candidate drug for ALI protection and providing avenues for clinical treatment.	Sufentanil	12-22	high mobility group box 1	Homo sapiens	48-53
33535837-11	2021	CONCLUSION: Sufentanil regulated the miR-129-5p/HMGB1 axis to enhance IkappaB-alpha expression, suggesting that sufentanil represents a candidate drug for ALI protection and providing avenues for clinical treatment.	Sufentanil	112-122	high mobility group box 1	Homo sapiens	48-53
32216030-0	2021	Adsorption kinetics for high mobility group box 1 (HMGB1) protein in a polyacrylonitrile hemofiltration membrane.	polyacrylonitrile	71-88	high mobility group box 1	Homo sapiens	24-49
32216030-0	2021	Adsorption kinetics for high mobility group box 1 (HMGB1) protein in a polyacrylonitrile hemofiltration membrane.	polyacrylonitrile	71-88	high mobility group box 1	Homo sapiens	51-56
32216030-2	2021	We previously reported that a polyacrylonitrile (AN69ST) membrane rapidly adsorbed HMGB1.	polyacrylonitrile	30-47	high mobility group box 1	Homo sapiens	83-88
33515401-3	2021	Our study illustrates an example of drug repositioning of Biapenem (BIPM), a carbapenem antibiotic, for the modulation of HMGB1-induced septic responses.	biapenem	58-66	high mobility group box 1	Homo sapiens	122-127
33515401-3	2021	Our study illustrates an example of drug repositioning of Biapenem (BIPM), a carbapenem antibiotic, for the modulation of HMGB1-induced septic responses.	biapenem	68-72	high mobility group box 1	Homo sapiens	122-127
33515401-3	2021	Our study illustrates an example of drug repositioning of Biapenem (BIPM), a carbapenem antibiotic, for the modulation of HMGB1-induced septic responses.	Carbapenems	77-87	high mobility group box 1	Homo sapiens	122-127
33509758-5	2021	Treatment with dihydromyricetin obviously suppressed the proliferation and migration of BGC-823 cells, significantly reduced the expression levels of cyclin D1, cyclin E1 and Ncadherin, enhanced E-cadherin expression, inhibited the phosphorylation of Akt and stat3, and downregulated HMGB1 expression in the cells.	dihydromyricetin	15-31	high mobility group box 1	Homo sapiens	284-289
33509758-7	2021	CONCLUSIONS: Dihydromyricetin inhibits the proliferation and migration of BGC-823 cells through suppressing the activation of Akt/stat3 signaling pathways and HMGB1 expression.	dihydromyricetin	13-29	high mobility group box 1	Homo sapiens	159-164
33440377-5	2021	Acrylonitrile 69-based oXiris membranes can remove endotoxin and high-mobility group box 1 protein.	Acrylonitrile	0-13	high mobility group box 1	Homo sapiens	65-90
33573541-1	2021	Oleanolic acid can inhibit edema and exhibit obvious inhibitory activity to inflammatory by activating of the pituitary-adrenal cortical system, inhibiting the synthesis or release of PGs, inhibiting endotoxin-mediated release of HMGB1 by endothelial cells or regulating MAPK, PI3K/Akt/NF-kappaB/ICAM-1/JAK/STAT signaling pathways, etc.	Oleanolic Acid	0-14	high mobility group box 1	Homo sapiens	230-235
33242463-5	2021	Mechanistically, tumor HIF1alpha signaling activated by chemo-induced ROS drives the transcription of HMGB1 to promote more macrophage infiltration into CRC tumor.	ros	70-73	high mobility group box 1	Homo sapiens	102-107
33505216-10	2021	GA is capable of inhibiting toll-like receptors as well as high-mobility group box 1.	Glycyrrhetinic Acid	0-2	high mobility group box 1	Homo sapiens	59-84
33422068-2	2021	Ring-stage parasite mRNA, measured by sbp1 quantitative reverse-transcriptase PCR (qRT-PCR), was previously reported to persist after ACT treatment and hypothesized to reflect temporary arrest of the growth of ring-stage parasites (dormancy) following exposure to artemisinins.	Artemisinins	264-276	high mobility group box 1	Homo sapiens	38-42
32852122-9	2021	HMGB1 facilitated the proliferation of iNKT cells co-cultured with DCs and macrophages, which was found to be inhibited by heparin.	Heparin	123-130	high mobility group box 1	Homo sapiens	0-5
33414419-0	2021	Gefitinib initiates sterile inflammation by promoting IL-1beta and HMGB1 release via two distinct mechanisms.	Gefitinib	0-9	high mobility group box 1	Homo sapiens	67-72
33414419-3	2021	Here, we provide evidence that gefitinib elicits pro-inflammatory responses by promoting mature-interleukin-1beta (IL-1beta) and high-mobility group box 1 (HMGB1) release.	Gefitinib	31-40	high mobility group box 1	Homo sapiens	129-154
33414419-3	2021	Here, we provide evidence that gefitinib elicits pro-inflammatory responses by promoting mature-interleukin-1beta (IL-1beta) and high-mobility group box 1 (HMGB1) release.	Gefitinib	31-40	high mobility group box 1	Homo sapiens	156-161
33414419-5	2021	Notably, gefitinib also stimulated HMGB1 release, which is, however, not mediated by the NLRP3 inflammasome.	Gefitinib	9-18	high mobility group box 1	Homo sapiens	35-40
33414419-6	2021	On the other hand, gefitinib-driven mtROS promoted the accumulation of gammaH2AX, a hallmark of DNA damage, leading to the activation of poly (ADP-ribose) polymerase-1 (PARP-1) and subsequent active release of HMGB1.	Gefitinib	19-28	high mobility group box 1	Homo sapiens	210-215
33414419-7	2021	Together our results reveal the potential ability of gefitinib to initiate sterile inflammation via two distinct mechanisms, and identified IL-1beta and HMGB1 as key determinants of gefitinib-induced inflammation that may provide insights into gefitinib-induced interstitial pneumonitis.	Gefitinib	182-191	high mobility group box 1	Homo sapiens	153-158
33414419-7	2021	Together our results reveal the potential ability of gefitinib to initiate sterile inflammation via two distinct mechanisms, and identified IL-1beta and HMGB1 as key determinants of gefitinib-induced inflammation that may provide insights into gefitinib-induced interstitial pneumonitis.	Gefitinib	182-191	high mobility group box 1	Homo sapiens	153-158
33485134-13	2021	were analyzed for remission rates after first anthracycline based induction therapy, in those who did not experience a complete remission significantly enhanced HMGB1 surface expression was seen (98 vs. 94%; p < 0.05; n = 20).	Anthracyclines	46-59	high mobility group box 1	Homo sapiens	161-166
32902022-0	2021	MiR-381-3p inhibits high glucose-induced vascular smooth muscle cell proliferation and migration by targeting HMGB1.	mir-381-3p	0-10	high mobility group box 1	Homo sapiens	110-115
31888389-2	2021	Collismycin C inhibited the HMGB1 release and downregulated HMGB1-mediated inflammatory responses in human endothelial cells.	collismycin A	0-13	high mobility group box 1	Homo sapiens	28-33
31888389-2	2021	Collismycin C inhibited the HMGB1 release and downregulated HMGB1-mediated inflammatory responses in human endothelial cells.	collismycin A	0-13	high mobility group box 1	Homo sapiens	60-65
32902022-0	2021	MiR-381-3p inhibits high glucose-induced vascular smooth muscle cell proliferation and migration by targeting HMGB1.	Glucose	25-32	high mobility group box 1	Homo sapiens	110-115
32902022-13	2021	CONCLUSION: MiR-381-3p targets HMGB1 to suppress the inflammation, oxidative stress, proliferation and migration of high-glucose-induced VSMCs by targeting HMGB1.	Glucose	121-128	high mobility group box 1	Homo sapiens	31-36
32902022-13	2021	CONCLUSION: MiR-381-3p targets HMGB1 to suppress the inflammation, oxidative stress, proliferation and migration of high-glucose-induced VSMCs by targeting HMGB1.	Glucose	121-128	high mobility group box 1	Homo sapiens	156-161
33347772-6	2021	Results: GLY protected against loss of cell viability induced by HG and significantly reduced HMGB1, IL-1beta, TLR2, TLR4, NLRP3, COX2, SOD2, HO-1, GPX2, and GR1.	Glycyrrhizic Acid	9-12	high mobility group box 1	Homo sapiens	94-99
33128580-3	2021	Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines.	Tetradecanoylphorbol Acetate	198-229	high mobility group box 1	Homo sapiens	129-134
33128580-3	2021	Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines.	Tetradecanoylphorbol Acetate	231-234	high mobility group box 1	Homo sapiens	129-134
33128580-3	2021	Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines.	Tretinoin	240-263	high mobility group box 1	Homo sapiens	129-134
33128580-3	2021	Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines.	Tretinoin	265-269	high mobility group box 1	Homo sapiens	129-134
33128580-4	2021	On the other hand, chidamide, an orally histone deacetylase inhibitor, decreases HMGB1 expression significantly in AML cells with concomitant upregulation of TGFBI expression, and confers therapeutic effect on AML by inducing cell differentiation, apoptosis and inhibiting cell proliferation.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	19-28	high mobility group box 1	Homo sapiens	81-86
33128580-5	2021	In conclusion, our findings provide additional insights that HMGB1 is a promising therapeutic target of AML, and also present experimental evidence for the clinical application of chidamide as a novel agent in AML therapy by downregulating HMGB1 expression.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	180-189	high mobility group box 1	Homo sapiens	240-245
33128580-8	2021	Chidamide, a selective HDAC inhibitor, confers promising therapeutic effect for AML via downregulating HMGB1 expression.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	0-9	high mobility group box 1	Homo sapiens	103-108
33030958-10	2021	We identified that HMGB1 secreted by breast cancer cells promotes fibroblast activation via RAGE/aerobic glycolysis, and activated fibroblasts enhance breast cancer cell metastasis through increased lactate.	Lactic Acid	199-206	high mobility group box 1	Homo sapiens	19-24
33313438-7	2020	Importantly, genetic (using AGER siRNA) or pharmacological (using glycyrrhizin, chloroquine, hydroxychloroquine, and FPS-ZM1) inhibition of the HMGB1-AGER pathway blocks ACE2 expression.	Glycyrrhizic Acid	66-78	high mobility group box 1	Homo sapiens	144-149
33420996-0	2021	Immunoaffinity-Based Liquid Chromatography Mass Spectrometric Assay to Accurately Quantify the Protein Concentration of HMGB1 in EDTA Plasma.	Edetic Acid	129-133	high mobility group box 1	Homo sapiens	120-125
33086122-3	2020	The pharmacological activities essentially derive from the capacity of DMC to interact with the protein targets HMGB1 and AMPK.	2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone	71-74	high mobility group box 1	Homo sapiens	112-117
33086122-4	2020	Upon binding to HMGB1, DMC inhibits the nucleocytoplasmic transfer of the protein and its extracellular secretion, thereby blocking its alarmin function.	2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone	23-26	high mobility group box 1	Homo sapiens	16-21
33086122-6	2020	AMPK activation by DMC reinforces inhibition of HMGB1, to further reduce the release of the alarmin protein, likely contributing to the anticancer effects.	2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone	19-22	high mobility group box 1	Homo sapiens	48-53
33086122-7	2020	The characterization of a tight control of DMC over the AMPK-HMGB1 axis not only helps to explain the known activities of DMC but also suggests opportunities to use this chalcone to treat other pathological conditions such as the acute respiratory distress syndrome (which affects patients with COVID-19).	2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone	43-46	high mobility group box 1	Homo sapiens	61-66
33086122-7	2020	The characterization of a tight control of DMC over the AMPK-HMGB1 axis not only helps to explain the known activities of DMC but also suggests opportunities to use this chalcone to treat other pathological conditions such as the acute respiratory distress syndrome (which affects patients with COVID-19).	2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone	122-125	high mobility group box 1	Homo sapiens	61-66
33086122-7	2020	The characterization of a tight control of DMC over the AMPK-HMGB1 axis not only helps to explain the known activities of DMC but also suggests opportunities to use this chalcone to treat other pathological conditions such as the acute respiratory distress syndrome (which affects patients with COVID-19).	Chalcone	170-178	high mobility group box 1	Homo sapiens	61-66
33380312-0	2020	Retraction Note to: Redox modification of cysteine residues regulates the cytokine activity of high mobility group box-1 (HMGB1).	Cysteine	42-50	high mobility group box 1	Homo sapiens	95-120
33380312-0	2020	Retraction Note to: Redox modification of cysteine residues regulates the cytokine activity of high mobility group box-1 (HMGB1).	Cysteine	42-50	high mobility group box 1	Homo sapiens	122-127
33321563-0	2021	Synergistic Tumoricidal Effects of Alpha-Lipoic Acid and Radiotherapy on Human Breast Cancer Cells Via HMGB1.	Thioctic Acid	35-52	high mobility group box 1	Homo sapiens	103-108
33321563-8	2021	In addition, ALA significantly enhanced radiation-induced cellular senescence, which was shown by increased HMGB1 expression in the cytosol fraction compared to the control, increased p53 expression compared to the control, activation of p38 as well as NF-kappaB, and G2/M cell cycle arrest.	Thioctic Acid	13-16	high mobility group box 1	Homo sapiens	108-113
33313438-7	2020	Importantly, genetic (using AGER siRNA) or pharmacological (using glycyrrhizin, chloroquine, hydroxychloroquine, and FPS-ZM1) inhibition of the HMGB1-AGER pathway blocks ACE2 expression.	Chloroquine	80-91	high mobility group box 1	Homo sapiens	144-149
33313438-7	2020	Importantly, genetic (using AGER siRNA) or pharmacological (using glycyrrhizin, chloroquine, hydroxychloroquine, and FPS-ZM1) inhibition of the HMGB1-AGER pathway blocks ACE2 expression.	Hydroxychloroquine	93-111	high mobility group box 1	Homo sapiens	144-149
33288764-4	2020	Here, we show that gemcitabine, a standard chemotherapy for various solid tumors, triggers hallmark immunostimualtory DAMP release (e.g., calreticulin, HSP70, and HMGB1); however, is unable to induce ICD.	gemcitabine	19-30	high mobility group box 1	Homo sapiens	163-168
33287126-0	2020	Role of HMGB1/TLR4 Axis in Ischemia/Reperfusion-Impaired Extracellular Glutamate Clearance in Primary Astrocytes.	Glutamic Acid	71-80	high mobility group box 1	Homo sapiens	8-13
33287126-4	2020	(2) Methods: We investigated the mechanism of the HMGB1/TLR4 axis in extracellular glutamate clearance in primary astrocytes exposed to ischemia/reperfusion by using OGD/R (oxygen-glucose deprivation/reoxygenation) model.	Glutamic Acid	83-92	high mobility group box 1	Homo sapiens	50-55
33287126-5	2020	(3) Results: OGD/R insult activated the HMGB1/TLR4 axis for reducing the activity of glutamate clearance by inhibiting GLAST (glutamate aspartate transporter) expression in primary astrocytes.	Glutamic Acid	85-94	high mobility group box 1	Homo sapiens	40-45
33287126-6	2020	Interestingly, OGD/R-untreated astrocytes showed impairment of glutamate clearance after exposure to exogenous HMGB1 or conditioned medium from OGD/R-treated astrocytes culture.	Glutamic Acid	63-72	high mobility group box 1	Homo sapiens	111-116
33287126-7	2020	Inhibition of HMGB1 or TLR4 effectively prevented impaired glutamate clearance, which was induced by OGD/R, exogenous HMGB1, or conditioned medium from OGD/R-treated astrocytes.	Glutamic Acid	59-68	high mobility group box 1	Homo sapiens	14-19
33287126-7	2020	Inhibition of HMGB1 or TLR4 effectively prevented impaired glutamate clearance, which was induced by OGD/R, exogenous HMGB1, or conditioned medium from OGD/R-treated astrocytes.	Glutamic Acid	59-68	high mobility group box 1	Homo sapiens	118-123
33287126-8	2020	Furthermore, glycyrrhizic acid attenuated OGD/R-induced impairment of astrocytic glutamate clearance mediated by the HMGB1-TLR4 axis.	Glycyrrhizic Acid	13-30	high mobility group box 1	Homo sapiens	117-122
33287126-8	2020	Furthermore, glycyrrhizic acid attenuated OGD/R-induced impairment of astrocytic glutamate clearance mediated by the HMGB1-TLR4 axis.	Glutamic Acid	81-90	high mobility group box 1	Homo sapiens	117-122
33274007-0	2020	Protective Effect of miR-204 on Doxorubicin-Induced Cardiomyocyte Injury via HMGB1.	Doxorubicin	32-43	high mobility group box 1	Homo sapiens	77-82
33012199-6	2020	Moreover, only human pulmonary artery smooth muscle cell death induced a release of dimeric HMGB1, found to be mitochondrial reactive oxygen species dependent, and TLR4 (toll-like receptor 4) activation.	Reactive Oxygen Species	125-148	high mobility group box 1	Homo sapiens	92-97
33049495-8	2020	Juglanin also inhibits the inflammatory response by suppressing OSS-induced expressions of IL-1beta, MCP-1, and HMGB1.	juglanin	0-8	high mobility group box 1	Homo sapiens	112-117
32998017-0	2020	Paclitaxel alleviates the sepsis-induced acute kidney injury via lnc-MALAT1/miR-370-3p/HMGB1 axis.	Paclitaxel	0-10	high mobility group box 1	Homo sapiens	87-92
32998017-7	2020	What"s more, miR-370-3p targeted HMGB1 which was induced in serum and cells of sepsis.	mir-370-3p	13-23	high mobility group box 1	Homo sapiens	33-38
32998017-8	2020	Knockdown of miR-370-3p inhibited the expression of HMGB1 and suppressed the proliferation but promoted the apoptosis of HK-2 cells injured by LPS as well as the expression of TNF-alpha, IL-6 and IL-1beta.	mir-370-3p	13-23	high mobility group box 1	Homo sapiens	52-57
32998017-9	2020	Besides, paclitaxel restrained the expression of HMGB1 via regulating lnc-MALAT1/miR-370-3p axis.	Paclitaxel	9-19	high mobility group box 1	Homo sapiens	49-54
33274007-13	2020	In summary, our study showed that miR-204 protected against DOX-induced cardiac injury via the inhibition of HMGB1, and increasing miR-204 expression may be a new treatment option for patients with DOX-induced cardiac injury.	Doxorubicin	60-63	high mobility group box 1	Homo sapiens	109-114
33274007-13	2020	In summary, our study showed that miR-204 protected against DOX-induced cardiac injury via the inhibition of HMGB1, and increasing miR-204 expression may be a new treatment option for patients with DOX-induced cardiac injury.	Doxorubicin	198-201	high mobility group box 1	Homo sapiens	109-114
33091813-0	2020	Paeonol promotes the phagocytic ability of macrophages through confining HMGB1 to the nucleus.	paeonol	0-7	high mobility group box 1	Homo sapiens	73-78
33091813-5	2020	We found that paeonol could inhibit the translocation of HMGB1 from the nucleus to the cytoplasm, it may have an impact on phagocytosis.	paeonol	14-21	high mobility group box 1	Homo sapiens	57-62
33091813-8	2020	Our results showed that paeonol promotes the phagocytosis of macrophages through confining HMGB1 to the nucleus.	paeonol	24-31	high mobility group box 1	Homo sapiens	91-96
32998017-10	2020	SIGNIFICANCE: Paclitaxel could protect against LPS-induced AKI via the regulation of lnc-MALAT1/miR-370-3p/HMGB1 axis and the expression of TNF-alpha, IL-6 and IL-1beta, revealing that paclitaxel might act as a therapy drug in reducing sepsis-associated AKI.	Paclitaxel	14-24	high mobility group box 1	Homo sapiens	107-112
33174035-10	2020	miR-143-3p overexpression attenuated the Der p1-induced inflammatory response and apoptosis of BEAS-2B cells by targeting high mobility group box 1 (HMGB1).	mir-143-3p	0-10	high mobility group box 1	Homo sapiens	122-147
33174035-10	2020	miR-143-3p overexpression attenuated the Der p1-induced inflammatory response and apoptosis of BEAS-2B cells by targeting high mobility group box 1 (HMGB1).	mir-143-3p	0-10	high mobility group box 1	Homo sapiens	149-154
33324614-0	2020	Discovery of 5,5"-Methylenedi-2,3-Cresotic Acid as a Potent Inhibitor of the Chemotactic Activity of the HMGB1 CXCL12 Heterocomplex Using Virtual Screening and NMR Validation.	5,5"-methylenedi-2,3-cresotic acid	13-47	high mobility group box 1	Homo sapiens	105-110
33324614-7	2020	We identified 5,5"-methylenedi-2,3-cresotic acid (2a) as a binder of both HMGB1 and CXCL12; 2a also targets the HMGB1 CXCL12 heterocomplex.	5,5"-methylenedi-2,3-cresotic acid	14-48	high mobility group box 1	Homo sapiens	74-79
33324614-7	2020	We identified 5,5"-methylenedi-2,3-cresotic acid (2a) as a binder of both HMGB1 and CXCL12; 2a also targets the HMGB1 CXCL12 heterocomplex.	5,5"-methylenedi-2,3-cresotic acid	14-48	high mobility group box 1	Homo sapiens	112-117
33182652-5	2020	EW-7197, AG-1478 and the TNFalpha antibody prevented hyperpermeability induced by HMGB1 and inflammatory cytokines in 2.5D culture.	NSC334073	0-2	high mobility group box 1	Homo sapiens	82-87
32931793-13	2020	Inhibition of HMGB1 expression correlated with increased basal phospholipid production and SP-B expression in the lung lining.	Phospholipids	63-75	high mobility group box 1	Homo sapiens	14-19
32898630-5	2020	In vitro studies showed that combination of laser assisted indocyanine green-mediated photothermal therapy and doxorubicin-mediated chemotherapy effectively eradicated cancer cells and resulted in the highest level of damage-associated molecular pattern presentation (calreticulin, high mobility group box 1, and adenosine triphosphate) compared to the individual treatments alone.	Indocyanine Green	59-76	high mobility group box 1	Homo sapiens	282-307
32898630-5	2020	In vitro studies showed that combination of laser assisted indocyanine green-mediated photothermal therapy and doxorubicin-mediated chemotherapy effectively eradicated cancer cells and resulted in the highest level of damage-associated molecular pattern presentation (calreticulin, high mobility group box 1, and adenosine triphosphate) compared to the individual treatments alone.	Doxorubicin	111-122	high mobility group box 1	Homo sapiens	282-307
33182652-7	2020	EW-7197, AG-1478 and the TNFalpha antibody prevented the increase in cell metabolism induced by HMGB1 and inflammatory cytokines in 2D culture.	NSC334073	0-2	high mobility group box 1	Homo sapiens	96-101
32860758-2	2020	The high mobility group Box 1 (HMGB1) protein is a DNA-binding protein which exerts robust inflammatory actions, however, its role in ketoprofen-induced gastric damage has not been explored.	Ketoprofen	134-144	high mobility group box 1	Homo sapiens	4-29
31504866-12	2020	We noted a negative correlation between HMGB1, NGF, Il-6, and lidocaine concentrations after surgery.	Lidocaine	62-71	high mobility group box 1	Homo sapiens	40-45
33158052-0	2020	Morin Hydrate Sensitizes Hepatoma Cells and Xenograft Tumor towards Cisplatin by Downregulating PARP-1-HMGB1 Mediated Autophagy.	morin	0-13	high mobility group box 1	Homo sapiens	103-108
33158052-6	2020	In addition, CP-induced PARP-1 activation led to ADP-ribosylation of HMGB1, which consequently developed autophagy as evident by the LC3I/II ratio.	Adenosine Diphosphate	49-52	high mobility group box 1	Homo sapiens	69-74
33158052-8	2020	CP-Mh abrogates the PARP-1 expression and significantly reduced HMGB1-cytoplasmic translocation with subsequent inhibition of the HMGB1-Beclin1 complex formation.	cp-mh	0-5	high mobility group box 1	Homo sapiens	64-69
33158052-8	2020	CP-Mh abrogates the PARP-1 expression and significantly reduced HMGB1-cytoplasmic translocation with subsequent inhibition of the HMGB1-Beclin1 complex formation.	cp-mh	0-5	high mobility group box 1	Homo sapiens	130-135
33106070-8	2020	In addition, DHA decreased protein expression of TNF receptor, receptor interacting protein kinase 1, RIP3 and phosphorylation of mixed lineage kinase-like protein, phosphoglycerate mutase family 5, dynamin-related protein 1 and high mobility group box-1 protein.	Docosahexaenoic Acids	13-16	high mobility group box 1	Homo sapiens	229-254
33455114-1	2020	PURPOSE: To explore the role of micro ribonucleic acid (miR)-218 in cervical cancer (CC) and the regulatory mechanism between the high mobility group box 1 (HMGB1)/receptor for advanced glycation end-product (RAGE) pathway and miR-218.	micro ribonucleic acid	32-54	high mobility group box 1	Homo sapiens	157-162
33455114-8	2020	Moreover, miR-218 was observed to directly regulate the HMGB1/RAGE signaling pathway in a targeted manner to affect the proliferation and migration of CC cells.	mir-218	10-17	high mobility group box 1	Homo sapiens	56-61
33455114-9	2020	CONCLUSIONS: MiR-218 inhibits the HMGB1/RAGE pathway to suppress the proliferation, migration and invasion of CC cells.	mir-218	13-20	high mobility group box 1	Homo sapiens	34-39
33070867-0	2020	Retraction notice to "Molecular forms of HMGB1 and keratin-18 as mechanistic biomarkers for mode of cell death and prognosis during clinical acetaminophen hepatotoxicity": J Hepatol 56(2012)1070-1079.	Acetaminophen	141-154	high mobility group box 1	Homo sapiens	41-46
33012373-0	2020	Retraction Notice to "Ketamine Reduces LPS-Induced HMGB1 Through HO-1 and Nrf2/ p38 MAPK" [Journal of Surgical Research 194 (2015) 599-613].	Ketamine	22-30	high mobility group box 1	Homo sapiens	51-56
32860758-2	2020	The high mobility group Box 1 (HMGB1) protein is a DNA-binding protein which exerts robust inflammatory actions, however, its role in ketoprofen-induced gastric damage has not been explored.	Ketoprofen	134-144	high mobility group box 1	Homo sapiens	31-36
33017561-7	2021	Additionally, geldanamycin, an HSP90AA1 inhibitor, reduced HMGB1 secretion.	geldanamycin	14-26	high mobility group box 1	Homo sapiens	59-64
33193406-3	2020	This study investigates whether increased HMGB1 levels are found in the intestinal mucosa of ulcerative colitis (UC) patients, and whether an anti-HMGB1 neutralizing-antibody (HnAb) can inhibit the intestinal inflammation elicited by dextran sulfate sodium (DSS) in mice.	Dextran Sulfate	234-256	high mobility group box 1	Homo sapiens	147-152
33193406-3	2020	This study investigates whether increased HMGB1 levels are found in the intestinal mucosa of ulcerative colitis (UC) patients, and whether an anti-HMGB1 neutralizing-antibody (HnAb) can inhibit the intestinal inflammation elicited by dextran sulfate sodium (DSS) in mice.	Dextran Sulfate	258-261	high mobility group box 1	Homo sapiens	147-152
33076532-0	2020	Nonhistone Proteins HMGB1 and HMGB2 Differentially Modulate the Response of Human Embryonic Stem Cells and the Progenitor Cells to the Anticancer Drug Etoposide.	Etoposide	151-160	high mobility group box 1	Homo sapiens	20-25
33076532-1	2020	HMGB1 and HMGB2 proteins are abundantly expressed in human embryonic stem cells (hESCs) and hESC-derived progenitor cells (neuroectodermal cells, hNECs), though their functional roles in pluripotency and the mechanisms underlying their differentiation in response to the anticancer drug etoposide remain to be elucidated.	Etoposide	287-296	high mobility group box 1	Homo sapiens	0-5
33076532-3	2020	The objective of this work was to determine whether HMGB1/2 proteins could modulate the sensitivity of hESCs and hESC-derived progenitor cells (hNECs) to etoposide.	Etoposide	154-163	high mobility group box 1	Homo sapiens	52-59
33076532-4	2020	We observed that HMGB1 KD knockdown (KD) and, to a lesser extent, HMGB2 KD enhanced the sensitivity of hESCs to etoposide.	Etoposide	112-121	high mobility group box 1	Homo sapiens	17-22
33076532-5	2020	Enhanced accumulation of 53BP1 on telomeres was detected by confocal microscopy in both untreated and etoposide-treated HMGB1 KD hESCs and hNECs, indicating that the loss of HMGB1 could destabilize telomeres.	Etoposide	102-111	high mobility group box 1	Homo sapiens	120-125
33076532-5	2020	Enhanced accumulation of 53BP1 on telomeres was detected by confocal microscopy in both untreated and etoposide-treated HMGB1 KD hESCs and hNECs, indicating that the loss of HMGB1 could destabilize telomeres.	Etoposide	102-111	high mobility group box 1	Homo sapiens	174-179
33076532-10	2020	Collectively, we have demonstrated that HMGB1 or HMGB2 differentially modulate the impact of etoposide treatment on human embryonic stem cells and their progenitor cells, suggesting possible strategies for the enhancement of the efficacy of this anticancer drug.	Etoposide	93-102	high mobility group box 1	Homo sapiens	40-45
33056943-0	2020	Epigallocatechin Gallate (EGCG) Improves Anti-Angiogenic State, Cell Viability, and Hypoxia-Induced Endothelial Dysfunction by Downregulating High Mobility Group Box 1 (HMGB1) in Preeclampsia.	epigallocatechin gallate	0-24	high mobility group box 1	Homo sapiens	142-167
33056943-0	2020	Epigallocatechin Gallate (EGCG) Improves Anti-Angiogenic State, Cell Viability, and Hypoxia-Induced Endothelial Dysfunction by Downregulating High Mobility Group Box 1 (HMGB1) in Preeclampsia.	epigallocatechin gallate	0-24	high mobility group box 1	Homo sapiens	169-174
33056943-0	2020	Epigallocatechin Gallate (EGCG) Improves Anti-Angiogenic State, Cell Viability, and Hypoxia-Induced Endothelial Dysfunction by Downregulating High Mobility Group Box 1 (HMGB1) in Preeclampsia.	epigallocatechin gallate	26-30	high mobility group box 1	Homo sapiens	142-167
33056943-0	2020	Epigallocatechin Gallate (EGCG) Improves Anti-Angiogenic State, Cell Viability, and Hypoxia-Induced Endothelial Dysfunction by Downregulating High Mobility Group Box 1 (HMGB1) in Preeclampsia.	epigallocatechin gallate	26-30	high mobility group box 1	Homo sapiens	169-174
33056943-2	2020	This study assessed whether epigallocatechin gallate (EGCG) could reduce the production of anti-angiogenic factors, improve cell viability, and suppress endothelial dysfunction in vitro via regulating high mobility group box 1 (HMGB1) in preeclampsia.	epigallocatechin gallate	28-52	high mobility group box 1	Homo sapiens	201-226
33056943-2	2020	This study assessed whether epigallocatechin gallate (EGCG) could reduce the production of anti-angiogenic factors, improve cell viability, and suppress endothelial dysfunction in vitro via regulating high mobility group box 1 (HMGB1) in preeclampsia.	epigallocatechin gallate	28-52	high mobility group box 1	Homo sapiens	228-233
33056943-2	2020	This study assessed whether epigallocatechin gallate (EGCG) could reduce the production of anti-angiogenic factors, improve cell viability, and suppress endothelial dysfunction in vitro via regulating high mobility group box 1 (HMGB1) in preeclampsia.	epigallocatechin gallate	54-58	high mobility group box 1	Homo sapiens	201-226
33056943-2	2020	This study assessed whether epigallocatechin gallate (EGCG) could reduce the production of anti-angiogenic factors, improve cell viability, and suppress endothelial dysfunction in vitro via regulating high mobility group box 1 (HMGB1) in preeclampsia.	epigallocatechin gallate	54-58	high mobility group box 1	Homo sapiens	228-233
33056943-5	2020	RESULTS EGCG inhibited HMGB1 expression in hypoxic trophoblast cells in a dose-dependent manner.	epigallocatechin gallate	8-12	high mobility group box 1	Homo sapiens	23-28
33056943-6	2020	In addition, EGCG relieved anti-angiogenic state and endothelial dysfunction in hypoxic trophoblast cells by downregulating HMGB1.	epigallocatechin gallate	13-17	high mobility group box 1	Homo sapiens	124-129
33056943-7	2020	Moreover, EGCG dose-dependently promoted cell proliferation by downregulating HMGB1.	epigallocatechin gallate	10-14	high mobility group box 1	Homo sapiens	78-83
33056943-8	2020	CONCLUSIONS Taken together, our data show the protective role of EGCG in preeclampsia and revealed EGCG-mediated effects on the production of anti-angiogenic factors, cell viability, and endothelial dysfunction through downregulating HMGB1.	epigallocatechin gallate	99-103	high mobility group box 1	Homo sapiens	234-239
32999071-4	2020	We previously demonstrated that, upon asbestos exposure, HM and reactive macrophages releases the high mobility group box 1 (HMGB1) protein that becomes detectable in the tissues near asbestos deposits where HMGB1 triggers chronic inflammation.	Asbestos	38-46	high mobility group box 1	Homo sapiens	125-130
32999071-4	2020	We previously demonstrated that, upon asbestos exposure, HM and reactive macrophages releases the high mobility group box 1 (HMGB1) protein that becomes detectable in the tissues near asbestos deposits where HMGB1 triggers chronic inflammation.	Asbestos	38-46	high mobility group box 1	Homo sapiens	208-213
32999071-4	2020	We previously demonstrated that, upon asbestos exposure, HM and reactive macrophages releases the high mobility group box 1 (HMGB1) protein that becomes detectable in the tissues near asbestos deposits where HMGB1 triggers chronic inflammation.	Asbestos	184-192	high mobility group box 1	Homo sapiens	125-130
32999071-4	2020	We previously demonstrated that, upon asbestos exposure, HM and reactive macrophages releases the high mobility group box 1 (HMGB1) protein that becomes detectable in the tissues near asbestos deposits where HMGB1 triggers chronic inflammation.	Asbestos	184-192	high mobility group box 1	Homo sapiens	208-213
33023630-8	2020	RESULTS: DEX, but not IgG, significantly inhibited apoptosis caused by inflammatory stimuli, resulting in effective reduction of HMGB1 and IL-1alpha protein release by HCAECs.	Dexamethasone	9-12	high mobility group box 1	Homo sapiens	129-134
33017561-11	2021	The multivesicular body formation inhibitor GW4869 dramatically decreased HMGB1 secretion under HMGB1 secretion-inducing conditions.	GW 4869	44-50	high mobility group box 1	Homo sapiens	74-79
33017561-11	2021	The multivesicular body formation inhibitor GW4869 dramatically decreased HMGB1 secretion under HMGB1 secretion-inducing conditions.	GW 4869	44-50	high mobility group box 1	Homo sapiens	96-101
32436353-0	2020	Hypoxia-responsive miR-141-3p is involved in the progression of breast cancer via mediating HMGB1/HIF-1alpha signaling pathway.	mir-141-3p	19-29	high mobility group box 1	Homo sapiens	92-97
32388677-4	2020	Mechanistically, in the GC cells under the 5-FU treatment, reactive oxygen species is accumulated and then induces the activation of HIF1alpha signaling to drive the expression of high-mobility group box 1, which leads to more macrophage"s infiltration into GC tumor.	Fluorouracil	43-47	high mobility group box 1	Homo sapiens	180-205
32388677-4	2020	Mechanistically, in the GC cells under the 5-FU treatment, reactive oxygen species is accumulated and then induces the activation of HIF1alpha signaling to drive the expression of high-mobility group box 1, which leads to more macrophage"s infiltration into GC tumor.	Oxygen	68-74	high mobility group box 1	Homo sapiens	180-205
32623356-0	2020	N-glycosylation of High Mobility Group Box 1 protein (HMGB1) modulates the interaction with glycyrrhizin: A molecular modeling study.	Glycyrrhizic Acid	92-104	high mobility group box 1	Homo sapiens	54-59
32623356-5	2020	In cells, HMGB1 is N-glycosylated at three asparagine residues located in boxes A and B, and these N-glycans are essential for the nucleocytoplasmic transport of the protein.	Nitrogen	19-20	high mobility group box 1	Homo sapiens	10-15
32623356-5	2020	In cells, HMGB1 is N-glycosylated at three asparagine residues located in boxes A and B, and these N-glycans are essential for the nucleocytoplasmic transport of the protein.	Asparagine	43-53	high mobility group box 1	Homo sapiens	10-15
32623356-5	2020	In cells, HMGB1 is N-glycosylated at three asparagine residues located in boxes A and B, and these N-glycans are essential for the nucleocytoplasmic transport of the protein.	n-glycans	99-108	high mobility group box 1	Homo sapiens	10-15
32623356-7	2020	Here we have investigated the effect of the N-glycosylation of HMGB1 on its interaction with GLR using molecular modelling, after incorporation of three N-glycans on a Human HMGB1 structure (PDB code 2YRQ).	Nitrogen	44-45	high mobility group box 1	Homo sapiens	63-68
32623356-7	2020	Here we have investigated the effect of the N-glycosylation of HMGB1 on its interaction with GLR using molecular modelling, after incorporation of three N-glycans on a Human HMGB1 structure (PDB code 2YRQ).	n-glycans	153-162	high mobility group box 1	Homo sapiens	63-68
32623356-13	2020	The effects of the N-glycans are mostly indirect, but in one case a direct contact with the drug, via a carbohydrate-carbohydrate interaction, was observed with 18beta-GLR bound to Box-B of glycosylated HMGB1.	n-glycans	19-28	high mobility group box 1	Homo sapiens	203-208
32623356-13	2020	The effects of the N-glycans are mostly indirect, but in one case a direct contact with the drug, via a carbohydrate-carbohydrate interaction, was observed with 18beta-GLR bound to Box-B of glycosylated HMGB1.	Carbohydrates	104-116	high mobility group box 1	Homo sapiens	203-208
32623356-13	2020	The effects of the N-glycans are mostly indirect, but in one case a direct contact with the drug, via a carbohydrate-carbohydrate interaction, was observed with 18beta-GLR bound to Box-B of glycosylated HMGB1.	Carbohydrates	117-129	high mobility group box 1	Homo sapiens	203-208
32623356-14	2020	For the first time, it is shown (at least in silico) that N-glycosylation, one of the many post-translational modifications of HMGB1, can affect drug binding.	Nitrogen	58-59	high mobility group box 1	Homo sapiens	127-132
32623356-0	2020	N-glycosylation of High Mobility Group Box 1 protein (HMGB1) modulates the interaction with glycyrrhizin: A molecular modeling study.	Nitrogen	0-1	high mobility group box 1	Homo sapiens	19-44
32623356-0	2020	N-glycosylation of High Mobility Group Box 1 protein (HMGB1) modulates the interaction with glycyrrhizin: A molecular modeling study.	Nitrogen	0-1	high mobility group box 1	Homo sapiens	54-59
32623356-0	2020	N-glycosylation of High Mobility Group Box 1 protein (HMGB1) modulates the interaction with glycyrrhizin: A molecular modeling study.	Glycyrrhizic Acid	92-104	high mobility group box 1	Homo sapiens	19-44
32945389-7	2020	The results of the present study demonstrated that the expression levels of circ_0010283 and HMGB1 were significantly upregulated in ox-LDL-induced VSMCs compared with those in VSMCs without ox-LDL induction, whereas the expression of miR-370-3p was downregulated.	mir-370-3p	235-245	high mobility group box 1	Homo sapiens	93-98
32945389-9	2020	In addition, miR-370-3p was demonstrated to be a target of circ_0010283 and to target HMGB1; thus, circ_0010283 regulated HMGB1 expression via miR-370-3p.	mir-370-3p	13-23	high mobility group box 1	Homo sapiens	86-91
32945389-9	2020	In addition, miR-370-3p was demonstrated to be a target of circ_0010283 and to target HMGB1; thus, circ_0010283 regulated HMGB1 expression via miR-370-3p.	mir-370-3p	13-23	high mobility group box 1	Homo sapiens	122-127
32945389-11	2020	Additionally, the miR-370-3p-mediated suppressive effects on cell viability and migration were rescued by overexpression of HMGB1.	mir-370-3p	18-28	high mobility group box 1	Homo sapiens	124-129
32436353-2	2020	The present study was aimed to investigate whether hypoxia-responsive miR-141-3p was implicated in the pathogenesis of breast cancer via mediating HMGB1/HIF-1alpha signaling pathway.	mir-141-3p	70-80	high mobility group box 1	Homo sapiens	147-152
32436353-10	2020	Mechanistically, hypoxia-related HMGB1/HIF-1alpha signaling pathway might be a possible target of miR-141-3p to prevent the development of breast cancer.	mir-141-3p	98-108	high mobility group box 1	Homo sapiens	33-38
32436353-11	2020	CONCLUSIONS: Our finding provides a new mechanism that miR-141-3p could prevent hypoxia-induced breast tumorigenesis by post-transcriptional repression of HMGB1/HIF-1alpha signaling pathway.	mir-141-3p	55-65	high mobility group box 1	Homo sapiens	155-160
31872339-0	2020	Glycyrrhizin Prevents Hemorrhagic Transformation and Improves Neurological Outcome in Ischemic Stroke with Delayed Thrombolysis Through Targeting Peroxynitrite-Mediated HMGB1 Signaling.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	169-174
32857676-5	2020	Pretreatment with EW-7197 prevented the changes of all tight junction molecules induced by HMGB1.	vactosertib	18-25	high mobility group box 1	Homo sapiens	91-96
32857676-6	2020	In 2.5D Matrigel culture, treatment with HMGB1 induced permeability of FITC-dextran (FD-4) into the lumen, whereas pretreatment with EW-7197 prevented the hyperpermeability of FD-4 into the lumen caused by HMGB1.	fluorescein isothiocyanate dextran	71-83	high mobility group box 1	Homo sapiens	41-46
32857676-6	2020	In 2.5D Matrigel culture, treatment with HMGB1 induced permeability of FITC-dextran (FD-4) into the lumen, whereas pretreatment with EW-7197 prevented the hyperpermeability of FD-4 into the lumen caused by HMGB1.	vactosertib	133-140	high mobility group box 1	Homo sapiens	206-211
31872339-0	2020	Glycyrrhizin Prevents Hemorrhagic Transformation and Improves Neurological Outcome in Ischemic Stroke with Delayed Thrombolysis Through Targeting Peroxynitrite-Mediated HMGB1 Signaling.	Peroxynitrous Acid	146-159	high mobility group box 1	Homo sapiens	169-174
31872339-12	2020	In conclusion, peroxynitrite-mediated HMGB1/TLR2 signaling contributes to hemorrhagic transformation, and glycyrrhizin could be a potential adjuvant therapy to attenuate hemorrhagic transformation, possibly through inhibiting the ONOO-/HMGB1/TLR2 signaling cascades.	Peroxynitrous Acid	15-28	high mobility group box 1	Homo sapiens	38-43
31872339-12	2020	In conclusion, peroxynitrite-mediated HMGB1/TLR2 signaling contributes to hemorrhagic transformation, and glycyrrhizin could be a potential adjuvant therapy to attenuate hemorrhagic transformation, possibly through inhibiting the ONOO-/HMGB1/TLR2 signaling cascades.	Peroxynitrous Acid	15-28	high mobility group box 1	Homo sapiens	236-241
31872339-2	2020	However, the roles of ONOO- in mediating HMGB1 expression and its impacts on hemorrhagic transformation (HT) in ischemic brain injury with delayed t-PA treatment remain unclear.	tetramethylammonium peroxynitrite	22-26	high mobility group box 1	Homo sapiens	41-46
31872339-12	2020	In conclusion, peroxynitrite-mediated HMGB1/TLR2 signaling contributes to hemorrhagic transformation, and glycyrrhizin could be a potential adjuvant therapy to attenuate hemorrhagic transformation, possibly through inhibiting the ONOO-/HMGB1/TLR2 signaling cascades.	Glycyrrhizic Acid	106-118	high mobility group box 1	Homo sapiens	236-241
31872339-3	2020	In the present study, we tested the hypothesis that ONOO- could directly mediate the activation and release of HMGB1 in ischemic brains with delayed t-PA treatment.	tetramethylammonium peroxynitrite	52-56	high mobility group box 1	Homo sapiens	111-116
31872339-4	2020	With clinical studies, we found that plasma nitrotyrosine (NT, a surrogate marker of ONOO-) was positively correlated with HMGB1 level in acute ischemic stroke patients.	Nitrotyrosine	44-57	high mobility group box 1	Homo sapiens	123-128
32446815-4	2020	The role of HMGB1 in DNA damage in an aflatoxin-induced lung inflammatory environment was investigated in this study.	Aflatoxins	38-47	high mobility group box 1	Homo sapiens	12-17
31872339-4	2020	With clinical studies, we found that plasma nitrotyrosine (NT, a surrogate marker of ONOO-) was positively correlated with HMGB1 level in acute ischemic stroke patients.	nt	59-61	high mobility group box 1	Homo sapiens	123-128
31872339-4	2020	With clinical studies, we found that plasma nitrotyrosine (NT, a surrogate marker of ONOO-) was positively correlated with HMGB1 level in acute ischemic stroke patients.	tetramethylammonium peroxynitrite	85-89	high mobility group box 1	Homo sapiens	123-128
31872339-7	2020	ONOO- donor SIN-1 directly induced expression of HMGB1 and its receptor TLR2 in naive rat brains in vivo and induced HMGB1 in brain microvascular endothelial b.End3 cells in vitro.	tetramethylammonium peroxynitrite	0-4	high mobility group box 1	Homo sapiens	49-54
31872339-8	2020	Those results suggest that ONOO- could activate HMGB1/TLR2/MMP-9 signaling.	tetramethylammonium peroxynitrite	27-31	high mobility group box 1	Homo sapiens	48-53
31872339-9	2020	We then addressed whether glycyrrhizin, a natural HMGB1 inhibitor, could inhibit ONOO- production and the antioxidant properties of glycyrrhizin contribute to the inhibition of HMGB1 and the neuroprotective effects on attenuating hemorrhagic transformation in ischemic stroke with delayed t-PA treatment.	Glycyrrhizic Acid	26-38	high mobility group box 1	Homo sapiens	50-55
31872339-9	2020	We then addressed whether glycyrrhizin, a natural HMGB1 inhibitor, could inhibit ONOO- production and the antioxidant properties of glycyrrhizin contribute to the inhibition of HMGB1 and the neuroprotective effects on attenuating hemorrhagic transformation in ischemic stroke with delayed t-PA treatment.	Glycyrrhizic Acid	26-38	high mobility group box 1	Homo sapiens	177-182
31872339-10	2020	Glycyrrhizin treatment downregulated the expressions of NADPH oxidase p47 phox and p67 phox and iNOS, inhibited superoxide and ONOO- production, reduced the expression of HMGB1, TLR2, MMP-9, preserved type IV collagen and claudin-5 in ischemic brains.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	171-176
32963505-5	2020	TNF-alpha-treated human periodontal ligament stem cell (hPDLSC) model was established, and was administrated with 1, 2 or 5 mM glycyrrhizin for 24 h. After treatment, the expression of HMGB1and inflammatory cytokines was monitored.	Glycyrrhizic Acid	127-139	high mobility group box 1	Homo sapiens	185-190
32553625-0	2020	Dimethyl fumarate prevents osteoclastogenesis by decreasing NFATc1 expression, inhibiting of erk and p38 MAPK phosphorylation, and suppressing of HMGB1 release.	Dimethyl Fumarate	0-17	high mobility group box 1	Homo sapiens	146-151
32553625-8	2020	We also found that DMF inhibited the extracellular release of high mobility group box 1, associated with an up-regulation of heme oxygenase-1, likely mediated through Nrf2 activation.	Dimethyl Fumarate	19-22	high mobility group box 1	Homo sapiens	62-87
32963505-7	2020	Glycyrrhizin significantly prevented TNF-alpha-induced expression of HMGB1 (691.5 +- 136.4 vs 142.8 +- 57.3 pg/mL), IL-6 (388.1 +- 85.2 vs 189.4 +- 61.2 pg/mL) and IL-1beta (176.3 +- 47.2 vs 53.9 +- 25.7 pg/mL) in hPDLSC.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	69-74
32954194-5	2020	We also found that ropivacaine could inhibit the secretion of the high-mobility group box 1 protein and improve cell viability.	Ropivacaine	19-30	high mobility group box 1	Homo sapiens	66-91
33013386-14	2020	In conclusion, we showed for the first time a hepatoprotective effect for AU in liver IRI, which acted by inhibiting the HMGB1/TLR-4/NF-kappaB signaling pathway, oxidative stress, and apoptosis.	aucubin	74-76	high mobility group box 1	Homo sapiens	121-126
32320818-6	2020	CONCLUSION: LncRNA ZFAS1 could bind to miR-129 to promote HMGB1 expression, thereby affecting the endocrine disturbance, proliferation and apoptosis of ovarian granulosa cells in PCOS.	mir-129	39-46	high mobility group box 1	Homo sapiens	58-63
32833553-8	2020	Knockdown or block of HMGB1 relieved the CCl4-induced liver fibrosis.	Carbon Tetrachloride	41-45	high mobility group box 1	Homo sapiens	22-27
32497617-2	2020	HMGB1 is a danger associated protein pattern receptor which can sense high glucose as a stressor.	Glucose	75-82	high mobility group box 1	Homo sapiens	0-5
32437849-3	2020	RGG-motif proteins Scd6 and Sbp1 are translation-repressors and decapping-activators that localize to and affect the assembly of RNA granules in response to sodium azide stress.	Sodium Azide	157-169	high mobility group box 1	Homo sapiens	28-32
32874136-8	2020	Additionally, in both the rabbit trauma model and cellular injury model, CAA combined with high-dosage of VB6 inhibited the expression of inflammatory factors (IL-6, TNF-alpha and IL-1beta) and proteins (HMGB1, TLR4 and p-p65) in HMGB1/TLR4/NF-kappaB pathway.	caa	73-76	high mobility group box 1	Homo sapiens	204-209
32771683-6	2020	High Mobility Group Box 1 (HMGB1) is a mediator of lethality in trauma and sepsis and our mechanistic studies revealed that disulfide and oxidized forms of HMGB1 bind to the gp91phox subunit of NOX2, and thus decrease the neutrophil respiratory burst and bacterial killing.	Disulfides	124-133	high mobility group box 1	Homo sapiens	0-25
32771683-6	2020	High Mobility Group Box 1 (HMGB1) is a mediator of lethality in trauma and sepsis and our mechanistic studies revealed that disulfide and oxidized forms of HMGB1 bind to the gp91phox subunit of NOX2, and thus decrease the neutrophil respiratory burst and bacterial killing.	Disulfides	124-133	high mobility group box 1	Homo sapiens	27-32
32874136-0	2020	Compound amino acid combined with high-dose vitamin B6 attenuate traumatic coagulopathy via inhibiting inflammation by HMGB1/TLR4/NF-kappaB pathway.	Vitamin B 6	44-54	high mobility group box 1	Homo sapiens	119-124
32553931-0	2020	Magnoflorine inhibits the malignant phenotypes and increases cisplatin sensitivity of osteosarcoma cells via regulating miR-410-3p/HMGB1/NF-kappaB pathway.	magnoflorine	0-12	high mobility group box 1	Homo sapiens	131-136
32553931-8	2020	To explore the potential mechanism, we assayed the influence of magnoflorine on the miR-410-3p/HMGB1/NF-kappaB signaling pathway.	magnoflorine	64-76	high mobility group box 1	Homo sapiens	95-100
32553931-8	2020	To explore the potential mechanism, we assayed the influence of magnoflorine on the miR-410-3p/HMGB1/NF-kappaB signaling pathway.	mir-410	84-91	high mobility group box 1	Homo sapiens	95-100
32553931-12	2020	Magnoflorine significantly suppressed HMGB1 expression and NF-kappaB activation, but upregulated miR-410-3p level.	magnoflorine	0-12	high mobility group box 1	Homo sapiens	38-43
32553931-13	2020	Overexpression of HMGB1 promoted NF-kappaB activation and reversed the effects of magnoflorine on the viability, invasion, EMT and cisplatin sensitivity of OS cells.	magnoflorine	82-94	high mobility group box 1	Homo sapiens	18-23
32553931-13	2020	Overexpression of HMGB1 promoted NF-kappaB activation and reversed the effects of magnoflorine on the viability, invasion, EMT and cisplatin sensitivity of OS cells.	Cisplatin	131-140	high mobility group box 1	Homo sapiens	18-23
32553931-15	2020	And miR-410-3p inhibitor abrogated the influence of magnoflorine on HMGB1 expression in OS cells.	mir-410-3p	4-14	high mobility group box 1	Homo sapiens	68-73
32553931-15	2020	And miR-410-3p inhibitor abrogated the influence of magnoflorine on HMGB1 expression in OS cells.	magnoflorine	52-64	high mobility group box 1	Homo sapiens	68-73
32553931-16	2020	SIGNIFICANCE: Magnoflorine inhibited the malignant phenotypes and increased cisplatin sensitivity of OS cells via modulating miR-410-3p/HMGB1/NF-kappaB pathway.	magnoflorine	14-26	high mobility group box 1	Homo sapiens	136-141
32874136-8	2020	Additionally, in both the rabbit trauma model and cellular injury model, CAA combined with high-dosage of VB6 inhibited the expression of inflammatory factors (IL-6, TNF-alpha and IL-1beta) and proteins (HMGB1, TLR4 and p-p65) in HMGB1/TLR4/NF-kappaB pathway.	caa	73-76	high mobility group box 1	Homo sapiens	230-235
32874136-9	2020	Most importantly, over-expression of HMGB1 reversed the effect of CAA and VB6 in HUVECs and EA.hy926 cells injury model.	caa	66-69	high mobility group box 1	Homo sapiens	37-42
32867128-13	2020	HMGB1 silencing causes loss of response to paclitaxel, whereas silencing of HMGB2 slightly increases sensitivity to olaparib.	Paclitaxel	43-53	high mobility group box 1	Homo sapiens	0-5
32874136-10	2020	Conclusion: CAA combined with high-dosage of VB6 alleviated TC and inhibited the expression and secretion of inflammatory factors by inhibiting HMGB1-mediated TLR4/NF-kappaB pathway.	caa	12-15	high mobility group box 1	Homo sapiens	144-149
32867128-14	2020	Silencing of either HMGB1 or HMGB2 increases sensitivity to carboplatin.	Carboplatin	60-71	high mobility group box 1	Homo sapiens	20-25
32824279-0	2020	N-(2"-Hydroxyphenyl)-2-Propylpentanamide (HO-AAVPA) Inhibits HDAC1 and Increases the Translocation of HMGB1 Levels in Human Cervical Cancer Cells.	N-(2-hydroxyphenyl)-2-propylpentanamide	0-40	high mobility group box 1	Homo sapiens	102-107
32824279-6	2020	Furthermore, an increase in ROS production was observed after the treatment with HO-AAVPA, which also could contribute to HMGB1 translocation.	ros	28-31	high mobility group box 1	Homo sapiens	122-127
32754040-0	2020	Berberine Ameliorates Subarachnoid Hemorrhage Injury via Induction of Sirtuin 1 and Inhibiting HMGB1/Nf-kappaB Pathway.	Berberine	0-9	high mobility group box 1	Homo sapiens	95-100
32724408-12	2020	In conclusion, miR-505-3p inhibited the development of glioma by targeting HMGB1 and regulating AKT expression.	mir-505-3p	15-25	high mobility group box 1	Homo sapiens	75-80
32275943-0	2020	HMGB1 release promotes paclitaxel resistance in castration-resistant prostate cancer cells via activating c-Myc expression.	Paclitaxel	23-33	high mobility group box 1	Homo sapiens	0-5
32275943-3	2020	In this study, we reported that PTX-induced constant HMGB1 expression and release confers to PTX resistance in mCRPC cells via activating and sustaining c-Myc signaling.	Paclitaxel	32-35	high mobility group box 1	Homo sapiens	53-58
32275943-3	2020	In this study, we reported that PTX-induced constant HMGB1 expression and release confers to PTX resistance in mCRPC cells via activating and sustaining c-Myc signaling.	Paclitaxel	93-96	high mobility group box 1	Homo sapiens	53-58
32275943-4	2020	PTX upregulated HMGB1 expression and triggered its release in human mCRPC cells.	Paclitaxel	0-3	high mobility group box 1	Homo sapiens	16-21
32275943-5	2020	Silencing HMGB1 by RNAi and blocking HMGB1 release by glycyrrhizin or HMGB1 neutralizing antibody sensitized the response of PTX-resistant mCRPC cells to PTX.	Glycyrrhizic Acid	54-66	high mobility group box 1	Homo sapiens	37-42
32275943-5	2020	Silencing HMGB1 by RNAi and blocking HMGB1 release by glycyrrhizin or HMGB1 neutralizing antibody sensitized the response of PTX-resistant mCRPC cells to PTX.	Glycyrrhizic Acid	54-66	high mobility group box 1	Homo sapiens	37-42
32275943-5	2020	Silencing HMGB1 by RNAi and blocking HMGB1 release by glycyrrhizin or HMGB1 neutralizing antibody sensitized the response of PTX-resistant mCRPC cells to PTX.	Paclitaxel	125-128	high mobility group box 1	Homo sapiens	10-15
32275943-5	2020	Silencing HMGB1 by RNAi and blocking HMGB1 release by glycyrrhizin or HMGB1 neutralizing antibody sensitized the response of PTX-resistant mCRPC cells to PTX.	Paclitaxel	125-128	high mobility group box 1	Homo sapiens	37-42
32275943-5	2020	Silencing HMGB1 by RNAi and blocking HMGB1 release by glycyrrhizin or HMGB1 neutralizing antibody sensitized the response of PTX-resistant mCRPC cells to PTX.	Paclitaxel	125-128	high mobility group box 1	Homo sapiens	37-42
32275943-5	2020	Silencing HMGB1 by RNAi and blocking HMGB1 release by glycyrrhizin or HMGB1 neutralizing antibody sensitized the response of PTX-resistant mCRPC cells to PTX.	Paclitaxel	154-157	high mobility group box 1	Homo sapiens	37-42
32275943-5	2020	Silencing HMGB1 by RNAi and blocking HMGB1 release by glycyrrhizin or HMGB1 neutralizing antibody sensitized the response of PTX-resistant mCRPC cells to PTX.	Paclitaxel	154-157	high mobility group box 1	Homo sapiens	37-42
32275943-8	2020	Therefore, HMGB1/c-Myc axis is critical in the development of PTX resistance, and targeting HMGB1/c-Myc axis would counteract PTX resistance in mCRPC cells.	Paclitaxel	62-65	high mobility group box 1	Homo sapiens	11-16
32275943-8	2020	Therefore, HMGB1/c-Myc axis is critical in the development of PTX resistance, and targeting HMGB1/c-Myc axis would counteract PTX resistance in mCRPC cells.	Paclitaxel	126-129	high mobility group box 1	Homo sapiens	92-97
32282121-7	2020	Finally, we proved that miR-141-3p decreased the level of MUAC5AC in LPS-treated NECs through regulating HMGB1.	mir-141-3p	24-34	high mobility group box 1	Homo sapiens	105-110
32282121-8	2020	In conclusion, miR-141-3p inhibited LPS-induced MUAC5AC production and the apoptosis of LPS-treated NECs by targeting HMGB1.	mir-141-3p	15-25	high mobility group box 1	Homo sapiens	118-123
32722545-9	2020	Several molecules, such as glycyrrhizin (GA), have proven effective in reducing diabetic damage to the retina through the inhibition of HMGB1.	Glycyrrhizic Acid	27-39	high mobility group box 1	Homo sapiens	136-141
32722545-9	2020	Several molecules, such as glycyrrhizin (GA), have proven effective in reducing diabetic damage to the retina through the inhibition of HMGB1.	Gallium	41-43	high mobility group box 1	Homo sapiens	136-141
32683852-11	2020	Regarding the mechanism, circFANCL served as a sponge of miR-337-3p that was a tumor suppressor in glioma and circFANCL targeted miR-337-3p to regulate HMGB1 that was a target gene of miR-337-3p.	circfancl	25-34	high mobility group box 1	Homo sapiens	152-157
32683852-11	2020	Regarding the mechanism, circFANCL served as a sponge of miR-337-3p that was a tumor suppressor in glioma and circFANCL targeted miR-337-3p to regulate HMGB1 that was a target gene of miR-337-3p.	circfancl	110-119	high mobility group box 1	Homo sapiens	152-157
32683852-12	2020	Furthermore, HMGB1 down-regulation was responsible for the repression of glioma progression caused by knockdown of circFANCL.	circfancl	115-124	high mobility group box 1	Homo sapiens	13-18
32683852-13	2020	CONCLUSIONS: Through the illustration of oncogenic function of circFANCL in glioma by the miR-337-3p/HMGB1 axis, we believed that circFANCL might be a great target in the early diagnosis and late treatment of glioma.	circfancl	63-72	high mobility group box 1	Homo sapiens	101-106
32683852-13	2020	CONCLUSIONS: Through the illustration of oncogenic function of circFANCL in glioma by the miR-337-3p/HMGB1 axis, we believed that circFANCL might be a great target in the early diagnosis and late treatment of glioma.	circfancl	130-139	high mobility group box 1	Homo sapiens	101-106
32471717-6	2020	Similarly, inhibition for ERK (PD98059), NF-kappaB (BAY11-7082) and c-Jun (c-Jun peptide), respectively, also suppressed the HMGB1 cytoplasm translocation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	31-38	high mobility group box 1	Homo sapiens	125-130
32754040-6	2020	Moreover, berberine significantly inhibited high mobile group box 1 (HMGB1)/nuclear factor-kappaB (Nf-kappaB)-dependent pathway and enhanced sirtuin 1 (SIRT1) expression after SAH.	Berberine	10-19	high mobility group box 1	Homo sapiens	44-67
32754040-6	2020	Moreover, berberine significantly inhibited high mobile group box 1 (HMGB1)/nuclear factor-kappaB (Nf-kappaB)-dependent pathway and enhanced sirtuin 1 (SIRT1) expression after SAH.	Berberine	10-19	high mobility group box 1	Homo sapiens	69-74
32754040-7	2020	Treatment with ex527, a selective SIRT1 inhibitor, reversed berberine-induced SIRT1 activation and inhibitory effects on HMGB1/Nf-kappaB activation.	6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide	15-20	high mobility group box 1	Homo sapiens	121-126
32754040-9	2020	Taken together, these findings suggest that berberine provides beneficial effects against SAH-triggered cerebral inflammation by inhibiting HMGB1/Nf-kappaB pathway, which may be modulated by SIRT1 activation.	Berberine	44-53	high mobility group box 1	Homo sapiens	140-145
32469087-7	2020	Concurrently, HMGB1 impaired insulin sensitivities by attenuating the abundance of insulin receptor substrate-1, Akt phosphorylation, GLUT4 translocation, and glucose uptake in granulosa cells, which were reversed by blocking autophagy pathways with siRNA-mediated knockdown of ATG7 or with chloroquine and bafilomycin A1, the lysosome inhibitors.	Glucose	159-166	high mobility group box 1	Homo sapiens	14-19
32469087-7	2020	Concurrently, HMGB1 impaired insulin sensitivities by attenuating the abundance of insulin receptor substrate-1, Akt phosphorylation, GLUT4 translocation, and glucose uptake in granulosa cells, which were reversed by blocking autophagy pathways with siRNA-mediated knockdown of ATG7 or with chloroquine and bafilomycin A1, the lysosome inhibitors.	Chloroquine	291-302	high mobility group box 1	Homo sapiens	14-19
32469087-7	2020	Concurrently, HMGB1 impaired insulin sensitivities by attenuating the abundance of insulin receptor substrate-1, Akt phosphorylation, GLUT4 translocation, and glucose uptake in granulosa cells, which were reversed by blocking autophagy pathways with siRNA-mediated knockdown of ATG7 or with chloroquine and bafilomycin A1, the lysosome inhibitors.	bafilomycin A1	307-321	high mobility group box 1	Homo sapiens	14-19
32347316-6	2020	RESULTS: In hydrogen peroxide (H2O2)-stimulated HL7702 cells, HBx triggered the release of pro-inflammatory mediators apoptosis-associated speck-like protein containing a CARD (ASC), interleukin (IL)-1beta, IL-18, and high-mobility group box 1 (HMGB1); activated NLRP3; and initiated pro-inflammatory cell death (pyroptosis).	Hydrogen Peroxide	12-29	high mobility group box 1	Homo sapiens	218-243
32054355-0	2020	HMGB1 is increased in adolescents with polycystic ovary syndrome (PCOS) and decreases after treatment with myo-inositol (MYO) in combination with alpha-lipoic acid (ALA).	5-O-methyl-myo-inositol	107-119	high mobility group box 1	Homo sapiens	0-5
32054355-0	2020	HMGB1 is increased in adolescents with polycystic ovary syndrome (PCOS) and decreases after treatment with myo-inositol (MYO) in combination with alpha-lipoic acid (ALA).	5-O-methyl-myo-inositol	121-124	high mobility group box 1	Homo sapiens	0-5
32054355-0	2020	HMGB1 is increased in adolescents with polycystic ovary syndrome (PCOS) and decreases after treatment with myo-inositol (MYO) in combination with alpha-lipoic acid (ALA).	Thioctic Acid	146-163	high mobility group box 1	Homo sapiens	0-5
32054355-0	2020	HMGB1 is increased in adolescents with polycystic ovary syndrome (PCOS) and decreases after treatment with myo-inositol (MYO) in combination with alpha-lipoic acid (ALA).	Thioctic Acid	165-168	high mobility group box 1	Homo sapiens	0-5
32054355-4	2020	The aim of this study was to verify changes in HMGB1, in metabolic and endocrine parameters in adolescents with PCOS compared with controls and after treatment with a combination of MYO + ALA.	5-O-methyl-myo-inositol	182-185	high mobility group box 1	Homo sapiens	47-52
32054355-4	2020	The aim of this study was to verify changes in HMGB1, in metabolic and endocrine parameters in adolescents with PCOS compared with controls and after treatment with a combination of MYO + ALA.	Thioctic Acid	188-191	high mobility group box 1	Homo sapiens	47-52
32416454-0	2020	Glycyrrhetinic acid alleviates hepatic inflammation injury in viral hepatitis disease via a HMGB1-TLR4 signaling pathway.	Glycyrrhetinic Acid	0-19	high mobility group box 1	Homo sapiens	92-97
32606157-6	2020	RESULTS: HMGB1 levels increased with increasing dietary cholesterol, and a negative correlation was found between HMGB1 levels and thrombus formation time.	Cholesterol	56-67	high mobility group box 1	Homo sapiens	9-14
32416454-6	2020	We also employed a murine hepatitis virus (MHV) infection model to illustrate that GA treatment inhibited activation of hepatic inflammatory responses by blocking high-mobility group box 1 (HMGB1) cytokine activity.	Glycyrrhetinic Acid	83-85	high mobility group box 1	Homo sapiens	163-188
32347316-6	2020	RESULTS: In hydrogen peroxide (H2O2)-stimulated HL7702 cells, HBx triggered the release of pro-inflammatory mediators apoptosis-associated speck-like protein containing a CARD (ASC), interleukin (IL)-1beta, IL-18, and high-mobility group box 1 (HMGB1); activated NLRP3; and initiated pro-inflammatory cell death (pyroptosis).	Hydrogen Peroxide	12-29	high mobility group box 1	Homo sapiens	245-250
32416454-6	2020	We also employed a murine hepatitis virus (MHV) infection model to illustrate that GA treatment inhibited activation of hepatic inflammatory responses by blocking high-mobility group box 1 (HMGB1) cytokine activity.	Glycyrrhetinic Acid	83-85	high mobility group box 1	Homo sapiens	190-195
32416454-8	2020	Thus, our findings characterize GA as a hepatoprotective therapy agent in hepatic infectious disease not only by suppressing HMGB1 release and blocking HMGB1 cytokine activity, but also via an underlying viral-induced HMGB1-TLR4 immunological regulation axis that occurs during the cytokine storm.	Glycyrrhetinic Acid	32-34	high mobility group box 1	Homo sapiens	125-130
32347316-6	2020	RESULTS: In hydrogen peroxide (H2O2)-stimulated HL7702 cells, HBx triggered the release of pro-inflammatory mediators apoptosis-associated speck-like protein containing a CARD (ASC), interleukin (IL)-1beta, IL-18, and high-mobility group box 1 (HMGB1); activated NLRP3; and initiated pro-inflammatory cell death (pyroptosis).	Hydrogen Peroxide	31-35	high mobility group box 1	Homo sapiens	218-243
32416454-8	2020	Thus, our findings characterize GA as a hepatoprotective therapy agent in hepatic infectious disease not only by suppressing HMGB1 release and blocking HMGB1 cytokine activity, but also via an underlying viral-induced HMGB1-TLR4 immunological regulation axis that occurs during the cytokine storm.	Glycyrrhetinic Acid	32-34	high mobility group box 1	Homo sapiens	152-157
32347316-6	2020	RESULTS: In hydrogen peroxide (H2O2)-stimulated HL7702 cells, HBx triggered the release of pro-inflammatory mediators apoptosis-associated speck-like protein containing a CARD (ASC), interleukin (IL)-1beta, IL-18, and high-mobility group box 1 (HMGB1); activated NLRP3; and initiated pro-inflammatory cell death (pyroptosis).	Hydrogen Peroxide	31-35	high mobility group box 1	Homo sapiens	245-250
32416454-8	2020	Thus, our findings characterize GA as a hepatoprotective therapy agent in hepatic infectious disease not only by suppressing HMGB1 release and blocking HMGB1 cytokine activity, but also via an underlying viral-induced HMGB1-TLR4 immunological regulation axis that occurs during the cytokine storm.	Glycyrrhetinic Acid	32-34	high mobility group box 1	Homo sapiens	152-157
32602358-0	2021	Glycyrrhizin, an HMGB1 inhibitor, Suppresses Interleukin-1beta-Induced Inflammatory Responses in Chondrocytes from Patients with Osteoarthritis.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	17-22
32612147-8	2020	8-NitroG formation in A549 cells was also largely suppressed by small interfering RNA (siRNA) for high-mobility group box-1 (HMGB1), receptor for advanced glycation and end products (AGER, RAGE) and Toll-like receptor 9 (TLR9).	8-nitrog	0-8	high mobility group box 1	Homo sapiens	98-123
32612147-8	2020	8-NitroG formation in A549 cells was also largely suppressed by small interfering RNA (siRNA) for high-mobility group box-1 (HMGB1), receptor for advanced glycation and end products (AGER, RAGE) and Toll-like receptor 9 (TLR9).	8-nitrog	0-8	high mobility group box 1	Homo sapiens	125-130
32612147-9	2020	These results suggest that indium compounds induce inflammation-mediated DNA damage in lung epithelial cells via the HMGB1-RAGE-TLR9 pathway.	Indium	27-33	high mobility group box 1	Homo sapiens	117-122
32602358-8	2021	HMGB1 inhibition by glycyrrhizin improved cell viability of chondrocytes treated with IL-1beta.	Glycyrrhizic Acid	20-32	high mobility group box 1	Homo sapiens	0-5
32602358-9	2021	Glycyrrhizin suppressed IL-1beta-induced upregulation of HMGB1 and inflammatory mediators and cytokines, including PGE2, NO, proinflammatory cytokines, and MMPs.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	57-62
32602358-3	2021	This study aimed to investigate how inhibition of HMGB1 by glycyrrhizin might affect inflammatory responses and viability of OA patient-derived chondrocytes treated with IL-1beta.	Glycyrrhizic Acid	59-71	high mobility group box 1	Homo sapiens	50-55
32423802-8	2020	Treatment with EW-7197, a transforming growth factor-beta (TGF-beta) type I receptor kinase inhibitor, prevented all the effects of HMGB1 in Calu-3 cells.	vactosertib	15-22	high mobility group box 1	Homo sapiens	132-137
32600307-0	2020	The alpha7 nicotinic acetylcholine receptor agonist, GTS-21, attenuates hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation.	3-(2,4-dimethoxybenzylidene)anabaseine	53-59	high mobility group box 1	Homo sapiens	156-161
32600316-5	2020	This comprehension was recently reinforced by results reported in Molecular Medicine by Sitapara and coworkers demonstrating that administration of an alpha7 nicotinic acetylcholine receptor agonist attenuated hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation.	sitapara	88-96	high mobility group box 1	Homo sapiens	294-299
32423802-10	2020	The effects of HMGB1 contribute to TGF-beta signaling and EW-7197 shows potential for use in therapy for HMGB1-induced airway inflammation.	vactosertib	58-65	high mobility group box 1	Homo sapiens	105-110
32587593-5	2020	We currently investigated that peroxiredoxins I and II (PrxI/II) induce the intramolecular disulfide bond formation of HMGB1 in the nucleus.	Disulfides	91-100	high mobility group box 1	Homo sapiens	119-124
32636835-2	2020	HMGB1 binds to its specific receptors not only to activate the nuclear factor (NF)-kappaB and mitogen-activated protein kinase (MAPK) pathways but also to regulate the activation of the phosphatidylinositol 3"-kinase/protein kinase B/mammalian target of the rapamycin (PI3K/AKT/mTOR) pathway.	Sirolimus	258-267	high mobility group box 1	Homo sapiens	0-5
32321806-0	2020	PCV2 Induces Reactive Oxygen Species To Promote Nucleocytoplasmic Translocation of the Viral DNA Binding Protein HMGB1 To Enhance Its Replication.	Reactive Oxygen Species	13-36	high mobility group box 1	Homo sapiens	113-118
32321806-4	2020	Here, we demonstrate that nuclear HMGB1 negatively regulated PCV2 replication as shown by overexpression of HMGB1 or blockage of its nucleocytoplasmic translocation with ethyl pyruvate.	ethyl pyruvate	170-184	high mobility group box 1	Homo sapiens	34-39
32321806-8	2020	Elevation of reactive oxygen species (ROS) induced by PCV2 infection was closely associated with cytosolic translocation of nuclear HMGB1.	Reactive Oxygen Species	13-36	high mobility group box 1	Homo sapiens	132-137
32321806-8	2020	Elevation of reactive oxygen species (ROS) induced by PCV2 infection was closely associated with cytosolic translocation of nuclear HMGB1.	Reactive Oxygen Species	38-41	high mobility group box 1	Homo sapiens	132-137
32321806-9	2020	Treatment of PCV2-infected cells with ethyl pyruvate or N-acetylcysteine downregulated PCV2-induced ROS production, suppressed nucleocytoplasmic HMGB1 translocation, and decreased PCV2 replication.	ethyl pyruvate	38-52	high mobility group box 1	Homo sapiens	145-150
32321806-9	2020	Treatment of PCV2-infected cells with ethyl pyruvate or N-acetylcysteine downregulated PCV2-induced ROS production, suppressed nucleocytoplasmic HMGB1 translocation, and decreased PCV2 replication.	Acetylcysteine	56-72	high mobility group box 1	Homo sapiens	145-150
32321806-13	2020	PCV2 then upregulates host reactive oxygen species (ROS) to prevent sequestration of its genome by expelling nuclear HMGB1 into the cytosol.	Reactive Oxygen Species	27-50	high mobility group box 1	Homo sapiens	117-122
32321806-13	2020	PCV2 then upregulates host reactive oxygen species (ROS) to prevent sequestration of its genome by expelling nuclear HMGB1 into the cytosol.	Reactive Oxygen Species	52-55	high mobility group box 1	Homo sapiens	117-122
32321806-15	2020	This study also provides insight into the justification and pharmacological basis of antioxidants as an adjunct therapy in PCV2 infection or possibly other diseases caused by the viruses that deploy the ROS-HMGB1 interaction favoring their replication.	Reactive Oxygen Species	203-206	high mobility group box 1	Homo sapiens	207-212
32587593-6	2020	Disulfide HMGB1 is preferentially transported out of the nucleus by binding to the nuclear exportin chromosome-region maintenance 1 (CRM1).	Disulfides	0-9	high mobility group box 1	Homo sapiens	10-15
32587593-7	2020	We determined the kinetics of HMGB1 oxidation in bone marrow-derived macrophage as early as a few minutes after lipopolysaccharide treatment, peaking at 4 h while disulfide HMGB1 accumulation was observed within the cells, starting to secrete in the late time point.	Disulfides	163-172	high mobility group box 1	Homo sapiens	173-178
32419317-5	2020	THP-1 cells were induced to differentiate into M1 macrophages, then challenged with either CC-5013 or an HMGB1 inhibitor, glycyrrhizin.	Glycyrrhizic Acid	122-134	high mobility group box 1	Homo sapiens	105-110
32642410-0	2020	MiR-142-3p enhances chemosensitivity of breast cancer cells and inhibits autophagy by targeting HMGB1.	mir-142-3p	0-10	high mobility group box 1	Homo sapiens	96-101
32642410-6	2020	Moreover, overexpression of HMGB1 dramatically reversed the promotion of apoptosis and inhibition of autophagy mediated by miR-142-3p up-regulation.	mir-142-3p	123-133	high mobility group box 1	Homo sapiens	28-33
32642410-7	2020	In conclusion, miR-142-3p overexpression may inhibit autophagy and promote the drug sensitivity of breast cancer cells to DOX by targeting HMGB1.	mir-142-3p	15-25	high mobility group box 1	Homo sapiens	139-144
32642410-7	2020	In conclusion, miR-142-3p overexpression may inhibit autophagy and promote the drug sensitivity of breast cancer cells to DOX by targeting HMGB1.	Doxorubicin	122-125	high mobility group box 1	Homo sapiens	139-144
32642410-8	2020	The miR-142-3p/HMGB1 axis might be a novel target to regulate the drug resistance of breast cancer patients.	mir-142-3p	4-14	high mobility group box 1	Homo sapiens	15-20
32251024-6	2020	Experiments with anti-N-methyl-D-aspartate antibodies show that HMGB1 and C1q were essential to activate microglia which, in turn, remodel damaged neurons in vivo.	N-Methylaspartate	22-42	high mobility group box 1	Homo sapiens	64-69
32169518-7	2020	HMGB1 concentration in plasma was higher in the URSA group than the control group.	ursa	48-52	high mobility group box 1	Homo sapiens	0-5
32277430-8	2020	Furthermore, reduction in the levels of high-mobility group box 1 protein, inhibitor of kappa B protein-alpha, matrix metalloproteinase-9 and C-reactive protein are some other important hesperidin-derived hepatoprotective mechanisms.	Hesperidin	186-196	high mobility group box 1	Homo sapiens	40-65
32633407-8	2020	Lipopolysaccharide (LPS) was used in stimulating the macrophages to activate inflammatory response and recombined human HMGB1 was used to resist the function of GL to explore whether GL acted via the target of HMGB1.	Glycyrrhizic Acid	161-163	high mobility group box 1	Homo sapiens	120-125
32359123-5	2020	Serum HMGB1 level was also positively correlated with HbA1c and negatively correlated with nitric oxide (NO) in diabetic patients.	Nitric Oxide	91-103	high mobility group box 1	Homo sapiens	6-11
32169518-8	2020	Furthermore, the levels of HMGB1 of subjects with URSA could be reduced by administrating low doses of aspirin (ASPL).	Aspirin	103-110	high mobility group box 1	Homo sapiens	27-32
32514250-4	2020	To observe the relationship between HMGB1, GPX4 and inflammation or ROS, Western blot assays were adopted.	Reactive Oxygen Species	68-71	high mobility group box 1	Homo sapiens	36-41
32514250-8	2020	Furthermore, by utilizing siHMGB1 and its inhibitor, our discoveries demonstrate that HMGB1 knockdown can inhibit inflammation and reactive oxygen species (ROS) accumulation via NF-kB.	Reactive Oxygen Species	131-154	high mobility group box 1	Homo sapiens	28-33
32514250-8	2020	Furthermore, by utilizing siHMGB1 and its inhibitor, our discoveries demonstrate that HMGB1 knockdown can inhibit inflammation and reactive oxygen species (ROS) accumulation via NF-kB.	Reactive Oxygen Species	156-159	high mobility group box 1	Homo sapiens	28-33
32523550-7	2020	In line with the supposed switch to a pro-inflammatory phenotype known as the senescence associated secretory phenotype (SASP), we found that both RS and DS upregulated IL-1beta and released HMGB-1 from the nucleus, while RS also showed IL-6 upregulation.	ds	154-156	high mobility group box 1	Homo sapiens	191-197
32466385-12	2020	Treatment with PROG reduced HMGB1 release and NLRP3 inflammasome activation, and enhanced autophagy in stressed and unstressed ischemic animals.	Progesterone	15-19	high mobility group box 1	Homo sapiens	28-33
32489326-0	2020	LncRNA NNT-AS1 contributes to the cisplatin resistance of cervical cancer through NNT-AS1/miR-186/HMGB1 axis.	Cisplatin	34-43	high mobility group box 1	Homo sapiens	98-103
31978425-6	2020	Additionally, our findings demonstrate that nobiletin potently ameliorated IL-21-induced increased production of reactive oxygen species and 4-hydroxynonenal, increased expression of interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and high-mobility group box 1 (HMGB1), and decreased mitochondrial membrane potential.	nobiletin	44-53	high mobility group box 1	Homo sapiens	250-275
31978425-6	2020	Additionally, our findings demonstrate that nobiletin potently ameliorated IL-21-induced increased production of reactive oxygen species and 4-hydroxynonenal, increased expression of interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and high-mobility group box 1 (HMGB1), and decreased mitochondrial membrane potential.	nobiletin	44-53	high mobility group box 1	Homo sapiens	277-282
32536835-0	2020	Aloin promotes cell apoptosis by targeting HMGB1-TLR4-ERK axis in human melanoma cells.	alloin	0-5	high mobility group box 1	Homo sapiens	43-48
32536835-7	2020	Furthermore, HMGB1 release was significantly inhibited in melanoma cancer cells treated with ALO.	alloin	93-96	high mobility group box 1	Homo sapiens	13-18
32536835-8	2020	Knockdown of HMGB1 could enhance melanoma cell death that is induced by ALO treatment.	alloin	72-75	high mobility group box 1	Homo sapiens	13-18
32523355-15	2020	Conclusion: HMGB1 promotes NHEJ via interaction with Ku70 resulting in resistance to IR and cisplatin.	Cisplatin	92-101	high mobility group box 1	Homo sapiens	12-17
32523355-16	2020	Inhibition of HMGB1 by glycyrrhizin is a potential therapeutic regimen to treat cisplatin and IR resistant NPC patients.	Glycyrrhizic Acid	23-35	high mobility group box 1	Homo sapiens	14-19
32523355-16	2020	Inhibition of HMGB1 by glycyrrhizin is a potential therapeutic regimen to treat cisplatin and IR resistant NPC patients.	Cisplatin	80-89	high mobility group box 1	Homo sapiens	14-19
32403440-5	2020	KEY RESULTS: Incubation of human CM with HMGB-1 or histones is associated with changes in calcium handling, a reduction of cell viability and a substantial reduction of the mitochondrial respiratory capacity.	Calcium	90-97	high mobility group box 1	Homo sapiens	41-47
32380958-4	2020	Disulfide-HMGB1 triggers TLR4 receptors generating pro-inflammatory cytokine release.	Disulfides	0-9	high mobility group box 1	Homo sapiens	10-15
32380958-9	2020	Extracellular HMGB1 generally exists in vivo bound to other molecules, including PAMPs and DAMPs.	dinitrophenyl-aminopropyl-methylamine	91-96	high mobility group box 1	Homo sapiens	14-19
32431618-0	2020	Quercetin Attenuates d-GaLN-Induced L02 Cell Damage by Suppressing Oxidative Stress and Mitochondrial Apoptosis via Inhibition of HMGB1.	Quercetin	0-9	high mobility group box 1	Homo sapiens	130-135
32431618-4	2020	Quercetin (Que), as an antioxidant, is a potential phytochemical with hepatocyte protection and is also considered to be an inhibitor of HMGB1.	Quercetin	0-9	high mobility group box 1	Homo sapiens	137-142
32431618-4	2020	Quercetin (Que), as an antioxidant, is a potential phytochemical with hepatocyte protection and is also considered to be an inhibitor of HMGB1.	Quercetin	0-3	high mobility group box 1	Homo sapiens	137-142
32431618-6	2020	The present study explored whether the hepatoprotective effect of Que antagonizes HMGB1, and subsequent molecular signaling events.	Quercetin	66-69	high mobility group box 1	Homo sapiens	82-87
32431618-9	2020	Further research showed that after transfection with HMGB1 short hairpin RNA (shRNA), cell viability was improved, and intracellular ROS production and apoptosis were suppressed.	Reactive Oxygen Species	133-136	high mobility group box 1	Homo sapiens	53-58
32431618-10	2020	When co-treated with Que, the expression of HMGB1 was decreased significantly, the expression of proteins in the corresponding signal pathway were further reduced, and the production of ROS and apoptosis were further suppressed.	Quercetin	21-24	high mobility group box 1	Homo sapiens	44-49
32431618-10	2020	When co-treated with Que, the expression of HMGB1 was decreased significantly, the expression of proteins in the corresponding signal pathway were further reduced, and the production of ROS and apoptosis were further suppressed.	Reactive Oxygen Species	186-189	high mobility group box 1	Homo sapiens	44-49
32431618-12	2020	Taken together, these results indicate that Que significantly improves d-GaLN-induced cellular damage by inhibiting oxidative stress and mitochondrial apoptosis via inhibiting HMGB1.	Quercetin	44-47	high mobility group box 1	Homo sapiens	176-181
32456685-1	2020	BACKGROUND: Chemotherapeutics can stimulate immune antitumor response by inducing immunogenic cell death (ICD), which is activated by Damage-Associated Molecular Patterns (DAMPs) like the exposure of calreticulin (CRT) on the cell surface, the release of ATP and the secretion of High Mobility Group Box 1 (HMGB1).	Adenosine Triphosphate	255-258	high mobility group box 1	Homo sapiens	280-305
32456685-1	2020	BACKGROUND: Chemotherapeutics can stimulate immune antitumor response by inducing immunogenic cell death (ICD), which is activated by Damage-Associated Molecular Patterns (DAMPs) like the exposure of calreticulin (CRT) on the cell surface, the release of ATP and the secretion of High Mobility Group Box 1 (HMGB1).	Adenosine Triphosphate	255-258	high mobility group box 1	Homo sapiens	307-312
32514327-5	2020	Consistent with experimental data, the acidic tail was predicted to adopt an extended conformation that allows it to make a range of hydrogen-bonding and electrostatic interactions with the box-like domains that stabilize the overall structure of HMGB1.	Hydrogen	133-141	high mobility group box 1	Homo sapiens	247-252
32523355-11	2020	Mutational analysis revealed that serine 155 of Ku70 was required for its direct interaction with HMGB1.	Serine	34-40	high mobility group box 1	Homo sapiens	98-103
32523355-13	2020	Deficiency of HMGB1 sensitized wild-type (WT) and resistant NPC cells to IR and cisplatin.	Cisplatin	80-89	high mobility group box 1	Homo sapiens	14-19
32523355-14	2020	Glycyrrhizin, which is HMGB1 inhibitor, impaired DNA binding of HMGB1 and exhibited excellent synergy with IR and cisplatin.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	23-28
32523355-14	2020	Glycyrrhizin, which is HMGB1 inhibitor, impaired DNA binding of HMGB1 and exhibited excellent synergy with IR and cisplatin.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	64-69
32014690-6	2020	Here we found that TDI induced pyroptosis in 16HBE cells, as evidenced by enhanced expressions of caspase-1 and elevated levels of LDH, IL-1beta and HMGB1.	Toluene 2,4-Diisocyanate	19-22	high mobility group box 1	Homo sapiens	149-154
32588826-4	2020	Ethanol consumption leads to activation of neuroimmune signaling in the central nervous system through many types of Toll-like receptors (TLRs), as well as the release of their endogenous agonists (HMGB1 protein, S100 protein, heat shock proteins, extracellular matrix breakdown proteins).	Ethanol	0-7	high mobility group box 1	Homo sapiens	198-203
32252560-8	2020	In this regard, glycyrrhetic acid (GA), the active component of Glycyrrhiza glabra, can efficiently block HMGB1.	Glycyrrhetinic Acid	16-33	high mobility group box 1	Homo sapiens	106-111
32252560-8	2020	In this regard, glycyrrhetic acid (GA), the active component of Glycyrrhiza glabra, can efficiently block HMGB1.	Glycyrrhetinic Acid	35-37	high mobility group box 1	Homo sapiens	106-111
32246277-6	2020	Radiotherapy induces so-called "immunogenic cell death", which involves cell surface translocation of calreticulin and extracellular release of high-mobility group protein box 1 (HMGB-1) and adenosine-5"-triphosphate (ATP).	Adenosine Triphosphate	218-221	high mobility group box 1	Homo sapiens	179-185
31846033-0	2020	Corrigendum to "Carbon Nanomaterials Stimulate HMGB1 Release From Macrophages and Induce Cell Migration and Invasion".	Carbon	16-22	high mobility group box 1	Homo sapiens	47-52
32440094-10	2020	Results: Our findings demonstrate that laquinimod reduced the expression of key inflammatory cytokines and chemokines, including IL-6, MCP-1, and HMGB1.	laquinimod	39-49	high mobility group box 1	Homo sapiens	146-151
32489453-1	2020	Purpose: We aimed to investigate the association of single-nucleotide polymorphisms (SNPs) in HMGB1, REV3L, and NFE2L2 with prognosis in lung cancer patients with platinum-based chemotherapy.	Platinum	163-171	high mobility group box 1	Homo sapiens	94-99
32489453-4	2020	Results: The results revealed that patients carrying TC or CC genotype in REV3L rs462779 (HR=0.67, 95% CI=0.51-0.90, P=0.007) and AG or GG genotype in HMGB1 rs1045411 (HR=0.61, 95% CI=0.38-0.99, P=0.046) had a better overall survival.	Technetium	53-55	high mobility group box 1	Homo sapiens	151-156
32489453-9	2020	The REV3L rs462779 and HMGB1 rs1045411 may serve as prognosis markers in lung cancer patients with platinum-based chemotherapy.	Platinum	99-107	high mobility group box 1	Homo sapiens	23-28
32340172-0	2020	Glycyrrhizin Inhibits PEDV Infection and Proinflammatory Cytokine Secretion via the HMGB1/TLR4-MAPK p38 Pathway.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	84-89
32340172-8	2020	Collectively, our data indicated that GLY inhibited PEDV infection and decreased proinflammatory cytokine secretion via the HMGB1/TLR4-mitogen-activated protein kinase (MAPK) p38 pathway.	Glycyrrhizic Acid	38-41	high mobility group box 1	Homo sapiens	124-129
31928132-6	2020	We further demonstrated that SIRT6 and PARP1 activation were required for chemotherapy-induced ADP-ribosylation of HMGB1 in leukemic cells and then influenced the acetylation of HMGB1, finally promoting the autophagy of leukemic cells mediated by HMGB1 translocation.	Adenosine Diphosphate	95-98	high mobility group box 1	Homo sapiens	115-120
32328193-0	2020	Self-enforcing HMGB1/NF-kappaB/HIF-1alpha Feedback Loop Promotes Cisplatin Resistance in Hepatocellular Carcinoma Cells.	Cisplatin	65-74	high mobility group box 1	Homo sapiens	15-20
32328193-6	2020	Further, we showed that HMGB1 has an important role in mediating cisplatin resistance via an HMGB1/ nuclear factor kappa-B (NF-kappaB)/ hypoxia inducible factor-1alpha (HIF-1alpha) feedback loop.	Cisplatin	65-74	high mobility group box 1	Homo sapiens	24-29
32328193-6	2020	Further, we showed that HMGB1 has an important role in mediating cisplatin resistance via an HMGB1/ nuclear factor kappa-B (NF-kappaB)/ hypoxia inducible factor-1alpha (HIF-1alpha) feedback loop.	Cisplatin	65-74	high mobility group box 1	Homo sapiens	93-98
32328193-7	2020	The study findings reveal an unappreciated molecular mechanism of HMGB1-mediated cisplatin resistance and may provide a new clue in cancer therapy.	Cisplatin	81-90	high mobility group box 1	Homo sapiens	66-71
31928132-0	2020	SIRT6-PARP1 is involved in HMGB1 polyADP-ribosylation and acetylation and promotes chemotherapy-induced autophagy in leukemia.	Adenosine Diphosphate	33-40	high mobility group box 1	Homo sapiens	27-32
32331368-5	2020	In Pgp-expressing/doxorubicin-resistant cells, Tariquidar and R-3 increased doxorubicin accumulation and toxicity, reduced Pgp activity, and increased CRT translocation and ATP and HMGB1 release.	tariquidar	47-57	high mobility group box 1	Homo sapiens	181-186
32035144-4	2020	Our results showed that hesperetin significantly relieved the symptoms of DSS -induced colitis and increased the expressions of zonula occludens-1 (ZO-1), occludin and mucin2 (MUC-2) as well as the decrease of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-18, HMGB1 and IL-6.	hesperetin	24-34	high mobility group box 1	Homo sapiens	282-287
32328059-7	2020	Caspase-11/GsdmD was responsible for HMGB1 translocation from nucleus to the cytoplasm via calcium changing-induced phosphorylation of calcium-calmodulin kinase kinase (camkk)beta during endotoxemia.	Calcium	91-98	high mobility group box 1	Homo sapiens	37-42
32328059-10	2020	These findings provide a novel mechanism that TLR4 signaling results in an increase in caspase-11 expression, as well as increased exosome release, while caspase-11/GsdmD activation/cleavage leads to accumulation of HMGB1 in the cytoplasm through a process associated with the release of calcium from the endoplasmic reticulum and camkkbeta activation.	Calcium	288-295	high mobility group box 1	Homo sapiens	216-221
32329842-1	2020	OBJECTIVE: The aim of this study was to investigate the effects of micro ribonucleic acid (miR)-129-5p on the proliferation and apoptosis of gastric cancer cells via targeted repression on the expression of high mobility group protein B1 (HMGB1).	micro ribonucleic acid	67-89	high mobility group box 1	Homo sapiens	207-237
32329842-1	2020	OBJECTIVE: The aim of this study was to investigate the effects of micro ribonucleic acid (miR)-129-5p on the proliferation and apoptosis of gastric cancer cells via targeted repression on the expression of high mobility group protein B1 (HMGB1).	micro ribonucleic acid	67-89	high mobility group box 1	Homo sapiens	239-244
32329842-1	2020	OBJECTIVE: The aim of this study was to investigate the effects of micro ribonucleic acid (miR)-129-5p on the proliferation and apoptosis of gastric cancer cells via targeted repression on the expression of high mobility group protein B1 (HMGB1).	methionylisoleucylarginine	91-94	high mobility group box 1	Homo sapiens	207-237
32329842-1	2020	OBJECTIVE: The aim of this study was to investigate the effects of micro ribonucleic acid (miR)-129-5p on the proliferation and apoptosis of gastric cancer cells via targeted repression on the expression of high mobility group protein B1 (HMGB1).	methionylisoleucylarginine	91-94	high mobility group box 1	Homo sapiens	239-244
32329842-1	2020	OBJECTIVE: The aim of this study was to investigate the effects of micro ribonucleic acid (miR)-129-5p on the proliferation and apoptosis of gastric cancer cells via targeted repression on the expression of high mobility group protein B1 (HMGB1).	-129-5p	95-102	high mobility group box 1	Homo sapiens	207-237
32329842-1	2020	OBJECTIVE: The aim of this study was to investigate the effects of micro ribonucleic acid (miR)-129-5p on the proliferation and apoptosis of gastric cancer cells via targeted repression on the expression of high mobility group protein B1 (HMGB1).	-129-5p	95-102	high mobility group box 1	Homo sapiens	239-244
32095984-10	2020	Uric acid and HMGB1 siRNA inhibited HMGB1 acetylation to prevent its transport from the nucleus to the cytoplasm.	Uric Acid	0-9	high mobility group box 1	Homo sapiens	36-41
32095984-12	2020	These data indicated that uric acid may prevent cell injury mainly by inhibiting HMGB1 acetylation to regulate TLR4/NF-kappaB pathways and reduce the levels of inflammatory factors.	Uric Acid	26-35	high mobility group box 1	Homo sapiens	81-86
32095984-0	2020	The protective effect of uric acid in reducing TLR4/NF-kappaB activation through the inhibition of HMGB1 acetylation in a model of ischemia-reperfusion injury in vitro.	Uric Acid	25-34	high mobility group box 1	Homo sapiens	99-104
31802434-0	2020	HMGB1 Is a Therapeutic Target and Biomarker in Diazepam-Refractory Status Epilepticus with Wide Time Window.	Diazepam	47-55	high mobility group box 1	Homo sapiens	0-5
31802434-2	2020	Here, we investigated the proinflammatory cytokine high mobility group box-1 (HMGB1) as a candidate therapeutic target for diazepam (DZP)-refractory SE.	Diazepam	123-131	high mobility group box 1	Homo sapiens	51-76
31858421-0	2020	HMGB1 Mediates Paraquat-Induced Neuroinflammatory Responses via Activating RAGE Signaling Pathway.	Paraquat	15-23	high mobility group box 1	Homo sapiens	0-5
31802434-2	2020	Here, we investigated the proinflammatory cytokine high mobility group box-1 (HMGB1) as a candidate therapeutic target for diazepam (DZP)-refractory SE.	Diazepam	123-131	high mobility group box 1	Homo sapiens	78-83
31858421-3	2020	High-mobility group box 1 (HMGB1) has been proven to be relevant to the neuroinflammation involved in PD; however, whether and how HMGB1 exerts modulatory effects in nervous system upon PQ exposure remain elusive.	Paraquat	186-188	high mobility group box 1	Homo sapiens	131-136
31858421-4	2020	Therefore, the present study investigated the underlying association between HMGB1 and PQ exposure in SH-SY5Y cells, which is a well-established in vitro model for PD research.	Paraquat	87-89	high mobility group box 1	Homo sapiens	77-82
31802434-2	2020	Here, we investigated the proinflammatory cytokine high mobility group box-1 (HMGB1) as a candidate therapeutic target for diazepam (DZP)-refractory SE.	Diazepam	133-136	high mobility group box 1	Homo sapiens	51-76
31858421-5	2020	We observed that HMGB1 was markedly increased in a concentration and time-dependent manner upon PQ exposure, and the elevated HMGB1 could be translocated into cytosol and then released to the extracellular milieu of SH-SY5Y cells.	Paraquat	96-98	high mobility group box 1	Homo sapiens	17-22
31802434-2	2020	Here, we investigated the proinflammatory cytokine high mobility group box-1 (HMGB1) as a candidate therapeutic target for diazepam (DZP)-refractory SE.	Diazepam	133-136	high mobility group box 1	Homo sapiens	78-83
31858421-7	2020	These results suggested that HMGB1 is involved in the PQ-induced neuron death via activating RAGE signaling pathways and promoting neuroinflammatory responses.	Paraquat	54-56	high mobility group box 1	Homo sapiens	29-34
31802434-4	2020	Exogenous HMGB1 was sufficient to directly induce DZP-refractory SE in nonrefractory SE.	Diazepam	50-53	high mobility group box 1	Homo sapiens	10-15
31802434-5	2020	Neutralization of HMGB1 with an anti-HMGB1 monoclonal antibody decreased the incidence of SE and alleviated the severity of seizure activity in DZP-refractory SE, which was mediated by a Toll-like receptor 4 (TLR4)-dependent pathway.	Diazepam	144-147	high mobility group box 1	Homo sapiens	18-23
31802434-5	2020	Neutralization of HMGB1 with an anti-HMGB1 monoclonal antibody decreased the incidence of SE and alleviated the severity of seizure activity in DZP-refractory SE, which was mediated by a Toll-like receptor 4 (TLR4)-dependent pathway.	Diazepam	144-147	high mobility group box 1	Homo sapiens	37-42
31802434-6	2020	Importantly, anti-HMGB1 mAb reversed DZP-refractory SE with a wide time window, extending the therapeutic window from 30 to 180 min.	Diazepam	37-40	high mobility group box 1	Homo sapiens	18-23
31802434-7	2020	Furthermore, we found the upregulation of plasma HMGB1 level is closely correlated with the therapeutic response of anti-HMGB1 mAb in DZP-refractory SE.	Diazepam	134-137	high mobility group box 1	Homo sapiens	49-54
31802434-7	2020	Furthermore, we found the upregulation of plasma HMGB1 level is closely correlated with the therapeutic response of anti-HMGB1 mAb in DZP-refractory SE.	Diazepam	134-137	high mobility group box 1	Homo sapiens	121-126
31802434-8	2020	All these results indicated that HMGB1 is a potential therapeutic target and a useful predictive biomarker in DZP-refractory SE.	Diazepam	110-113	high mobility group box 1	Homo sapiens	33-38
32221312-0	2020	New insights in acetaminophen toxicity: HMGB1 contributes by itself to amplify hepatocyte necrosis in vitro through the TLR4-TRIF-RIPK3 axis.	Acetaminophen	16-29	high mobility group box 1	Homo sapiens	40-45
32098696-0	2020	Propofol upregulates miR-320a and reduces HMGB1 by downregulating ANRIL to inhibit PTC cell malignant behaviors.	Propofol	0-8	high mobility group box 1	Homo sapiens	42-47
32098696-15	2020	CONCLUSION: Propofol upregulated miR-320a and reduced HMGB1 by downregulating ANRIL and inactivating the Wnt/beta-catenin and NF-kappaB pathways, thus preventing PTC cell malignant behaviors.	Propofol	12-20	high mobility group box 1	Homo sapiens	54-59
31962109-7	2020	Phoenixin-14 attenuated oxidative stress via downregulation of ROS and NOX1 and inhibited HMGB1 expression.	phoenixin	0-9	high mobility group box 1	Homo sapiens	90-95
32221312-1	2020	Extracellular release of HMGB1 contributes to acetaminophen-induced liver injury.	Acetaminophen	46-59	high mobility group box 1	Homo sapiens	25-30
32221312-3	2020	Here we studied, in vitro, the role of HMGB1 in amplifying the acetaminophen-induced hepatocyte necrosis process.	Acetaminophen	63-76	high mobility group box 1	Homo sapiens	39-44
32221312-5	2020	We confirmed that addition of acetaminophen induced HepaRG cell death and HMGB1 release.	Acetaminophen	30-43	high mobility group box 1	Homo sapiens	74-79
32221312-6	2020	We showed that inhibition of HMGB1 decreased acetaminophen-induced HepaRG cell death, suggesting a feedforward effect.	Acetaminophen	45-58	high mobility group box 1	Homo sapiens	29-34
32221312-11	2020	Our data support that released HMGB1 from acetaminophen-stressed hepatocytes induced necrosis of neighboring hepatocytes by TLR4-TRIF-RIPK3- pathway.	Acetaminophen	42-55	high mobility group box 1	Homo sapiens	31-36
32221312-12	2020	This in vitro study gives new insights in the role of HMGB1 in the amplification of acetaminophen-induced toxicity.	Acetaminophen	84-97	high mobility group box 1	Homo sapiens	54-59
32161598-4	2020	In our study, we observed that low-dose gemcitabine treatment enhanced the immunogenicity of lung cancer by increasing the exposure of calreticulin, high mobility group box 1, and upregulating expression of NKG2D ligands.	gemcitabine	40-51	high mobility group box 1	Homo sapiens	149-174
32265930-5	2020	Disulfide HMGB1 activates the TLR4 complex by binding to MD-2.	Disulfides	0-9	high mobility group box 1	Homo sapiens	10-15
32188725-4	2020	Here, we found that a heparan sulfate (HS) octadecasaccharide (18-mer-HP or hepatoprotective 18-mer) displays potent hepatoprotection by targeting the HMGB1/RAGE axis.	Heparitin Sulfate	22-37	high mobility group box 1	Homo sapiens	151-156
32188725-4	2020	Here, we found that a heparan sulfate (HS) octadecasaccharide (18-mer-HP or hepatoprotective 18-mer) displays potent hepatoprotection by targeting the HMGB1/RAGE axis.	Heparitin Sulfate	39-41	high mobility group box 1	Homo sapiens	151-156
32188725-4	2020	Here, we found that a heparan sulfate (HS) octadecasaccharide (18-mer-HP or hepatoprotective 18-mer) displays potent hepatoprotection by targeting the HMGB1/RAGE axis.	octadecasaccharide	43-61	high mobility group box 1	Homo sapiens	151-156
32188725-6	2020	Furthermore, purified syndecan-1, but not syndecan-1 core protein, binds to HMGB1, suggesting that HMGB1 binds to HS polysaccharide side chains of syndecan-1.	Heparitin Sulfate	114-116	high mobility group box 1	Homo sapiens	99-104
32188725-6	2020	Furthermore, purified syndecan-1, but not syndecan-1 core protein, binds to HMGB1, suggesting that HMGB1 binds to HS polysaccharide side chains of syndecan-1.	Polysaccharides	117-131	high mobility group box 1	Homo sapiens	99-104
32169964-0	2020	Expression of Concern: HMGB1 and Its Hyperacetylated Isoform are Sensitive and Specific Serum Biomarkers to Detect Asbestos Exposure and to Identify Mesothelioma Patients.	Asbestos	115-123	high mobility group box 1	Homo sapiens	23-28
31879132-0	2020	Corrigendum to "HMGB1 contributes to adriamycin-induced cardiotoxicity via up-regulating autophagy" [Toxicol.	Doxorubicin	37-47	high mobility group box 1	Homo sapiens	16-21
32208365-4	2020	Correlations between metformin concentration and high-mobility group box 1 (HMGB1) and miR-142-3p levels were assessed.	Metformin	21-30	high mobility group box 1	Homo sapiens	76-81
32208365-7	2020	HMGB1 gene expression correlated negatively with metformin concentration, whereas miR-142-3p expression correlated positively with metformin concentration.	Metformin	49-58	high mobility group box 1	Homo sapiens	0-5
32208365-8	2020	In addition, mimic-induced miR-142-3p elevation resulted in decreased HMGB1 and LC3II levels and elevated p62 levels in the high-glucose condition, whereas miR-142-3p knockdown had the reverse effects, and metformin abolished those effects.	Glucose	129-136	high mobility group box 1	Homo sapiens	70-75
32208365-9	2020	Metformin inhibits high glucose-induced VSMC hyperproliferation and increased migration by inducing miR-142-3p-mediated inhibition of HMGB1 expression via the HMGB1-autophagy related pathway.	Metformin	0-9	high mobility group box 1	Homo sapiens	134-139
32208365-9	2020	Metformin inhibits high glucose-induced VSMC hyperproliferation and increased migration by inducing miR-142-3p-mediated inhibition of HMGB1 expression via the HMGB1-autophagy related pathway.	Metformin	0-9	high mobility group box 1	Homo sapiens	159-164
32208365-9	2020	Metformin inhibits high glucose-induced VSMC hyperproliferation and increased migration by inducing miR-142-3p-mediated inhibition of HMGB1 expression via the HMGB1-autophagy related pathway.	Glucose	24-31	high mobility group box 1	Homo sapiens	134-139
32208365-9	2020	Metformin inhibits high glucose-induced VSMC hyperproliferation and increased migration by inducing miR-142-3p-mediated inhibition of HMGB1 expression via the HMGB1-autophagy related pathway.	Glucose	24-31	high mobility group box 1	Homo sapiens	159-164
32191778-0	2020	Retraction: Inhibition of HMGB1-Induced Angiogenesis by Cilostazol via SIRT1 Activation in Synovial Fibroblasts from Rheumatoid Arthritis.	Cilostazol	56-66	high mobility group box 1	Homo sapiens	26-31
31913693-6	2020	In normal SAECs, HMGB-1 increased amiloride-sensitive Isc and ENaC Po from 0.15+-0.03 to 0.28+-0.04; p&lt;0.01.	Amiloride	34-43	high mobility group box 1	Homo sapiens	17-23
32089069-5	2020	Upregulation of miR-204 and downregulation of HMGB1 could repress TLR4/NF-kappaB pathway activation, degraded insulin release and testosterone (T) leveland ascended ovarian coefficient, boosted cell proliferation and restrained apoptosis of granulosa cells.	Testosterone	130-142	high mobility group box 1	Homo sapiens	46-51
32036391-7	2020	HMGB1 can inhibit mutant huntingtin aggregation, protecting against polyglutamine-induced neurotoxicity and acting as a chaperon-like molecule, possibly via autophagy regulation.	polyglutamine	68-81	high mobility group box 1	Homo sapiens	0-5
31270920-2	2020	Previous studies showed that HMGB1 is increased in the lung and circulation of patients with acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF).	ae-ipf	146-152	high mobility group box 1	Homo sapiens	29-34
31270920-9	2020	Higher levels of HMGB1 were associated with earlier onset of AE in stable IPF patients and with shorter survival in AE-IPF patients (P = 0.030 and 0.001, respectively).	ae-ipf	116-122	high mobility group box 1	Homo sapiens	17-22
32296583-13	2020	Conclusions: Our results suggest that NETs produced by TINs mediate the crosstalk between glioma progression and the tumor microenvironment by regulating the HMGB1/RAGE/IL-8 axis.	tins	55-59	high mobility group box 1	Homo sapiens	158-163
31924647-12	2020	NSG mice with human hematopoietic system injected with the HMGB1 antagonist glycyrrhizin verified the in vitro effects of HMGB1.	Glycyrrhizic Acid	76-88	high mobility group box 1	Homo sapiens	59-64
31924647-12	2020	NSG mice with human hematopoietic system injected with the HMGB1 antagonist glycyrrhizin verified the in vitro effects of HMGB1.	Glycyrrhizic Acid	76-88	high mobility group box 1	Homo sapiens	122-127
31642155-5	2020	Vitamin D downstream signalling has also been checked in placenta (VDR, CYP27B1, Cathelicidin LL37) along with expression of inflammatory markers (S100A8, HMGB1, TLR2, pNF-kappaB) using Western blotting and immunohistochemistry.	Vitamin D	0-9	high mobility group box 1	Homo sapiens	155-160
32103987-6	2020	Results: Hypoxia enhanced the expressions of NRF-1/TFAM, boosted mtDNA copy number and ATP content and increased the number of mitochondria in pancreatic cancer cells while induction was suppressed by a knockdown of HMGB1.	Adenosine Triphosphate	87-90	high mobility group box 1	Homo sapiens	216-221
32103987-9	2020	A knockdown of HMGB1 attenuated hypoxia with AICAR (an AMPK activator)-induced expression of NRF-1, TFAM, PGC-1alpha, SIRT1 and the proteins of complexes I&amp; III and reduced the acetylation level of PGC-1alpha/SIRT1 activity.	Adenosine Monophosphate	156-159	high mobility group box 1	Homo sapiens	15-20
31056833-0	2020	Neuronal HMGB1 in nucleus accumbens regulates cocaine reward memory.	Cocaine	46-53	high mobility group box 1	Homo sapiens	9-14
31056833-4	2020	Here, we show that cocaine exposure induced the translocation and release of HMGB1 in the nucleus accumbens (NAc) neurons.	Cocaine	19-26	high mobility group box 1	Homo sapiens	77-82
31056833-5	2020	Gain and loss of HMGB1 in the NAc bidirectionally regulate cocaine-induced conditioned place preference.	Cocaine	59-66	high mobility group box 1	Homo sapiens	17-22
31056833-6	2020	From the nucleus to the cytosol, HMGB1 binds to glutamate receptor subunits (GluA2/GluN2B) on the membrane, which regulates cocaine-induced synaptic adaptation and the formation of cocaine-related memory.	Cocaine	124-131	high mobility group box 1	Homo sapiens	33-38
31056833-6	2020	From the nucleus to the cytosol, HMGB1 binds to glutamate receptor subunits (GluA2/GluN2B) on the membrane, which regulates cocaine-induced synaptic adaptation and the formation of cocaine-related memory.	Cocaine	181-188	high mobility group box 1	Homo sapiens	33-38
32019497-0	2020	Expression of Concern to: Redox modification of cysteine residues regulates the cytokine activity of high mobility group box-1 (HMGB1).	Cysteine	48-56	high mobility group box 1	Homo sapiens	101-126
32019497-0	2020	Expression of Concern to: Redox modification of cysteine residues regulates the cytokine activity of high mobility group box-1 (HMGB1).	Cysteine	48-56	high mobility group box 1	Homo sapiens	128-133
32117622-0	2020	Glycyrrhizin suppresses epithelial-mesenchymal transition by inhibiting high-mobility group box1 via the TGF-beta1/Smad2/3 pathway in lung epithelial cells.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	72-96
32117622-2	2020	Glycyrrhizin, an active component extracted from licorice plant, has been reported to treat a variety of inflammatory reactions through inhibiting high-mobility group box1 (HMGB1), which has been suggested to be a significant mediator in EMT process.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	147-171
32117622-2	2020	Glycyrrhizin, an active component extracted from licorice plant, has been reported to treat a variety of inflammatory reactions through inhibiting high-mobility group box1 (HMGB1), which has been suggested to be a significant mediator in EMT process.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	173-178
32117622-11	2020	Notably, we found that glycyrrhizin treatment effectively suppressed TGF-beta1-induced EMT process by inhibiting HMGB1.	Glycyrrhizic Acid	23-35	high mobility group box 1	Homo sapiens	113-118
32117622-14	2020	Glycyrrhizin significantly blocked the phosphorylation of Smad2/3 stimulated either by TGF-beta1 or by ectopic HMGB1 in A549 and BEAS-2B cells.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	111-116
32117622-16	2020	Importantly, glycyrrhizin can effectively block Smad2/3 signaling pathway through inhibiting HMGB1, thereby suppressing the EMT progress.	Glycyrrhizic Acid	13-25	high mobility group box 1	Homo sapiens	93-98
31802650-11	2020	Inhibition of miR-34a or overexpression of HMGB1 could effectively reverse elevated 5-FU sensitivity upon NEAT1 knockdown.	Fluorouracil	84-88	high mobility group box 1	Homo sapiens	43-48
32175381-4	2020	However, whether curcumin could effectively inhibit inflammation through the suppression of HMGB1 production or HMGB1-mediated inflammatory responses in Abeta-activated microglia is still unclear.	Curcumin	17-25	high mobility group box 1	Homo sapiens	92-97
32175381-4	2020	However, whether curcumin could effectively inhibit inflammation through the suppression of HMGB1 production or HMGB1-mediated inflammatory responses in Abeta-activated microglia is still unclear.	Curcumin	17-25	high mobility group box 1	Homo sapiens	112-117
31916113-0	2020	Restoration of calcium-induced differentiation potential and tight junction formation in HaCaT keratinocytes by functional attenuation of overexpressed high mobility group box-1 protein.	Calcium	15-22	high mobility group box 1	Homo sapiens	152-177
31916113-5	2020	In contrast, dipotassium glycyrrhizate (GK2), a soluble analogue of HMGB1-blocker Glycyrrhizin, down-regulated interferon-beta, a typical inflammatory cytokine induced by secreted HMGB1, and accelerated differentiation responses to the calcium treatment in these cells.	glycyrrhizic acid methyl ester	13-38	high mobility group box 1	Homo sapiens	68-73
31916113-5	2020	In contrast, dipotassium glycyrrhizate (GK2), a soluble analogue of HMGB1-blocker Glycyrrhizin, down-regulated interferon-beta, a typical inflammatory cytokine induced by secreted HMGB1, and accelerated differentiation responses to the calcium treatment in these cells.	glycyrrhizic acid methyl ester	13-38	high mobility group box 1	Homo sapiens	180-185
31916113-5	2020	In contrast, dipotassium glycyrrhizate (GK2), a soluble analogue of HMGB1-blocker Glycyrrhizin, down-regulated interferon-beta, a typical inflammatory cytokine induced by secreted HMGB1, and accelerated differentiation responses to the calcium treatment in these cells.	Glycyrrhizic Acid	82-94	high mobility group box 1	Homo sapiens	68-73
31916113-5	2020	In contrast, dipotassium glycyrrhizate (GK2), a soluble analogue of HMGB1-blocker Glycyrrhizin, down-regulated interferon-beta, a typical inflammatory cytokine induced by secreted HMGB1, and accelerated differentiation responses to the calcium treatment in these cells.	Glycyrrhizic Acid	82-94	high mobility group box 1	Homo sapiens	180-185
31916113-5	2020	In contrast, dipotassium glycyrrhizate (GK2), a soluble analogue of HMGB1-blocker Glycyrrhizin, down-regulated interferon-beta, a typical inflammatory cytokine induced by secreted HMGB1, and accelerated differentiation responses to the calcium treatment in these cells.	Calcium	236-243	high mobility group box 1	Homo sapiens	68-73
32560618-0	2020	Antigene and Antiproliferative Effects of Triplex-Forming Oligonucleotide (TFO) Targeted on hmgb1 Gene in Human Hepatoma Cells.	triplex-forming oligonucleotide	42-73	high mobility group box 1	Homo sapiens	92-97
31733186-7	2020	Additionally, Linagliptin inhibited AGEs-induced production of high mobility group box chromosomal protein 1 (HMGB-1), and the expression of matrix metalloproteases (MMPs)-2 and -9.	linagliptin	14-25	high mobility group box 1	Homo sapiens	110-116
32096202-11	2020	Melatonin repressed the HMGB1, TNF-alpha, and iNOS mRNA expression, NO production, and nuclear factor kappaB (NF-kappaB) activation in OGD/R challenged SH SY5Y cells.	Melatonin	0-9	high mobility group box 1	Homo sapiens	24-29
33308096-6	2020	Brucine also triggered cell stress and induced features of ICD, including calreticulin (CRT) exposure and high-mobility group box 1 (HMGB1) release in MDA-MB-231 and CT26 cancer cells.	brucine	0-7	high mobility group box 1	Homo sapiens	106-131
33308096-6	2020	Brucine also triggered cell stress and induced features of ICD, including calreticulin (CRT) exposure and high-mobility group box 1 (HMGB1) release in MDA-MB-231 and CT26 cancer cells.	brucine	0-7	high mobility group box 1	Homo sapiens	133-138
32560618-6	2020	RESULTS: Treatment of HepG2 cell with specific Triplex-forming Oligonucleotide significantly downregulated HMGB1 expression level at mRNA and protein levels by 50%, while the classical anticancer drugs, actinomycin/adriamycin as positive controls showed 65% and the combination of TFO and drug decreased by 70%.	triplex-forming oligonucleotide	47-78	high mobility group box 1	Homo sapiens	107-112
32560618-6	2020	RESULTS: Treatment of HepG2 cell with specific Triplex-forming Oligonucleotide significantly downregulated HMGB1 expression level at mRNA and protein levels by 50%, while the classical anticancer drugs, actinomycin/adriamycin as positive controls showed 65% and the combination of TFO and drug decreased by 70%.	Dactinomycin	203-214	high mobility group box 1	Homo sapiens	107-112
32560618-6	2020	RESULTS: Treatment of HepG2 cell with specific Triplex-forming Oligonucleotide significantly downregulated HMGB1 expression level at mRNA and protein levels by 50%, while the classical anticancer drugs, actinomycin/adriamycin as positive controls showed 65% and the combination of TFO and drug decreased by 70%.	Doxorubicin	215-225	high mobility group box 1	Homo sapiens	107-112
32560618-6	2020	RESULTS: Treatment of HepG2 cell with specific Triplex-forming Oligonucleotide significantly downregulated HMGB1 expression level at mRNA and protein levels by 50%, while the classical anticancer drugs, actinomycin/adriamycin as positive controls showed 65% and the combination of TFO and drug decreased by 70%.	tfo	281-284	high mobility group box 1	Homo sapiens	107-112
32560618-9	2020	CONCLUSION: Therefore, the ability of hmgb1 targeted triplex-forming oligonucleotide in combination with triplex selective anticancer drug holds promise in the treatment of malignancies associated with hmgb1 overexpression.	triplex-forming oligonucleotide	53-84	high mobility group box 1	Homo sapiens	38-43
32560618-0	2020	Antigene and Antiproliferative Effects of Triplex-Forming Oligonucleotide (TFO) Targeted on hmgb1 Gene in Human Hepatoma Cells.	tfo	75-78	high mobility group box 1	Homo sapiens	92-97
32560618-9	2020	CONCLUSION: Therefore, the ability of hmgb1 targeted triplex-forming oligonucleotide in combination with triplex selective anticancer drug holds promise in the treatment of malignancies associated with hmgb1 overexpression.	triplex-forming oligonucleotide	53-84	high mobility group box 1	Homo sapiens	202-207
31585890-5	2020	This protective effect of simvastatin was largely due to improved lysosome function that attenuated lysosome injury-mediated Nlrp3 inflammasome activation and subsequent release of high mobility group box protein-1 (HMGB1).	Simvastatin	26-37	high mobility group box 1	Homo sapiens	181-214
31676289-0	2020	MSU Crystals induce sterile IL-1beta secretion via P2X7 receptor activation and HMGB1 release.	Uric Acid	0-3	high mobility group box 1	Homo sapiens	80-85
31676289-11	2020	Moreover, MSU treatment induced HMGB1 release; pre-treatment with P2X7 antagonist reduced the amount of HMGB1 in cell supernatants.	Uric Acid	10-13	high mobility group box 1	Homo sapiens	32-37
31676289-11	2020	Moreover, MSU treatment induced HMGB1 release; pre-treatment with P2X7 antagonist reduced the amount of HMGB1 in cell supernatants.	Uric Acid	10-13	high mobility group box 1	Homo sapiens	104-109
31676289-12	2020	CONCLUSIONS: IL-1beta secretion induced by MSU depends on P2X7 receptor activation and involves HMGB1 release.	Uric Acid	43-46	high mobility group box 1	Homo sapiens	96-101
31676289-13	2020	GENERAL SIGNIFICANCE: We propose that cell activation caused by MSU crystals induces peritoneal macrophages and THP-1 cells to release ATP and HMGB1, causing IL-1beta secretion via P2X7 receptor activation.	Uric Acid	64-67	high mobility group box 1	Homo sapiens	143-148
32115500-0	2020	Docetaxel Upregulates HMGB1 Levels in Non-small Cell Lung Cancer.	Docetaxel	0-9	high mobility group box 1	Homo sapiens	22-27
32115500-6	2020	On the other hand, plasma levels of high-mobility group box 1 (HMGB1), a damage-associated molecular pattern (DAMP) protein, showed significant increase after docetaxel treatment.	Docetaxel	159-168	high mobility group box 1	Homo sapiens	36-61
32115500-6	2020	On the other hand, plasma levels of high-mobility group box 1 (HMGB1), a damage-associated molecular pattern (DAMP) protein, showed significant increase after docetaxel treatment.	Docetaxel	159-168	high mobility group box 1	Homo sapiens	63-68
32115500-9	2020	These findings imply that docetaxel could be involved in anti-tumor immunity via HMGB1.	Docetaxel	26-35	high mobility group box 1	Homo sapiens	81-86
33268671-0	2020	(-)-Epigallocatechin-3-gallate inhibits RANKL-induced osteoclastogenesis via downregulation of NFATc1 and suppression of HO-1-HMGB1-RAGE pathway.	epigallocatechin gallate	0-30	high mobility group box 1	Homo sapiens	126-131
33268671-8	2020	We also found that EGCG upregulated heme oxygenase-1 (HO-1) and suppressed the extracellular release of high-mobility group box 1 (HMGB1).	epigallocatechin gallate	19-23	high mobility group box 1	Homo sapiens	104-129
33268671-8	2020	We also found that EGCG upregulated heme oxygenase-1 (HO-1) and suppressed the extracellular release of high-mobility group box 1 (HMGB1).	epigallocatechin gallate	19-23	high mobility group box 1	Homo sapiens	131-136
33268671-9	2020	In addition, EGCG decreased the expression of the receptor for advanced glycation end products (RAGE), which is the receptor of HMGB1, in osteoclastogenesis.	epigallocatechin gallate	13-17	high mobility group box 1	Homo sapiens	128-133
33268671-10	2020	In summary, our study showed that EGCG could inhibit osteoclast differentiation through the downregulation of NFATc1 and the suppression of the HO-1-HMGB1-RAGE pathway.	epigallocatechin gallate	34-38	high mobility group box 1	Homo sapiens	149-154
31585890-5	2020	This protective effect of simvastatin was largely due to improved lysosome function that attenuated lysosome injury-mediated Nlrp3 inflammasome activation and subsequent release of high mobility group box protein-1 (HMGB1).	Simvastatin	26-37	high mobility group box 1	Homo sapiens	216-221
31875024-4	2019	A bioinformatics analysis predicted the binding of HMGB1 by the miR-548 cluster.	mir-548	64-71	high mobility group box 1	Homo sapiens	51-56
31769590-6	2020	Blockade of HMGB1 with chicken anti-HMGB1 polyclonal antibody (anti-HMGB1) or glycyrrhizin (Gly) attenuated the increase of LC3B-II and Beclin1, migration and p65 phosphorylation, suggesting the involvement of HMGB1 in autophagy, migration and NF-kappaB activation of lung macrophages.	Glycyrrhizic Acid	92-95	high mobility group box 1	Homo sapiens	12-17
31897190-6	2020	The results of the current study indicated that HMGB1 was localized to the nucleus and the cytoplasm, and it was determined to combine with the condensed chromosomes of proliferating cells in paraformaldehyde (PFA)-fixed glioma tissues.	paraform	192-208	high mobility group box 1	Homo sapiens	48-53
31897190-6	2020	The results of the current study indicated that HMGB1 was localized to the nucleus and the cytoplasm, and it was determined to combine with the condensed chromosomes of proliferating cells in paraformaldehyde (PFA)-fixed glioma tissues.	paraform	210-213	high mobility group box 1	Homo sapiens	48-53
31897190-7	2020	However, HMGB1 was also associated with interphase (but not mitotic chromosomes) when fixed with chilled methanol and 5% (v/v) acetic acid or PFA in vitro.	Methanol	105-113	high mobility group box 1	Homo sapiens	9-14
31897190-7	2020	However, HMGB1 was also associated with interphase (but not mitotic chromosomes) when fixed with chilled methanol and 5% (v/v) acetic acid or PFA in vitro.	Acetic Acid	127-138	high mobility group box 1	Homo sapiens	9-14
31897190-7	2020	However, HMGB1 was also associated with interphase (but not mitotic chromosomes) when fixed with chilled methanol and 5% (v/v) acetic acid or PFA in vitro.	paraform	142-145	high mobility group box 1	Homo sapiens	9-14
31806570-5	2020	Here, we found that the specific agonist of CB2R, GW405833 (GW) could induce intracellular HMGB1 degradation without influencing HMGB1 mRNA in peritoneal macrophages.	1-(2,3-dichlorobenzoyl)-5-methoxy-2-methyl-(2-(mopholin-4-yl)ethyl)-1H-indole	50-58	high mobility group box 1	Homo sapiens	91-96
31806570-5	2020	Here, we found that the specific agonist of CB2R, GW405833 (GW) could induce intracellular HMGB1 degradation without influencing HMGB1 mRNA in peritoneal macrophages.	1-(2,3-dichlorobenzoyl)-5-methoxy-2-methyl-(2-(mopholin-4-yl)ethyl)-1H-indole	50-52	high mobility group box 1	Homo sapiens	91-96
31806570-6	2020	Then we observed that autophagy inhibitor 3-methyladenine (3-MA) but not proteasome inhibitor MG-132 (MG) could block GW-induced HMGB1 degradation, which indicated that the autophagy-lysosome but not the ubiquitination pathway was involved in this process.	3-methyladenine	42-57	high mobility group box 1	Homo sapiens	129-134
31806570-6	2020	Then we observed that autophagy inhibitor 3-methyladenine (3-MA) but not proteasome inhibitor MG-132 (MG) could block GW-induced HMGB1 degradation, which indicated that the autophagy-lysosome but not the ubiquitination pathway was involved in this process.	3-methyladenine	59-63	high mobility group box 1	Homo sapiens	129-134
31806570-6	2020	Then we observed that autophagy inhibitor 3-methyladenine (3-MA) but not proteasome inhibitor MG-132 (MG) could block GW-induced HMGB1 degradation, which indicated that the autophagy-lysosome but not the ubiquitination pathway was involved in this process.	1-(2,3-dichlorobenzoyl)-5-methoxy-2-methyl-(2-(mopholin-4-yl)ethyl)-1H-indole	118-120	high mobility group box 1	Homo sapiens	129-134
31806570-8	2020	It also observed that inhibition of autophagy blocked GW-induced nuclear translocation of HMGB1 in macrophages.	1-(2,3-dichlorobenzoyl)-5-methoxy-2-methyl-(2-(mopholin-4-yl)ethyl)-1H-indole	54-56	high mobility group box 1	Homo sapiens	90-95
31897149-0	2020	Poly (ADP-ribosylation) of HMGB1 facilitates its acetylation and promotes HMGB1 translocation-associated chemotherapy-induced autophagy in leukaemia cells.	poly If	0-4	high mobility group box 1	Homo sapiens	27-32
31897149-0	2020	Poly (ADP-ribosylation) of HMGB1 facilitates its acetylation and promotes HMGB1 translocation-associated chemotherapy-induced autophagy in leukaemia cells.	poly If	0-4	high mobility group box 1	Homo sapiens	74-79
31897149-0	2020	Poly (ADP-ribosylation) of HMGB1 facilitates its acetylation and promotes HMGB1 translocation-associated chemotherapy-induced autophagy in leukaemia cells.	Adenosine Diphosphate	6-9	high mobility group box 1	Homo sapiens	27-32
31897149-0	2020	Poly (ADP-ribosylation) of HMGB1 facilitates its acetylation and promotes HMGB1 translocation-associated chemotherapy-induced autophagy in leukaemia cells.	Adenosine Diphosphate	6-9	high mobility group box 1	Homo sapiens	74-79
31897149-6	2020	It was further demonstrated that poly (ADP-ribosylation) of HMGB1 facilitates its acetylation, thereby inducing HMGB1 translocation and ultimately promoting chemotherapy-induced autophagy in leukaemic cells.	poly If	33-37	high mobility group box 1	Homo sapiens	60-65
31897149-6	2020	It was further demonstrated that poly (ADP-ribosylation) of HMGB1 facilitates its acetylation, thereby inducing HMGB1 translocation and ultimately promoting chemotherapy-induced autophagy in leukaemic cells.	poly If	33-37	high mobility group box 1	Homo sapiens	112-117
31897149-6	2020	It was further demonstrated that poly (ADP-ribosylation) of HMGB1 facilitates its acetylation, thereby inducing HMGB1 translocation and ultimately promoting chemotherapy-induced autophagy in leukaemic cells.	Adenosine Diphosphate	39-42	high mobility group box 1	Homo sapiens	60-65
31897149-6	2020	It was further demonstrated that poly (ADP-ribosylation) of HMGB1 facilitates its acetylation, thereby inducing HMGB1 translocation and ultimately promoting chemotherapy-induced autophagy in leukaemic cells.	Adenosine Diphosphate	39-42	high mobility group box 1	Homo sapiens	112-117
31905926-3	2019	Comparison of CDDP-sensitive cases with CDDP-resistant cases, the expression of c-met, HMGB1, and PCDHB9 was correlated with CDDP resistance.	Cisplatin	14-18	high mobility group box 1	Homo sapiens	87-92
31905926-3	2019	Comparison of CDDP-sensitive cases with CDDP-resistant cases, the expression of c-met, HMGB1, and PCDHB9 was correlated with CDDP resistance.	Cisplatin	40-44	high mobility group box 1	Homo sapiens	87-92
31905926-3	2019	Comparison of CDDP-sensitive cases with CDDP-resistant cases, the expression of c-met, HMGB1, and PCDHB9 was correlated with CDDP resistance.	Cisplatin	40-44	high mobility group box 1	Homo sapiens	87-92
31905926-4	2019	Among them, the expression of HMGB1 showed the most significant correlation with CDDP resistance in multivariate analysis.	Cisplatin	81-85	high mobility group box 1	Homo sapiens	30-35
31905926-5	2019	Treatment of TMK-1 and MKN74 human gastric cancer cell lines with ethyl pyruvate (EP) or tanshinone IIA (TAN), which are reported to inhibit HMGB1 signaling, showed a 4-5-fold increase in inhibition by CDDP.	ethyl pyruvate	66-80	high mobility group box 1	Homo sapiens	141-146
31905926-5	2019	Treatment of TMK-1 and MKN74 human gastric cancer cell lines with ethyl pyruvate (EP) or tanshinone IIA (TAN), which are reported to inhibit HMGB1 signaling, showed a 4-5-fold increase in inhibition by CDDP.	ethyl pyruvate	82-84	high mobility group box 1	Homo sapiens	141-146
31905926-5	2019	Treatment of TMK-1 and MKN74 human gastric cancer cell lines with ethyl pyruvate (EP) or tanshinone IIA (TAN), which are reported to inhibit HMGB1 signaling, showed a 4-5-fold increase in inhibition by CDDP.	tanshinone	89-103	high mobility group box 1	Homo sapiens	141-146
31905926-5	2019	Treatment of TMK-1 and MKN74 human gastric cancer cell lines with ethyl pyruvate (EP) or tanshinone IIA (TAN), which are reported to inhibit HMGB1 signaling, showed a 4-5-fold increase in inhibition by CDDP.	tanshinone	105-108	high mobility group box 1	Homo sapiens	141-146
31905926-6	2019	Treatment with EP or TAN also suppressed the expression of TLR4 and MyD88 in the HMGB1 signal transduction pathway and suppressed the activity of NFkappaB in both cell lines.	ethyl pyruvate	15-17	high mobility group box 1	Homo sapiens	81-86
31905926-6	2019	Treatment with EP or TAN also suppressed the expression of TLR4 and MyD88 in the HMGB1 signal transduction pathway and suppressed the activity of NFkappaB in both cell lines.	tanshinone	21-24	high mobility group box 1	Homo sapiens	81-86
31905926-7	2019	These results suggest that the expression of these cancer metastasis-related genes is also related to anticancer drug resistance and that suppression of HMGB1 may be particularly useful for CDDP sensitization.	Cisplatin	190-194	high mobility group box 1	Homo sapiens	153-158
31875024-9	2019	Moreover, forced expression of miR-548 suppressed HMGB1 and inflammatory cytokines in hAECs, which increased when treated with lipopolysaccharide.	mir-548	31-38	high mobility group box 1	Homo sapiens	50-55
31875024-10	2019	These results suggest miR-548 can alter the inflammatory responses in hAECs, and might be involved in the pathogenesis of preterm birth by regulating HMGB1.	mir-548	22-29	high mobility group box 1	Homo sapiens	150-155
31810939-3	2019	Previously, we identified an anticancer candidate, papaverine, that inhibited the HMGB1-RAGE interaction.	Papaverine	51-61	high mobility group box 1	Homo sapiens	82-87
31844158-4	2019	Acetylated HMGB1 (Ac-HMGB1) secreted by geminin-overexpressing cells activates RAGE and CXCR4 expression on mesenchymal stem cells (MSCs) located in tumor stroma.	Actinium	0-2	high mobility group box 1	Homo sapiens	11-16
31844158-4	2019	Acetylated HMGB1 (Ac-HMGB1) secreted by geminin-overexpressing cells activates RAGE and CXCR4 expression on mesenchymal stem cells (MSCs) located in tumor stroma.	Actinium	0-2	high mobility group box 1	Homo sapiens	21-26
31106593-6	2019	Furthermore, salicin inhibits IL-1beta-induced production of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1), vascular adhesion molecules such as intercellular cell adhesion molecule-1 (iCAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and high-mobility group protein 1 (HMGB-1).	salicin	13-20	high mobility group box 1	Homo sapiens	374-380
30945564-8	2019	Mechanistically, we show that vildagliptin suppresses FFA-induced expression of proteins of the NLRP3 inflammasome complex, including NLRP3, ASC, p20 and HMGB-1, and mitigates FFA-induced inactivation of the AMPK pathway.	Vildagliptin	30-42	high mobility group box 1	Homo sapiens	154-160
30945564-8	2019	Mechanistically, we show that vildagliptin suppresses FFA-induced expression of proteins of the NLRP3 inflammasome complex, including NLRP3, ASC, p20 and HMGB-1, and mitigates FFA-induced inactivation of the AMPK pathway.	Fatty Acids, Nonesterified	54-57	high mobility group box 1	Homo sapiens	154-160
30945564-11	2019	Collectively, we conclude that the protective role of vildagliptin in endothelial cells is mediated via suppression of the AMPK-NLRP3 inflammasome-HMGB-1 axis pathway.	Vildagliptin	54-66	high mobility group box 1	Homo sapiens	147-153
31666085-2	2019	Endothelial thrombomodulin (TM) promotes thrombin-induced degradation of HMGB1, and TMalpha, a recombinant human soluble TM, abolishes peripheral HMGB1-induced allodynia in mice.	tmalpha	84-91	high mobility group box 1	Homo sapiens	146-151
31514535-5	2019	We found that cilostazol significantly reduced NLRP3 inflammasome activation, as well as the activity of other related and harmful factors, including oxidative stress, expression of NADPH oxidase 4 (NOX-4), thioredoxin-interacting protein (TxNIP), high mobility group box 1 (HMGB-1), interleukin 1beta (IL-1beta) and IL-18.	Cilostazol	14-24	high mobility group box 1	Homo sapiens	248-273
31514535-5	2019	We found that cilostazol significantly reduced NLRP3 inflammasome activation, as well as the activity of other related and harmful factors, including oxidative stress, expression of NADPH oxidase 4 (NOX-4), thioredoxin-interacting protein (TxNIP), high mobility group box 1 (HMGB-1), interleukin 1beta (IL-1beta) and IL-18.	Cilostazol	14-24	high mobility group box 1	Homo sapiens	275-281
31418997-0	2019	Long noncoding RNA XIST enhances ethanol-induced hepatic stellate cells autophagy and activation via miR-29b/HMGB1 axis.	Ethanol	33-40	high mobility group box 1	Homo sapiens	109-114
31418997-12	2019	Collectively, XIST enhances ethanol-induced HSCs autophagy and activation via miR-29b/HMGB1 axis.	Ethanol	28-35	high mobility group box 1	Homo sapiens	86-91
31611261-7	2019	Mechanistically, hresistin promoted HMGB1 posttranslational lysine acetylation by preserving the NAD+-dependent deacetylase sirtuin (Sirt) 1 in human macrophages.	tyrosyl-lysine	60-66	high mobility group box 1	Homo sapiens	36-41
31849690-4	2019	In this pathological process, PM2.5 particles, excessive reactive oxygen species (ROS) derived from PM2.5, and certain components in PM2.5, such as ions and polyaromatic hydrocarbons (PAHs), have been implicated as potential EMT mediators that are linked to the activation of transforming growth factor beta (TGF-beta)/SMADs, NF-kappaB, growth factor (GF)/extracellular signal-regulated protein kinase (ERK), GF/phosphatidylinositol 3-kinase (PI3K)/Akt, wingless/integrated (Wnt)/beta-catenin, Notch, Hedgehog, high mobility group box B1 (HMGB1)-receptor for advanced glycation end-products (RAGE), and aryl hydrocarbon receptor (AHR) signaling cascades and to cytoskeleton rearrangement.	Hydrocarbons	184-188	high mobility group box 1	Homo sapiens	511-537
31849690-4	2019	In this pathological process, PM2.5 particles, excessive reactive oxygen species (ROS) derived from PM2.5, and certain components in PM2.5, such as ions and polyaromatic hydrocarbons (PAHs), have been implicated as potential EMT mediators that are linked to the activation of transforming growth factor beta (TGF-beta)/SMADs, NF-kappaB, growth factor (GF)/extracellular signal-regulated protein kinase (ERK), GF/phosphatidylinositol 3-kinase (PI3K)/Akt, wingless/integrated (Wnt)/beta-catenin, Notch, Hedgehog, high mobility group box B1 (HMGB1)-receptor for advanced glycation end-products (RAGE), and aryl hydrocarbon receptor (AHR) signaling cascades and to cytoskeleton rearrangement.	Hydrocarbons	184-188	high mobility group box 1	Homo sapiens	539-544
31570601-0	2019	HMGB1-C1q complexes regulate macrophage function by switching between leukotriene and specialized proresolving mediator biosynthesis.	Leukotrienes	70-81	high mobility group box 1	Homo sapiens	0-5
31570601-6	2019	Here, we show that HMGB1 induces leukotriene production through a RAGE-dependent pathway, while HMGB1 plus C1q induces specialized proresolving lipid mediators lipoxin A4, resolvin D1, and resolvin D2 through a RAGE- and LAIR-1-dependent pathway.	Leukotrienes	33-44	high mobility group box 1	Homo sapiens	19-24
31087368-3	2019	Here, we reported that high mobility group box 1 (HMGB1) was highly elevated in high glucose (HG)-treated mesangial cells, and induced the phosphorylation, nuclear translocation, and DNA binding activity of NF-kappaB via toll-like receptor 4 (TLR4).	Glucose	85-92	high mobility group box 1	Homo sapiens	23-48
31087368-3	2019	Here, we reported that high mobility group box 1 (HMGB1) was highly elevated in high glucose (HG)-treated mesangial cells, and induced the phosphorylation, nuclear translocation, and DNA binding activity of NF-kappaB via toll-like receptor 4 (TLR4).	Glucose	85-92	high mobility group box 1	Homo sapiens	50-55
31629951-0	2019	XIAOPI formula promotes breast cancer chemosensitivity via inhibiting CXCL1/HMGB1-mediated autophagy.	xiaopi formula	0-14	high mobility group box 1	Homo sapiens	76-81
31629951-11	2019	Taken together, XIAOPI formula is a potential adjuvant drug via inhibiting CXCL1/HMGB1-mediated autophagy for breast cancer treatment with good safety.	xiaopi formula	16-30	high mobility group box 1	Homo sapiens	81-86
31353785-2	2019	HMGB1 is implicated in hyperglycemia and excess glucose in trophoblast.	Glucose	48-55	high mobility group box 1	Homo sapiens	0-5
31545873-0	2019	Protective effect of glycyrrhizic acid on cerebral ischemia/reperfusion injury via inhibiting HMGB1-mediated TLR4/NF-kappaB pathway.	Glycyrrhizic Acid	21-38	high mobility group box 1	Homo sapiens	94-99
31545873-7	2019	Moreover, GA inhibited the expressions of high-mobility group protein box-1 (HMGB1)-mediated TLR4/NF-kappaB pathway.	Glycyrrhizic Acid	10-12	high mobility group box 1	Homo sapiens	42-75
31545873-7	2019	Moreover, GA inhibited the expressions of high-mobility group protein box-1 (HMGB1)-mediated TLR4/NF-kappaB pathway.	Glycyrrhizic Acid	10-12	high mobility group box 1	Homo sapiens	77-82
31545398-8	2019	The present study also demonstrated that bexarotene exerted an anti-inflammatory effect by downregulating expression of interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1, and high mobility group box-1.	Bexarotene	41-51	high mobility group box 1	Homo sapiens	186-211
31664305-0	2019	Upregulation of miR-129-5p increases the sensitivity to Taxol through inhibiting HMGB1-mediated cell autophagy in breast cancer MCF-7 cells.	Paclitaxel	56-61	high mobility group box 1	Homo sapiens	81-86
31754297-0	2019	miR- 26a Sensitizes Melanoma Cells To Dabrafenib Via Targeting HMGB1-Dependent Autophagy Pathways.	dabrafenib	38-48	high mobility group box 1	Homo sapiens	63-68
31754297-2	2019	Methods: In our study, we conducted a variety of studies, including quantitative PCR, Western blot, and autophagy and apoptosis assays to investigate the involvement of miR-26a and HMGB1 in modulation of dabrafenib sensitivity in human melanoma cell lines.	dabrafenib	204-214	high mobility group box 1	Homo sapiens	181-186
31754297-3	2019	Results: Our studies revealed that the expressions of miR-26a and HMGB1 were altered in two melanoma cell lines after dabrafenib treatment.	dabrafenib	118-128	high mobility group box 1	Homo sapiens	66-71
31664305-10	2019	We found that interference of HMGB1 enhanced the chemosensitivity of Taxol by inhibiting autophagy and inducing apoptosis in MCF-7 cells.	Paclitaxel	69-74	high mobility group box 1	Homo sapiens	30-35
31754297-4	2019	Additionally, dabrafenib caused autophagy in melanoma and this autophagic process was regulated by miR-26a via modifying HMGB1 expression.	dabrafenib	14-24	high mobility group box 1	Homo sapiens	121-126
31754297-5	2019	Furthermore, silencing HMGB1-inhibited autophagy induced by dabrafenib in melanoma cells.	dabrafenib	60-70	high mobility group box 1	Homo sapiens	23-28
31664305-11	2019	Taken together, our findings suggested that miR-129-5p increased the chemosensitivity of MCF-7 cells to Taxol through suppressing autophagy and enhancing apoptosis by inhibiting HMGB1.	Paclitaxel	104-109	high mobility group box 1	Homo sapiens	178-183
31754297-6	2019	Last, we verified that treatment with a miR-26a mimic and HMGB1 shRNA could increase the efficacy of dabrafenib in melanoma cells.	dabrafenib	101-111	high mobility group box 1	Homo sapiens	58-63
31664305-12	2019	Using miR-129-5p/HMGB1/autophagy-based therapeutic strategies may be a potential treatment for overcoming Taxol resistance in breast cancer.	Paclitaxel	106-111	high mobility group box 1	Homo sapiens	17-22
31754297-7	2019	Conclusion: Taken together, we showed that miR-26a is involved in the regulation of dabrafenib efficacy via a HMGB1-dependent autophagy pathway in melanoma cells.	dabrafenib	84-94	high mobility group box 1	Homo sapiens	110-115
31695615-9	2019	The plasma levels of IL-1beta, IL-6, TNF-alpha, HMGB1, and netrin-1 were significantly reduced with the treatment of minocycline.	Minocycline	117-128	high mobility group box 1	Homo sapiens	48-53
31284735-10	2019	Indeed, although WT MEF entered senescence accompanied by p21 increase, HMGB1 KO underwent apoptosis with p21 decrease by Dox treatment.	Doxorubicin	122-125	high mobility group box 1	Homo sapiens	72-77
31636696-3	2019	In addition, resveratrol treatment stimulated cell surface exposure of calreticulin, HMGB1 secretion and ATP release.	resveratrol	13-24	high mobility group box 1	Homo sapiens	85-90
31418171-2	2019	HMGB1 has several redox states: reduced HMGB1 recruits inflammatory cells to injured tissues forming a heterocomplex with CXCL12 and signaling via its receptor CXCR4; disulfide-containing HMGB1 binds to TLR4 and promotes inflammatory responses.	Disulfides	167-176	high mobility group box 1	Homo sapiens	0-5
31418171-3	2019	Here we show that diflunisal, an aspirin-like nonsteroidal anti-inflammatory drug (NSAID) that has been in clinical use for decades, specifically inhibits in vitro and in vivo the chemotactic activity of HMGB1 at nanomolar concentrations, at least in part by binding directly to both HMGB1 and CXCL12 and disrupting their heterocomplex.	Diflunisal	18-28	high mobility group box 1	Homo sapiens	204-209
31418171-3	2019	Here we show that diflunisal, an aspirin-like nonsteroidal anti-inflammatory drug (NSAID) that has been in clinical use for decades, specifically inhibits in vitro and in vivo the chemotactic activity of HMGB1 at nanomolar concentrations, at least in part by binding directly to both HMGB1 and CXCL12 and disrupting their heterocomplex.	Diflunisal	18-28	high mobility group box 1	Homo sapiens	284-289
31418171-3	2019	Here we show that diflunisal, an aspirin-like nonsteroidal anti-inflammatory drug (NSAID) that has been in clinical use for decades, specifically inhibits in vitro and in vivo the chemotactic activity of HMGB1 at nanomolar concentrations, at least in part by binding directly to both HMGB1 and CXCL12 and disrupting their heterocomplex.	Aspirin	33-40	high mobility group box 1	Homo sapiens	204-209
31284735-7	2019	In senescent B16-F10, SK-MEL-24, and LS174T cells treated with Dox, p21 levels were increased by persistent HMGB1 expression.	Doxorubicin	63-66	high mobility group box 1	Homo sapiens	108-113
31558702-6	2019	Mechanistically, HMGB1 binding with TLR2 receptor functions in a paracrine manner to affect CD133- pancreatic cancer cells dedifferentiation via activating Hippo-YAP pathway and HIF-1alpha expression in oxygen independent manner in vitro and in vivo.	Oxygen	203-209	high mobility group box 1	Homo sapiens	17-22
30998983-6	2019	Furthermore, cultured normal human melanocytes could release HMGB1 under treatment with hydrogen peroxide.	Hydrogen Peroxide	88-105	high mobility group box 1	Homo sapiens	61-66
31525576-0	2019	Cucurbitacin E ameliorates lipopolysaccharide-evoked injury, inflammation and MUC5AC expression in bronchial epithelial cells by restraining the HMGB1-TLR4-NF-kappaB signaling.	cucurbitacin E	0-14	high mobility group box 1	Homo sapiens	145-150
31547018-0	2019	HMGB1-triggered inflammation inhibition of notoginseng leaf triterpenes against cerebral ischemia and reperfusion injury via MAPK and NF-kappaB signaling pathways.	Triterpenes	60-71	high mobility group box 1	Homo sapiens	0-5
31527653-7	2019	After ex vivo trauma and/or CHX/TNF stimulation, addition of zVAD further enhanced expression of necroptosis-related markers as well as release of PGE2 and nitric oxide, which was in line with increased cell death and subsequent release of intracellular HMGB1 and dsDNA in CHX/TNF stimulated chondrocytes.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	61-65	high mobility group box 1	Homo sapiens	254-259
31607859-5	2019	HMGB1 was then passed through the impaired cell membrane to upregulate the receptor for advanced glycation end-products (RAGE), nuclear factor (NF)-kappaB, and inflammatory factors such as interleukin-6 (IL-6), interleukin-1 (IL-1beta), as well as NACHT, LRR and PYD domains-containing protein 3 (NLRP3).	Nalp5 protein, mouse	248-253	high mobility group box 1	Homo sapiens	0-5
31351069-7	2019	We also show that orexin A inhibits high glucose-induced expression of TxNIP, which is crucial to the activation of the NLRP3 inflammasome, as well as that of HMGB1.	Glucose	41-48	high mobility group box 1	Homo sapiens	159-164
31630719-6	2019	A significant positive correlation was found both between total cholesterol levels and HMGB1 values (r=0.846, p=0.000) and between LDL cholesterol and HMBG1 values (r=0.663, p=0.001).	Cholesterol	64-75	high mobility group box 1	Homo sapiens	87-92
31369761-2	2019	The aim of current study is to investigate whether melatonin would be protective in doxorubicin-induced beta (beta) cell toxicity via HMGB1/TLR2/TLR4/MAPK/NF-kB signaling pathway.	Melatonin	51-60	high mobility group box 1	Homo sapiens	134-139
31369761-2	2019	The aim of current study is to investigate whether melatonin would be protective in doxorubicin-induced beta (beta) cell toxicity via HMGB1/TLR2/TLR4/MAPK/NF-kB signaling pathway.	Doxorubicin	84-95	high mobility group box 1	Homo sapiens	134-139
31510019-7	2019	Co-culture blunted ethanol-induced high mobility group box protein 1 (HMGB1)-TLR responses, corresponding with reduced ethanol induction of several proinflammatory NFkappaB target genes.	Ethanol	19-26	high mobility group box 1	Homo sapiens	35-68
31510019-7	2019	Co-culture blunted ethanol-induced high mobility group box protein 1 (HMGB1)-TLR responses, corresponding with reduced ethanol induction of several proinflammatory NFkappaB target genes.	Ethanol	19-26	high mobility group box 1	Homo sapiens	70-75
31252267-13	2019	In conclusion, SNHG14 silencing suppressed NSCLC progression at least partly by miR-34a/HMGB1 axis in vitroand promoted NSCLC cell sensitivity to CDDP, highlighting that SNHG14 might be a potential target for NSCLC therapy.	Cisplatin	146-150	high mobility group box 1	Homo sapiens	88-93
30238832-5	2019	From our findings, we hypothesize that disulfide A-box fragment binds as an anchor toward the TLR4-MD-2 but does not facilitate the TLR4 dimer formation, thereby competing with the HMGb1-binding site and preventing HMGb1-induced signaling and downstream inflammation, whereas the pro-inflammatory B-box fragment retains the MD-2 active conformation and binds to both TLR4 proteins in the complex to aid TLR4 dimer formation, which activates the intracellular signaling for downstream inflammatory pathways and cytokine release.	Disulfides	39-48	high mobility group box 1	Homo sapiens	181-186
30238832-5	2019	From our findings, we hypothesize that disulfide A-box fragment binds as an anchor toward the TLR4-MD-2 but does not facilitate the TLR4 dimer formation, thereby competing with the HMGb1-binding site and preventing HMGb1-induced signaling and downstream inflammation, whereas the pro-inflammatory B-box fragment retains the MD-2 active conformation and binds to both TLR4 proteins in the complex to aid TLR4 dimer formation, which activates the intracellular signaling for downstream inflammatory pathways and cytokine release.	Disulfides	39-48	high mobility group box 1	Homo sapiens	215-220
30647411-6	2019	This protective effect of NecroX-7 was mediated by inhibition of HMGB1 release and downregulation of mitochondrial oxidative stress.	necrox-7	26-34	high mobility group box 1	Homo sapiens	65-70
31079281-6	2019	ROS increase the synthesis of Abeta, high-mobility group box 1(HMGB1), and S100 that interacts with RAGE to produce additional ROS resulting in enhancement of AD pathology.	Reactive Oxygen Species	0-3	high mobility group box 1	Homo sapiens	37-62
31079281-6	2019	ROS increase the synthesis of Abeta, high-mobility group box 1(HMGB1), and S100 that interacts with RAGE to produce additional ROS resulting in enhancement of AD pathology.	Reactive Oxygen Species	0-3	high mobility group box 1	Homo sapiens	63-68
31695540-10	2019	Serum HMGB1 levels were positively correlated with aspartate aminotransferase (rs =0.48, p&lt;0.01, Spearman"s rank correlation coefficient) and negatively correlated with fibrinogen (rs = -0.475, p=0.011) and hemoglobin (rs = -0.465, p=0.013).	Aspartic Acid	51-60	high mobility group box 1	Homo sapiens	6-11
31079281-6	2019	ROS increase the synthesis of Abeta, high-mobility group box 1(HMGB1), and S100 that interacts with RAGE to produce additional ROS resulting in enhancement of AD pathology.	Reactive Oxygen Species	127-130	high mobility group box 1	Homo sapiens	37-62
31079281-6	2019	ROS increase the synthesis of Abeta, high-mobility group box 1(HMGB1), and S100 that interacts with RAGE to produce additional ROS resulting in enhancement of AD pathology.	Reactive Oxygen Species	127-130	high mobility group box 1	Homo sapiens	63-68
31129968-6	2019	Ectopic expression of RIP3 promoted cisplatin-induced HepG2/DDP cells death, HMGB1 and LDH release.	Cisplatin	36-45	high mobility group box 1	Homo sapiens	77-82
31146014-0	2019	Hyperbaric oxygen inhibits the HMGB1/RAGE signaling pathway by upregulating Mir-107 expression in human osteoarthritic chondrocytes.	Oxygen	11-17	high mobility group box 1	Homo sapiens	31-36
31507595-3	2019	In suppressing activated T cells, it first sequesters the pro-inflammatory high mobility group Box 1 (HMGB1) protein, which facilitates its binding to the inhibitory sialic acid-binding immunoglobulin-like lectin-10 (Siglec-10) receptor.	N-Acetylneuraminic Acid	166-177	high mobility group box 1	Homo sapiens	75-100
31507595-3	2019	In suppressing activated T cells, it first sequesters the pro-inflammatory high mobility group Box 1 (HMGB1) protein, which facilitates its binding to the inhibitory sialic acid-binding immunoglobulin-like lectin-10 (Siglec-10) receptor.	N-Acetylneuraminic Acid	166-177	high mobility group box 1	Homo sapiens	102-107
31484595-3	2019	This study aimed to investigate the role of high mobility group box protein 1 (HMGB1) and the toll-like receptor 4 (TLR4) pathway in normal human gastric epithelial (GES-1) cells under clopidogrel exposure.	Clopidogrel	185-196	high mobility group box 1	Homo sapiens	44-77
31484595-3	2019	This study aimed to investigate the role of high mobility group box protein 1 (HMGB1) and the toll-like receptor 4 (TLR4) pathway in normal human gastric epithelial (GES-1) cells under clopidogrel exposure.	Clopidogrel	185-196	high mobility group box 1	Homo sapiens	79-84
31484595-5	2019	A laser scanning confocal microscope was used to determine the distribution of HMGB1 and TLR4 in clopidogrel-induced injury.	Clopidogrel	97-108	high mobility group box 1	Homo sapiens	79-84
31484595-8	2019	We found the expression of HMGB1 and TLR4 in the cytoplasm increased after clopidogrel administration.	Clopidogrel	75-86	high mobility group box 1	Homo sapiens	27-32
31484595-9	2019	Besides, inhibited TLR4, which is a receptor of HMGB1, prevented the injury and occludin reducing caused by clopidogrel challenge.	Clopidogrel	108-119	high mobility group box 1	Homo sapiens	48-53
31484595-10	2019	Furthermore, blocking HMGB1 or TLR4 activity by ethyl pyruvate (HMGB1 inhibitor) or cli-095(TLR4 inhibitor) can partially diminish the activation of p38MAPK.	ethyl pyruvate	48-62	high mobility group box 1	Homo sapiens	22-27
31484595-10	2019	Furthermore, blocking HMGB1 or TLR4 activity by ethyl pyruvate (HMGB1 inhibitor) or cli-095(TLR4 inhibitor) can partially diminish the activation of p38MAPK.	ethyl pyruvate	48-62	high mobility group box 1	Homo sapiens	64-69
31484595-10	2019	Furthermore, blocking HMGB1 or TLR4 activity by ethyl pyruvate (HMGB1 inhibitor) or cli-095(TLR4 inhibitor) can partially diminish the activation of p38MAPK.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	84-91	high mobility group box 1	Homo sapiens	22-27
31484595-11	2019	Gastric mucosal damages observed by clopidogrel challenge are associated with HMGB1, TLR4, through p38MAPK signal pathway.	Clopidogrel	36-47	high mobility group box 1	Homo sapiens	78-83
31507379-8	2019	In agreement, in vivo HMGB-1 blockage with glycyrrhizin, immediately after pilocarpine-induced status epilepticus (SE), reduced neuronal degeneration, reactive astrogliosis and microgliosis in the long term.	Glycyrrhizic Acid	43-55	high mobility group box 1	Homo sapiens	22-28
31507379-8	2019	In agreement, in vivo HMGB-1 blockage with glycyrrhizin, immediately after pilocarpine-induced status epilepticus (SE), reduced neuronal degeneration, reactive astrogliosis and microgliosis in the long term.	Pilocarpine	75-86	high mobility group box 1	Homo sapiens	22-28
31450620-4	2019	Suppression of HMGB1 with glycyrrhizin has therapeutic benefits in fibrotic diseases.	Glycyrrhizic Acid	26-38	high mobility group box 1	Homo sapiens	15-20
31552388-10	2019	Furthermore, HMGB1-mediated inflammation in depressive-like behaviors may be involved in Nod-like receptor family pyrin domain containing three (NLRP3) inflammasome and proinflammatory cytokines, abnormal kynurenine pathway and imbalance between neuroprotective and neurotoxic factors.	hydroxykynurenine glucoside	205-215	high mobility group box 1	Homo sapiens	13-18
31552388-11	2019	Conclusions: We found that stress-induced inflammation mediated by HMGB1 may affect motivational deficits through regulating dopamine pathway in corticostriatal neurocircuitry.	Dopamine	125-133	high mobility group box 1	Homo sapiens	67-72
31450620-12	2019	TGF-beta, Smad2/3, ERK1/2, and HMGB1 were decreased in glycyrrhizin-treated keloids.	Glycyrrhizic Acid	55-67	high mobility group box 1	Homo sapiens	31-36
31481891-6	2019	Raltegravir ameliorated pulmonary fibrosis by reducing the pathology score, collagen deposition, and expression of alpha-smooth muscle actin, NLRP3, HMGB1, TLR4, inhibitor of kappa B, p-NF-kappaB, HIF-1alpha, collagen I, and collagen III.	Raltegravir Potassium	0-11	high mobility group box 1	Homo sapiens	149-154
31190067-7	2019	Ker/ODC conditioned medium (CM) stimulated As-HaCaT but not parental HaCaT tumorsphere formation, and this was inhibited by glycyrrhizin, an inhibitor of HMGB1, and by TAK242, an inhibitor of the HMGB1 receptor TLR4.	lysylglutamylarginine	0-3	high mobility group box 1	Homo sapiens	154-159
31190067-7	2019	Ker/ODC conditioned medium (CM) stimulated As-HaCaT but not parental HaCaT tumorsphere formation, and this was inhibited by glycyrrhizin, an inhibitor of HMGB1, and by TAK242, an inhibitor of the HMGB1 receptor TLR4.	lysylglutamylarginine	0-3	high mobility group box 1	Homo sapiens	196-201
31190067-7	2019	Ker/ODC conditioned medium (CM) stimulated As-HaCaT but not parental HaCaT tumorsphere formation, and this was inhibited by glycyrrhizin, an inhibitor of HMGB1, and by TAK242, an inhibitor of the HMGB1 receptor TLR4.	Glycyrrhizic Acid	124-136	high mobility group box 1	Homo sapiens	154-159
31190067-7	2019	Ker/ODC conditioned medium (CM) stimulated As-HaCaT but not parental HaCaT tumorsphere formation, and this was inhibited by glycyrrhizin, an inhibitor of HMGB1, and by TAK242, an inhibitor of the HMGB1 receptor TLR4.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	168-174	high mobility group box 1	Homo sapiens	196-201
31190067-11	2019	These results show that polyamine-dependent release of HMGB1 promotes the expansion of stem cell-like subpopulations in arsenic-transformed keratinocytes while also increasing their invasiveness, suggesting that polyamines may be a potential therapeutic target for the prevention and treatment of arsenic-initiated skin cancers.	Polyamines	24-33	high mobility group box 1	Homo sapiens	55-60
31190067-11	2019	These results show that polyamine-dependent release of HMGB1 promotes the expansion of stem cell-like subpopulations in arsenic-transformed keratinocytes while also increasing their invasiveness, suggesting that polyamines may be a potential therapeutic target for the prevention and treatment of arsenic-initiated skin cancers.	Arsenic	120-127	high mobility group box 1	Homo sapiens	55-60
31190067-11	2019	These results show that polyamine-dependent release of HMGB1 promotes the expansion of stem cell-like subpopulations in arsenic-transformed keratinocytes while also increasing their invasiveness, suggesting that polyamines may be a potential therapeutic target for the prevention and treatment of arsenic-initiated skin cancers.	Polyamines	212-222	high mobility group box 1	Homo sapiens	55-60
31078691-6	2019	As with RU486, ADX mitigated the effects of stress on HMGB1 and CD200R1.	Adenylyl sulfate	15-18	high mobility group box 1	Homo sapiens	54-59
31218684-7	2019	Furthermore, higher amounts of HMGB1 was found in the plasma of BTI patients.	biotinamide	64-67	high mobility group box 1	Homo sapiens	31-36
31497226-0	2019	Glycyrrhizin suppresses inflammation and cell apoptosis by inhibition of HMGB1 via p38/p-JUK signaling pathway in attenuating intervertebral disc degeneration.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	73-78
31497226-2	2019	Previous studies have shown that glycyrrhizin (GL) is a valid inhibitor of the high-mobility group box-1 gene (HMGB1) which expressed much higher in an inflammatory condition.	Glycyrrhizic Acid	33-45	high mobility group box 1	Homo sapiens	79-104
31497226-2	2019	Previous studies have shown that glycyrrhizin (GL) is a valid inhibitor of the high-mobility group box-1 gene (HMGB1) which expressed much higher in an inflammatory condition.	Glycyrrhizic Acid	33-45	high mobility group box 1	Homo sapiens	111-116
31497226-2	2019	Previous studies have shown that glycyrrhizin (GL) is a valid inhibitor of the high-mobility group box-1 gene (HMGB1) which expressed much higher in an inflammatory condition.	Glycyrrhizic Acid	47-49	high mobility group box 1	Homo sapiens	79-104
31497226-2	2019	Previous studies have shown that glycyrrhizin (GL) is a valid inhibitor of the high-mobility group box-1 gene (HMGB1) which expressed much higher in an inflammatory condition.	Glycyrrhizic Acid	47-49	high mobility group box 1	Homo sapiens	111-116
31497226-3	2019	However, it is not known whether GL protects against IDD by the inhibition of HMGB1.	Glycyrrhizic Acid	33-35	high mobility group box 1	Homo sapiens	78-83
31497226-11	2019	These results suggested that GL prevented NP degradation via restraining inflammation and cell apoptosis by inhibition of HMGB1 via p38/p-JNK signaling pathway.	Glycyrrhizic Acid	29-31	high mobility group box 1	Homo sapiens	122-127
30938057-7	2019	Serum HMGB1 in LN patients correlated positively to the SLE Disease Activity Index (P < 0.0001), and 24 hours urinary proteins and negatively to creatinine clearance (P < 0.001).	Creatinine	145-155	high mobility group box 1	Homo sapiens	6-11
31162203-12	2019	In contrast, a second high mobility group box 1 protein wave peaking 3-6 hours after trauma in the most severely injured and physiologically deranged patients was consistently the most important predictor of outcome in our multivariable models, rendering all other predictor variables insignificant except for smaller contributions from age and sex, and of admission base excess for maximal creatinine concentration.	Creatinine	391-401	high mobility group box 1	Homo sapiens	22-47
31082723-0	2019	Melatonin alleviates circadian rhythm disruption exacerbating DSS-induced colitis by inhibiting the distribution of HMGB1 in intestinal tissues.	Melatonin	0-9	high mobility group box 1	Homo sapiens	116-121
31082723-3	2019	However, no exact mechanism has been illustrated among melatonin, disrupted circadian rhythm and inflammatory bowel disease, as well as regarding the effect of melatonin on HMGB1.	Melatonin	160-169	high mobility group box 1	Homo sapiens	173-178
31082723-5	2019	CRD aggravated DSS-induced colitis by worsening colonic inflammation and tissue injury, as well as by enhancing HMGB1 translocation, which could be reversed by ethyl pyruvate, an HMGB1 antagonist.	ethyl pyruvate	160-174	high mobility group box 1	Homo sapiens	112-117
31082723-5	2019	CRD aggravated DSS-induced colitis by worsening colonic inflammation and tissue injury, as well as by enhancing HMGB1 translocation, which could be reversed by ethyl pyruvate, an HMGB1 antagonist.	ethyl pyruvate	160-174	high mobility group box 1	Homo sapiens	179-184
31082723-6	2019	Moreover, melatonin treatment attenuated these disorders and the shuttling of HMGB1 in the intestinal epithelial cells (IECs), the effect of which could be partly reversed by the melatonin antagonist luzindole.	Melatonin	10-19	high mobility group box 1	Homo sapiens	78-83
31082723-6	2019	Moreover, melatonin treatment attenuated these disorders and the shuttling of HMGB1 in the intestinal epithelial cells (IECs), the effect of which could be partly reversed by the melatonin antagonist luzindole.	Melatonin	179-188	high mobility group box 1	Homo sapiens	78-83
31082723-6	2019	Moreover, melatonin treatment attenuated these disorders and the shuttling of HMGB1 in the intestinal epithelial cells (IECs), the effect of which could be partly reversed by the melatonin antagonist luzindole.	luzindole	200-209	high mobility group box 1	Homo sapiens	78-83
31082723-7	2019	The protective role of melatonin may be tightly related to the translocation of HMGB1 in IECs.	Melatonin	23-32	high mobility group box 1	Homo sapiens	80-85
30860623-6	2019	RESULTS: In vitro PUVA treatment induced the expression of several damage-associated molecular patterns (DAMPs) by dying T cells (calreticulin, high-mobility group box-1, and to a lesser extent heat shock proteins 70 and 90), especially upon T cell activation, leading to their phagocytosis by macrophages and dendritic cells (DCs).	puva	18-22	high mobility group box 1	Homo sapiens	144-169
31331356-9	2019	HMGB1-mediated AMPK, mTOR and p70S6K phosphorylation (p-AMPK, p-mTOR &amp; p-p70S6K) were detected by Western blot.	Adenosine Monophosphate	70-73	high mobility group box 1	Homo sapiens	0-5
31173265-0	2019	Ethyl pyruvate suppresses the growth, invasion and migration and induces the apoptosis of non-small cell lung cancer cells via the HMGB1/RAGE axis and the NF-kappaB/STAT3 pathway.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	131-136
31173265-1	2019	As an inhibitor of high mobility group protein B1 (HMGB1), ethyl pyruvate (EP) has been associated with various inflammatory diseases.	ethyl pyruvate	59-73	high mobility group box 1	Homo sapiens	19-49
31173265-1	2019	As an inhibitor of high mobility group protein B1 (HMGB1), ethyl pyruvate (EP) has been associated with various inflammatory diseases.	ethyl pyruvate	59-73	high mobility group box 1	Homo sapiens	51-56
31331356-3	2019	Here the authors intended to identify the role of HMGB1 in Hank"s balanced salt solution (HBSS)-induced autophagy, explore NIS protein degradation through a autophagy-lysosome pathway in thyroid cancer cells and elucidate the possible molecular mechanisms.	hank"s balanced salt solution	59-88	high mobility group box 1	Homo sapiens	50-55
31145943-0	2019	Inhibition of lncRNA TUG1 upregulates miR-142-3p to ameliorate myocardial injury during ischemia and reperfusion via targeting HMGB1- and Rac1-induced autophagy.	mir-142-3p	38-48	high mobility group box 1	Homo sapiens	127-132
31331356-12	2019	RESULTS: HMGB1 was a critical regulator of autophagy-mediated NIS degradation in HBSS-treated FTC-133/TPC-1 cells.	Nickel	62-65	high mobility group box 1	Homo sapiens	9-14
31336567-0	2019	High Mobility Group Box 1 Mediates TMAO-Induced Endothelial Dysfunction.	trimethyloxamine	35-39	high mobility group box 1	Homo sapiens	0-25
31336567-4	2019	The present study tested whether TMAO associated endothelial dysfunction results via HMGB1 activation.	trimethyloxamine	33-37	high mobility group box 1	Homo sapiens	85-90
31331356-3	2019	Here the authors intended to identify the role of HMGB1 in Hank"s balanced salt solution (HBSS)-induced autophagy, explore NIS protein degradation through a autophagy-lysosome pathway in thyroid cancer cells and elucidate the possible molecular mechanisms.	hbss	90-94	high mobility group box 1	Homo sapiens	50-55
31331356-12	2019	RESULTS: HMGB1 was a critical regulator of autophagy-mediated NIS degradation in HBSS-treated FTC-133/TPC-1 cells.	hbss	81-85	high mobility group box 1	Homo sapiens	9-14
31336567-5	2019	Biochemical and RT-PCR analysis showed that TMAO increased the HMGB1 expression in a dose-dependent manner in endothelial cells.	trimethyloxamine	44-48	high mobility group box 1	Homo sapiens	63-68
31331356-14	2019	HMGB1-knockdown dramatically suppressed autophagy, NIS degradation and boosted iodide uptake in HBSS-treated cells.	Nickel	51-54	high mobility group box 1	Homo sapiens	0-5
31336567-6	2019	However, prior treatment with glycyrrhizin, an HMGB1 binder, abolished the TMAO-induced HMGB1 production in endothelial cells.	Glycyrrhizic Acid	30-42	high mobility group box 1	Homo sapiens	47-52
31331356-14	2019	HMGB1-knockdown dramatically suppressed autophagy, NIS degradation and boosted iodide uptake in HBSS-treated cells.	Iodides	79-85	high mobility group box 1	Homo sapiens	0-5
31336567-6	2019	However, prior treatment with glycyrrhizin, an HMGB1 binder, abolished the TMAO-induced HMGB1 production in endothelial cells.	Glycyrrhizic Acid	30-42	high mobility group box 1	Homo sapiens	88-93
31331356-14	2019	HMGB1-knockdown dramatically suppressed autophagy, NIS degradation and boosted iodide uptake in HBSS-treated cells.	hbss	96-100	high mobility group box 1	Homo sapiens	0-5
31336567-6	2019	However, prior treatment with glycyrrhizin, an HMGB1 binder, abolished the TMAO-induced HMGB1 production in endothelial cells.	trimethyloxamine	75-79	high mobility group box 1	Homo sapiens	47-52
31336567-6	2019	However, prior treatment with glycyrrhizin, an HMGB1 binder, abolished the TMAO-induced HMGB1 production in endothelial cells.	trimethyloxamine	75-79	high mobility group box 1	Homo sapiens	88-93
31331356-15	2019	Moreover, HBSS enhanced ROS-sustained autophagy and promoted the cytosolic translocation of HMGB1.	hbss	10-14	high mobility group box 1	Homo sapiens	92-97
31336567-11	2019	In conclusion, our results demonstrate that HMGB1 is one of the important mediators of TMAO-induced endothelial dysfunction.	trimethyloxamine	87-91	high mobility group box 1	Homo sapiens	44-49
31331356-16	2019	A knockdown of HMGB1 suppressed LC3-II conversion and NIS degradation via an AMPK/mTOR-dependent signal pathway through a regulation of ROS generation, rather than ATP.	Nickel	54-57	high mobility group box 1	Homo sapiens	15-20
31331356-16	2019	A knockdown of HMGB1 suppressed LC3-II conversion and NIS degradation via an AMPK/mTOR-dependent signal pathway through a regulation of ROS generation, rather than ATP.	Reactive Oxygen Species	136-139	high mobility group box 1	Homo sapiens	15-20
31331356-16	2019	A knockdown of HMGB1 suppressed LC3-II conversion and NIS degradation via an AMPK/mTOR-dependent signal pathway through a regulation of ROS generation, rather than ATP.	Adenosine Triphosphate	164-167	high mobility group box 1	Homo sapiens	15-20
31331356-17	2019	Furthermore, these data were further supported by our in vivo experiment of xenografts formed by HMGB1 knockdown cells reverting the uptake of 99mTcO4- as compared with control shRNA-transfected cells in hunger group.	Sodium Pertechnetate Tc 99m	143-150	high mobility group box 1	Homo sapiens	97-102
31331356-18	2019	CONCLUSIONS: Acting as a critical regulator of autophagy-mediated NIS degradation via ROS/AMPK/mTOR pathway, HMGB1is a potential intervention target of radioiodine therapy in thyroid cancer.	Nickel	66-69	high mobility group box 1	Homo sapiens	109-114
31331356-18	2019	CONCLUSIONS: Acting as a critical regulator of autophagy-mediated NIS degradation via ROS/AMPK/mTOR pathway, HMGB1is a potential intervention target of radioiodine therapy in thyroid cancer.	Reactive Oxygen Species	86-89	high mobility group box 1	Homo sapiens	109-114
31331356-18	2019	CONCLUSIONS: Acting as a critical regulator of autophagy-mediated NIS degradation via ROS/AMPK/mTOR pathway, HMGB1is a potential intervention target of radioiodine therapy in thyroid cancer.	Iodine-131	152-163	high mobility group box 1	Homo sapiens	109-114
31189308-4	2019	Bioassay results showed that these oligomers significantly reversed the multidrug resistance of MCF-7/doxorubicin (DOX) cells and increased the sensitivity of U2 OS cells to DOX by downregulating the HMGB1 expression.	Doxorubicin	115-118	high mobility group box 1	Homo sapiens	200-205
31189308-4	2019	Bioassay results showed that these oligomers significantly reversed the multidrug resistance of MCF-7/doxorubicin (DOX) cells and increased the sensitivity of U2 OS cells to DOX by downregulating the HMGB1 expression.	Doxorubicin	174-177	high mobility group box 1	Homo sapiens	200-205
31311167-2	2019	De-regulation of the poly(ADP-ribose) polymerase 1 (PARP1)/high-mobility group box 1 (HMGB1) signaling pathway has been proposed as an important mechanism involved in cisplatin-resistance.	Cisplatin	167-176	high mobility group box 1	Homo sapiens	59-84
31324798-5	2019	beta-Lapachone-induced high mobility group box 1 (HMGB1) release activates the host TLR4/MyD88/type I interferon pathway and Batf3 dendritic cell-dependent cross-priming to bridge innate and adaptive immune responses against the tumor.	beta-lapachone	0-14	high mobility group box 1	Homo sapiens	23-48
31324798-5	2019	beta-Lapachone-induced high mobility group box 1 (HMGB1) release activates the host TLR4/MyD88/type I interferon pathway and Batf3 dendritic cell-dependent cross-priming to bridge innate and adaptive immune responses against the tumor.	beta-lapachone	0-14	high mobility group box 1	Homo sapiens	50-55
31311167-2	2019	De-regulation of the poly(ADP-ribose) polymerase 1 (PARP1)/high-mobility group box 1 (HMGB1) signaling pathway has been proposed as an important mechanism involved in cisplatin-resistance.	Cisplatin	167-176	high mobility group box 1	Homo sapiens	86-91
31311167-8	2019	The cisplatin/Morin hydrate combination was effective in the reversal of the HepG2DR cell resistance via suppression of PARP1-mediated autophagy by regulating the HMGB1 and microtubule-associated protein 1A/1B light chain 3B (LC3) I/II.	Cisplatin	4-13	high mobility group box 1	Homo sapiens	163-168
30977640-10	2019	PCB29-pQ-induced high-mobility group box 1 (HMGB1) release and subsequent binding to its receptors [toll-like receptor 2 (TLR2), TLR4, TLR9, and receptor for advanced glycation end products (RAGE)] are essential for the activation of NLRP3 inflammasome.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	0-8	high mobility group box 1	Homo sapiens	17-42
31284269-9	2019	Our data indicate that A2E-induced upregulation of HMGB1 Caveolin-1 and HMGB1 release may relate to RPE cell senescence and play a role in the pathogenesis of AMD.	N-retinylidene-N-retinylethanolamine	23-26	high mobility group box 1	Homo sapiens	51-56
31284269-9	2019	Our data indicate that A2E-induced upregulation of HMGB1 Caveolin-1 and HMGB1 release may relate to RPE cell senescence and play a role in the pathogenesis of AMD.	N-retinylidene-N-retinylethanolamine	23-26	high mobility group box 1	Homo sapiens	72-77
30613954-4	2019	Methods Serum HMGB1 was quantified in Malawian nevirapine-induced hypersensitivity, Taiwanese SJS/TEN and Spanish SJS/TEN cohorts.	Nevirapine	47-57	high mobility group box 1	Homo sapiens	14-19
31115516-0	2019	Fr-HMGB1 and ds-HMGB1 activate the kynurenine pathway via different mechanisms in association with depressive-like behavior.	Kynurenine	35-45	high mobility group box 1	Homo sapiens	3-8
31115516-0	2019	Fr-HMGB1 and ds-HMGB1 activate the kynurenine pathway via different mechanisms in association with depressive-like behavior.	Kynurenine	35-45	high mobility group box 1	Homo sapiens	16-21
31115516-2	2019	In the present study, the induction of depression via the kynurenine pathway by different redox states of HMGB1 was investigated in vivo and in vitro.	Kynurenine	58-68	high mobility group box 1	Homo sapiens	106-111
31115516-5	2019	Following intracerebroventricular injection of ds- and fr-HMGB1, behavioral tests were performed, revealing the presentation of depressive-like behavior, and essential proteins in the kynurenine pathway were demonstrated to be upregulated at the mRNA level, suggesting that ds- and fr-HMGB1 contributed to the development of this behavior via the kynurenine pathway.	Kynurenine	184-194	high mobility group box 1	Homo sapiens	58-63
31115516-5	2019	Following intracerebroventricular injection of ds- and fr-HMGB1, behavioral tests were performed, revealing the presentation of depressive-like behavior, and essential proteins in the kynurenine pathway were demonstrated to be upregulated at the mRNA level, suggesting that ds- and fr-HMGB1 contributed to the development of this behavior via the kynurenine pathway.	Kynurenine	184-194	high mobility group box 1	Homo sapiens	285-290
31115516-5	2019	Following intracerebroventricular injection of ds- and fr-HMGB1, behavioral tests were performed, revealing the presentation of depressive-like behavior, and essential proteins in the kynurenine pathway were demonstrated to be upregulated at the mRNA level, suggesting that ds- and fr-HMGB1 contributed to the development of this behavior via the kynurenine pathway.	Kynurenine	347-357	high mobility group box 1	Homo sapiens	58-63
31115516-6	2019	ds-HMGB1 directly activated the kynurenine pathway and cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in the hippocampal tissue.	Kynurenine	32-42	high mobility group box 1	Homo sapiens	3-8
31115516-7	2019	Conversely, fr-HMGB1 upregulated the aforementioned factors only following treatment with H2O2.	Hydrogen Peroxide	90-94	high mobility group box 1	Homo sapiens	15-20
31115516-8	2019	These findings indicated that ds-HMGB1 induced depression in a manner associated with the kynurenine pathway, whereas oxidation of fr-HMGB1 evoked activation of the kynurenine pathway, resulting in depressive behavior.	Kynurenine	90-100	high mobility group box 1	Homo sapiens	33-38
31115516-8	2019	These findings indicated that ds-HMGB1 induced depression in a manner associated with the kynurenine pathway, whereas oxidation of fr-HMGB1 evoked activation of the kynurenine pathway, resulting in depressive behavior.	Kynurenine	165-175	high mobility group box 1	Homo sapiens	134-139
31441407-0	2019	[Effect of unfractionated heparin on high mobility group box 1-mediated expression of vascular endothelial cadherin].	Heparin	26-33	high mobility group box 1	Homo sapiens	37-62
31441407-1	2019	OBJECTIVE: To observe the damage of high mobility group box 1 (HMGB1) on human umbilical vein endothelial cell (HUVEC) barrier permeability and the protective effect of unfractionated heparin (UFH), and to explore the down-regulated protection effect mechanism of UFH on HMGB1-mediated vascular endothelial cadherin (VE-cadherin) expression.	Heparin	264-267	high mobility group box 1	Homo sapiens	36-61
31441407-1	2019	OBJECTIVE: To observe the damage of high mobility group box 1 (HMGB1) on human umbilical vein endothelial cell (HUVEC) barrier permeability and the protective effect of unfractionated heparin (UFH), and to explore the down-regulated protection effect mechanism of UFH on HMGB1-mediated vascular endothelial cadherin (VE-cadherin) expression.	Heparin	264-267	high mobility group box 1	Homo sapiens	63-68
31298304-11	2019	RESULTS: In the presence of high glucose, hRECs cells proliferation was significantly reduced, Caspase-3 activity was enhanced, LDH and ROS levels were increased, SOD activity was declined with increased expression of HMGB-1, NF-kappaB, VEGF, as well as secretion of TNF-alpha and IL-1beta compared with control group (p &lt; 0.05).	Glucose	33-40	high mobility group box 1	Homo sapiens	218-224
31298304-11	2019	RESULTS: In the presence of high glucose, hRECs cells proliferation was significantly reduced, Caspase-3 activity was enhanced, LDH and ROS levels were increased, SOD activity was declined with increased expression of HMGB-1, NF-kappaB, VEGF, as well as secretion of TNF-alpha and IL-1beta compared with control group (p &lt; 0.05).	ros	136-139	high mobility group box 1	Homo sapiens	218-224
30946496-5	2019	HMGB1 function is also regulated by the redox status of critical cysteine residues within the protein, and is cell-type dependent.	Cysteine	65-73	high mobility group box 1	Homo sapiens	0-5
31247032-13	2019	MiR-19 only regulates the proliferation of HASM cells induced by HMGB1, but not PDGF, EGF, TGF-beta1.	mir-19	0-6	high mobility group box 1	Homo sapiens	65-70
31247032-14	2019	Furthermore, we demonstrated that miR-19 contributed to the promoting effects of HMGB1 on ASM cells by targeting PTEN 3"-UTR.	mir-19	34-40	high mobility group box 1	Homo sapiens	81-86
31333815-4	2019	Here, we used multi-microsecond molecular dynamics (MD) simulations to elucidate the effect of the disulfide bond on the structure and dynamics of HMGB1.	Disulfides	99-108	high mobility group box 1	Homo sapiens	147-152
31333815-5	2019	The results of the MD simulations show that the presence or lack of the disulfide bond between Cys23 and Cys45 modulates the conformational space explored by HMGB1, making the reduced protein more suitable to form a complex with CXCL12.	Disulfides	72-81	high mobility group box 1	Homo sapiens	158-163
30942231-7	2019	For this, we employ a three-dimensional colon cancer spheroid model and show for the first time that the treatment with KP1339, a ruthenium-based complex, triggers an ICD signature hallmarked by phosphorylation of PERK and eIF2alpha, exposure of calreticulin on the cell membrane, release of high mobility group box 1 and secretion of ATP.	Ruthenium	130-139	high mobility group box 1	Homo sapiens	292-317
30977640-10	2019	PCB29-pQ-induced high-mobility group box 1 (HMGB1) release and subsequent binding to its receptors [toll-like receptor 2 (TLR2), TLR4, TLR9, and receptor for advanced glycation end products (RAGE)] are essential for the activation of NLRP3 inflammasome.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	0-8	high mobility group box 1	Homo sapiens	44-49
30956264-0	2019	Triptolide Suppresses Growth of Breast Cancer by Targeting HMGB1 in Vitro and in Vivo.	triptolide	0-10	high mobility group box 1	Homo sapiens	59-64
31281467-5	2019	We found that after adjusting for other covariates, NSCLC patients who smoked and who respectively had CG, CT, and TC heterozygotes of HMGB1 rs2249825, rs1045411, and rs1360485, were at lower risk of developing mutant EGFR, compared to those patients with wild-type homozygotes.	cysteinylglycine	103-105	high mobility group box 1	Homo sapiens	135-140
31281467-5	2019	We found that after adjusting for other covariates, NSCLC patients who smoked and who respectively had CG, CT, and TC heterozygotes of HMGB1 rs2249825, rs1045411, and rs1360485, were at lower risk of developing mutant EGFR, compared to those patients with wild-type homozygotes.	Carbon Tetrachloride	107-109	high mobility group box 1	Homo sapiens	135-140
31281467-5	2019	We found that after adjusting for other covariates, NSCLC patients who smoked and who respectively had CG, CT, and TC heterozygotes of HMGB1 rs2249825, rs1045411, and rs1360485, were at lower risk of developing mutant EGFR, compared to those patients with wild-type homozygotes.	Technetium	115-117	high mobility group box 1	Homo sapiens	135-140
31281467-6	2019	Moreover, significant inverse associations between the CG and CG + GG genotypes of HMGB1 rs2249825 and the EGFR hotspot mutation, an exon 19 in-frame deletion, were also observed among NSCLC patients.	cysteinylglycine	55-57	high mobility group box 1	Homo sapiens	83-88
31281467-6	2019	Moreover, significant inverse associations between the CG and CG + GG genotypes of HMGB1 rs2249825 and the EGFR hotspot mutation, an exon 19 in-frame deletion, were also observed among NSCLC patients.	cysteinylglycine	62-64	high mobility group box 1	Homo sapiens	83-88
30956264-6	2019	Further studies evidenced that triptolide treatment not only inhibited HMGB1 mRNA expression, but also decreased supernatant level of HMGB1 in vitro.	triptolide	31-41	high mobility group box 1	Homo sapiens	134-139
30956264-3	2019	The therapeutic effect of triptolide on HMGB1 has not been reported.	triptolide	26-36	high mobility group box 1	Homo sapiens	40-45
30956264-8	2019	As well, triptolide enhanced the anti-proliferative activity of ethyl pyruvate (EP) (HMGB1 inhibitor).	triptolide	9-19	high mobility group box 1	Homo sapiens	85-90
30956264-8	2019	As well, triptolide enhanced the anti-proliferative activity of ethyl pyruvate (EP) (HMGB1 inhibitor).	ethyl pyruvate	64-78	high mobility group box 1	Homo sapiens	85-90
30956264-4	2019	Thus, our study aims to clarify the role of HMGB1 in triptolide-induced anti-growth effect on breast cancer in vitro and in vivo.	triptolide	53-63	high mobility group box 1	Homo sapiens	44-49
30956264-9	2019	Furthermore, downstream correlation factors (Toll-like receptor 4 (TLR4) and phosphorylated-nuclear factor-kappaB (NF-kappaB) p65) of HMGB1 were significantly decreased in vitro after triptolide treatment.	triptolide	184-194	high mobility group box 1	Homo sapiens	134-139
30956264-6	2019	Further studies evidenced that triptolide treatment not only inhibited HMGB1 mRNA expression, but also decreased supernatant level of HMGB1 in vitro.	triptolide	31-41	high mobility group box 1	Homo sapiens	71-76
30956264-11	2019	Meanwhile, immunohistochemical analyses showed that triptolide treatment significantly decreased the level of cytoplasmic HMGB1 and TLR4 expression, whereas the expression of NF-kappaB p65 was relatively higher in cytoplasm, and conversely lower in nucleus as compared to the control group.	triptolide	52-62	high mobility group box 1	Homo sapiens	122-127
30958608-0	2019	Dexmedetomidine protects against high mobility group box 1-induced cellular injury by inhibiting pyroptosis.	Dexmedetomidine	0-15	high mobility group box 1	Homo sapiens	33-58
30956264-12	2019	Collectively, these results demonstrate that triptolide suppresses the growth of breast cancer cells via reduction of HMGB1 expression in vitro and in vivo, which may provide new insights into the treament of breast cancer.	triptolide	45-55	high mobility group box 1	Homo sapiens	118-123
30853521-0	2019	N4-acetylcytidine is required for sustained NLRP3 inflammasome activation via HMGB1 pathway in microglia.	N-acetylcytidine	0-17	high mobility group box 1	Homo sapiens	78-83
30853521-3	2019	Here we reported that N4-acetylcytidine (N4A), a nucleoside metabolite, activated microglia and sustained NLRP3 inflammasome activation by inducing HMGB1 signaling.	N-acetylcytidine	22-39	high mobility group box 1	Homo sapiens	148-153
30958608-6	2019	We found that DEX protected against HMGB1-induced cell death of BMDMs.	Dexmedetomidine	14-17	high mobility group box 1	Homo sapiens	36-41
30958608-9	2019	Taken together, these findings demonstrate the protective effect of DEX in mediating HMGB1-induced cellular injury, thus indicating that DEX may be a potential therapeutic candidate for the management of infection and trauma-derived inflammation.	Dexmedetomidine	68-71	high mobility group box 1	Homo sapiens	85-90
30853521-3	2019	Here we reported that N4-acetylcytidine (N4A), a nucleoside metabolite, activated microglia and sustained NLRP3 inflammasome activation by inducing HMGB1 signaling.	CHEMBL3099812	41-44	high mobility group box 1	Homo sapiens	148-153
30958608-9	2019	Taken together, these findings demonstrate the protective effect of DEX in mediating HMGB1-induced cellular injury, thus indicating that DEX may be a potential therapeutic candidate for the management of infection and trauma-derived inflammation.	Dexmedetomidine	137-140	high mobility group box 1	Homo sapiens	85-90
30742880-8	2019	HMGB1 and p53 both serve as transcription factors that play crucial roles in the regulation of PCB29-pQ-induced autophagy and apoptosis.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	95-103	high mobility group box 1	Homo sapiens	0-5
30370641-5	2019	Bleomycin (BLM)-induced PF in Nrf2-knockout (Nrf2-/- ) and wild-type (WT) mice and transforming growth factor beta1 (TGF-beta1)-induced EMT in rat type II alveolar epithelial cell line (RLE-6TN) and human alveolar epithelial cell line (A549) were established to observe the relationship among Nrf2, HMGB1, and EMT by western blot and immunohistochemistry.	Bleomycin	0-9	high mobility group box 1	Homo sapiens	299-304
30742880-0	2019	Polychlorinated biphenyl quinone-induced signaling transition from autophagy to apoptosis is regulated by HMGB1 and p53 in human hepatoma HepG2 cells.	polychlorinated biphenyl quinone	0-32	high mobility group box 1	Homo sapiens	106-111
31177924-0	2019	Indomethacin down-regulating HMGB1 and TNF-alpha to prevent pancreatitis after endoscopic retrograde cholangiopancreatography.	Indomethacin	0-12	high mobility group box 1	Homo sapiens	29-34
31177924-11	2019	The levels of HMGB1 and TNF-alpha were significantly decreased in indomethacin group at 3 (p < .0001) and 24 h (p < .0001) after ERCP, compared to the control group.	Indomethacin	66-78	high mobility group box 1	Homo sapiens	14-19
31177924-13	2019	Conclusions: Rectal indomethacin could significantly reduce the risk of PEP by down-regulating the levels of HMGB1 and TNF-alpha.	Indomethacin	20-32	high mobility group box 1	Homo sapiens	109-114
31100066-3	2019	Previously, we identified an inhibitor of HMGB1/RAGE interaction, papaverine (a non-narcotic opium alkaloid), using a unique drug design system and drug repositioning approach.	Papaverine	66-76	high mobility group box 1	Homo sapiens	42-47
31100066-3	2019	Previously, we identified an inhibitor of HMGB1/RAGE interaction, papaverine (a non-narcotic opium alkaloid), using a unique drug design system and drug repositioning approach.	Opiate Alkaloids	93-107	high mobility group box 1	Homo sapiens	42-47
31100066-5	2019	HMGB1 supplementation in the culture medium promoted tumor cell growth in T98G cells, and this effect was canceled by papaverine.	Papaverine	118-128	high mobility group box 1	Homo sapiens	0-5
31100066-7	2019	As an HMGB1/RAGE inhibitor, papaverine also significantly inhibited cell proliferation in U87MG and T98G cells.	Papaverine	28-38	high mobility group box 1	Homo sapiens	6-11
30742880-9	2019	PCB29-pQ not only enhanced the expression of HMGB1 and p53 but also promoted their binding and cytosolic translocation.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	0-8	high mobility group box 1	Homo sapiens	45-50
30742880-10	2019	Interestingly, HMGB1 rather than p53 plays a primary role in 5 muM of PCB29-pQ-induced autophagy in the nucleus; however, p53 promoted apoptosis to a great extent in the cytosol at the dose of 15 muM PCB29-pQ.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	70-78	high mobility group box 1	Homo sapiens	15-20
30742880-10	2019	Interestingly, HMGB1 rather than p53 plays a primary role in 5 muM of PCB29-pQ-induced autophagy in the nucleus; however, p53 promoted apoptosis to a great extent in the cytosol at the dose of 15 muM PCB29-pQ.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	200-208	high mobility group box 1	Homo sapiens	15-20
30742880-11	2019	Together, HMGB1 and p53 provided a subtle balance between autophagy and apoptosis, thus determining the fate of PCB29-pQ-treated cells.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	112-120	high mobility group box 1	Homo sapiens	10-15
30990031-3	2019	Quantitative mass spectrometry results unambiguously revealed the predominant binding of HMGB1 and HMGB2, the well-established specific binders of 1,2-cisplatin-cross-linked DNA, to the cisplatin-cross-linked ODN, thus validating the accuracy and reliability of our strategy.	1,2-cisplatin	147-160	high mobility group box 1	Homo sapiens	89-94
31123414-0	2019	Downregulation of MALAT1 alleviates saturated fatty acid-induced myocardial inflammatory injury via the miR-26a/HMGB1/TLR4/NF-kappaB axis.	Fatty Acids	36-56	high mobility group box 1	Homo sapiens	112-117
30990031-3	2019	Quantitative mass spectrometry results unambiguously revealed the predominant binding of HMGB1 and HMGB2, the well-established specific binders of 1,2-cisplatin-cross-linked DNA, to the cisplatin-cross-linked ODN, thus validating the accuracy and reliability of our strategy.	Cisplatin	151-160	high mobility group box 1	Homo sapiens	89-94
30712242-0	2019	Cytosolic HMGB1 Mediates Autophagy Activation in an Emulsified Isoflurane Anesthesia Cell Model.	Isoflurane	63-73	high mobility group box 1	Homo sapiens	10-15
30767669-12	2019	NEW &amp; NOTEWORTHY This study shows for the first time to our knowledge that the plasma level of high mobility group box 1 (HMGB1) is elevated in hyperhomocysteinemia (HHcy) patients, and homocysteine promotes expression and secretion of HMGB1 partially regulated by neuropilin-1 in endothelial cells, which is involved in endothelial inflammation.	Adenosine Monophosphate	5-8	high mobility group box 1	Homo sapiens	99-124
30767669-12	2019	NEW &amp; NOTEWORTHY This study shows for the first time to our knowledge that the plasma level of high mobility group box 1 (HMGB1) is elevated in hyperhomocysteinemia (HHcy) patients, and homocysteine promotes expression and secretion of HMGB1 partially regulated by neuropilin-1 in endothelial cells, which is involved in endothelial inflammation.	Adenosine Monophosphate	5-8	high mobility group box 1	Homo sapiens	126-131
30767669-12	2019	NEW &amp; NOTEWORTHY This study shows for the first time to our knowledge that the plasma level of high mobility group box 1 (HMGB1) is elevated in hyperhomocysteinemia (HHcy) patients, and homocysteine promotes expression and secretion of HMGB1 partially regulated by neuropilin-1 in endothelial cells, which is involved in endothelial inflammation.	Homocysteine	153-165	high mobility group box 1	Homo sapiens	99-124
30767669-12	2019	NEW &amp; NOTEWORTHY This study shows for the first time to our knowledge that the plasma level of high mobility group box 1 (HMGB1) is elevated in hyperhomocysteinemia (HHcy) patients, and homocysteine promotes expression and secretion of HMGB1 partially regulated by neuropilin-1 in endothelial cells, which is involved in endothelial inflammation.	Homocysteine	153-165	high mobility group box 1	Homo sapiens	126-131
30822402-2	2019	KC1 and KC3, but not KC2, significantly reduced HMGB1 release in lipopolysaccharide (LPS)-activated human umbilical vein endothelial cells (HUVECs) and attenuated the cecal ligation and puncture (CLP)-induced release of HMGB1.	kc1	0-3	high mobility group box 1	Homo sapiens	48-53
30822402-2	2019	KC1 and KC3, but not KC2, significantly reduced HMGB1 release in lipopolysaccharide (LPS)-activated human umbilical vein endothelial cells (HUVECs) and attenuated the cecal ligation and puncture (CLP)-induced release of HMGB1.	kc1	0-3	high mobility group box 1	Homo sapiens	220-225
30822402-2	2019	KC1 and KC3, but not KC2, significantly reduced HMGB1 release in lipopolysaccharide (LPS)-activated human umbilical vein endothelial cells (HUVECs) and attenuated the cecal ligation and puncture (CLP)-induced release of HMGB1.	UNII-426P9HSR8I	8-11	high mobility group box 1	Homo sapiens	48-53
30822402-2	2019	KC1 and KC3, but not KC2, significantly reduced HMGB1 release in lipopolysaccharide (LPS)-activated human umbilical vein endothelial cells (HUVECs) and attenuated the cecal ligation and puncture (CLP)-induced release of HMGB1.	UNII-426P9HSR8I	8-11	high mobility group box 1	Homo sapiens	220-225
30712242-4	2019	However, the effect of intracellular HMGB1 during emulsified isoflurane (EI) exposure is poorly understood.	Isoflurane	61-71	high mobility group box 1	Homo sapiens	37-42
30712242-4	2019	However, the effect of intracellular HMGB1 during emulsified isoflurane (EI) exposure is poorly understood.	aziridine	73-75	high mobility group box 1	Homo sapiens	37-42
31040377-8	2019	Finally, blocking the receptor for advanced glycation end-products, a canonical HMGB1 receptor, inhibited HMGB1-induced PGE2 production and hair shaft elongation.	Dinoprostone	120-124	high mobility group box 1	Homo sapiens	80-85
30875490-6	2019	Further, a small dose of TMAO significantly increased TF expression and nuclear translocation of NF-kappaB with the synergistic action of low-dose of pro-atherosclerotic factors, such as TNF-alpha and HMGB1.	trimethyloxamine	25-29	high mobility group box 1	Homo sapiens	201-206
31040377-0	2019	HMGB1 promotes hair growth via the modulation of prostaglandin metabolism.	Prostaglandins	49-62	high mobility group box 1	Homo sapiens	0-5
31040377-7	2019	HMGB1 also stimulated prostaglandin E2 (PGE2) secretion from hDPCs.	Dinoprostone	22-38	high mobility group box 1	Homo sapiens	0-5
31040377-7	2019	HMGB1 also stimulated prostaglandin E2 (PGE2) secretion from hDPCs.	Dinoprostone	40-44	high mobility group box 1	Homo sapiens	0-5
31040377-8	2019	Finally, blocking the receptor for advanced glycation end-products, a canonical HMGB1 receptor, inhibited HMGB1-induced PGE2 production and hair shaft elongation.	Dinoprostone	120-124	high mobility group box 1	Homo sapiens	106-111
31040377-9	2019	Our results suggest that HMGB1 promotes hair growth via PGE2 secretion from hDPCs.	Dinoprostone	56-60	high mobility group box 1	Homo sapiens	25-30
31105713-2	2019	The dipotassium glycyrrhizate (DPG), a salt of the glycoconjugated triterpene glycyrrhizin, has been shown to inhibit the High Mobility Group Box 1 (HMGB1) protein, an allarmin strongly implicated in the pathogenesis of most inflammatory and auto-immune disorders.	Glycyrrhizic Acid	4-29	high mobility group box 1	Homo sapiens	122-147
31105713-2	2019	The dipotassium glycyrrhizate (DPG), a salt of the glycoconjugated triterpene glycyrrhizin, has been shown to inhibit the High Mobility Group Box 1 (HMGB1) protein, an allarmin strongly implicated in the pathogenesis of most inflammatory and auto-immune disorders.	Glycyrrhizic Acid	4-29	high mobility group box 1	Homo sapiens	149-154
31105713-2	2019	The dipotassium glycyrrhizate (DPG), a salt of the glycoconjugated triterpene glycyrrhizin, has been shown to inhibit the High Mobility Group Box 1 (HMGB1) protein, an allarmin strongly implicated in the pathogenesis of most inflammatory and auto-immune disorders.	Glycyrrhizic Acid	31-34	high mobility group box 1	Homo sapiens	122-147
31105713-2	2019	The dipotassium glycyrrhizate (DPG), a salt of the glycoconjugated triterpene glycyrrhizin, has been shown to inhibit the High Mobility Group Box 1 (HMGB1) protein, an allarmin strongly implicated in the pathogenesis of most inflammatory and auto-immune disorders.	Glycyrrhizic Acid	31-34	high mobility group box 1	Homo sapiens	149-154
31105713-2	2019	The dipotassium glycyrrhizate (DPG), a salt of the glycoconjugated triterpene glycyrrhizin, has been shown to inhibit the High Mobility Group Box 1 (HMGB1) protein, an allarmin strongly implicated in the pathogenesis of most inflammatory and auto-immune disorders.	Salts	39-43	high mobility group box 1	Homo sapiens	122-147
31105713-2	2019	The dipotassium glycyrrhizate (DPG), a salt of the glycoconjugated triterpene glycyrrhizin, has been shown to inhibit the High Mobility Group Box 1 (HMGB1) protein, an allarmin strongly implicated in the pathogenesis of most inflammatory and auto-immune disorders.	Salts	39-43	high mobility group box 1	Homo sapiens	149-154
31105713-2	2019	The dipotassium glycyrrhizate (DPG), a salt of the glycoconjugated triterpene glycyrrhizin, has been shown to inhibit the High Mobility Group Box 1 (HMGB1) protein, an allarmin strongly implicated in the pathogenesis of most inflammatory and auto-immune disorders.	Triterpenes	67-77	high mobility group box 1	Homo sapiens	122-147
31105713-2	2019	The dipotassium glycyrrhizate (DPG), a salt of the glycoconjugated triterpene glycyrrhizin, has been shown to inhibit the High Mobility Group Box 1 (HMGB1) protein, an allarmin strongly implicated in the pathogenesis of most inflammatory and auto-immune disorders.	Triterpenes	67-77	high mobility group box 1	Homo sapiens	149-154
30975096-7	2019	METHODS: Endocytosis was studied in cultured macrophages using Alexa Fluor-labeled HMGB1 or complexes of HMGB1 and Alexa Fluor-labeled LPS in the presence of an anti-HMGB1 monoclonal antibody (mAb), recombinant HMGB1 box A protein, acetylcholine, the nicotinic acetylcholine receptor subtype alpha 7 (alpha7 nAChR) agonist GTS-21, or a dynamin-specific inhibitor of endocytosis.	alexa fluor	63-74	high mobility group box 1	Homo sapiens	83-88
31114162-0	2019	The molecular mechanisms of Aloin induce gastric cancer cells apoptosis by targeting High Mobility Group Box 1.	alloin	28-33	high mobility group box 1	Homo sapiens	85-110
31114162-4	2019	We investigated the specific molecular mechanisms by which ALO-induced apoptosis by targeting HMGB1 in gastric cancer cells.	alloin	59-62	high mobility group box 1	Homo sapiens	94-99
31114162-13	2019	Blocking these signalling pathways by special inhibitors and HMGB1 knockdown could enhance ALO-induced HGC-27 cell apoptosis.	alloin	91-94	high mobility group box 1	Homo sapiens	61-66
31114162-14	2019	Conclusion: ALO- induced HGC-27 cell apoptosis by down-regulating expressions of HMGB1 and RAGE, inhibiting HMGB1 release and then suppressing rhHMGB1-induced activation of Akt-mTOR-P70S6K and ERK-P90RSK-CREB signalling pathways.	alloin	12-15	high mobility group box 1	Homo sapiens	81-86
31114162-14	2019	Conclusion: ALO- induced HGC-27 cell apoptosis by down-regulating expressions of HMGB1 and RAGE, inhibiting HMGB1 release and then suppressing rhHMGB1-induced activation of Akt-mTOR-P70S6K and ERK-P90RSK-CREB signalling pathways.	alloin	12-15	high mobility group box 1	Homo sapiens	108-113
31105821-6	2019	Notably, our findings indicate that sitagliptin possesses an anti-inflammatory effect against H/R-induced expression of IL-6, IL-8, and TNF-alpha as well as secretion of HMGB1.	Sitagliptin Phosphate	36-47	high mobility group box 1	Homo sapiens	170-175
30936310-0	2019	Correction for Bandala-Sanchez et al., CD52 glycan binds the proinflammatory B box of HMGB1 to engage the Siglec-10 receptor and suppress human T cell function.	Polysaccharides	44-50	high mobility group box 1	Homo sapiens	86-91
30970518-4	2019	In two AML cell lines and primary AML cells from two patients, etoposide induced necroptosis via cIAP1/2 degradation when caspase activity was inhibited by Z-VAD-fmk, but treatment with extracellular HMGB1 prevented this necroptosis.	Etoposide	63-72	high mobility group box 1	Homo sapiens	200-205
31105999-0	2019	HMGB1 regulates erastin-induced ferroptosis via RAS-JNK/p38 signaling in HL-60/NRASQ61L cells.	erastin	16-23	high mobility group box 1	Homo sapiens	0-5
31105999-5	2019	Erastin enhanced ROS levels, thereby promoting cytosolic translocation of HMGB1 and enhancing cell death.	erastin	0-7	high mobility group box 1	Homo sapiens	74-79
31105999-5	2019	Erastin enhanced ROS levels, thereby promoting cytosolic translocation of HMGB1 and enhancing cell death.	ros	17-20	high mobility group box 1	Homo sapiens	74-79
31105999-6	2019	Knockdown of HMGB1 decreased erastin-induced ROS generation and cell death in an iron-mediated lysosomal pathway in HL-60/NRASQ61L cells.	ros	45-48	high mobility group box 1	Homo sapiens	13-18
31105999-6	2019	Knockdown of HMGB1 decreased erastin-induced ROS generation and cell death in an iron-mediated lysosomal pathway in HL-60/NRASQ61L cells.	Iron	81-85	high mobility group box 1	Homo sapiens	13-18
30832473-0	2019	Glycyrrhizin Attenuates the Process of Epithelial-to-Mesenchymal Transition by Modulating HMGB1 Initiated Novel Signaling Pathway in Prostate Cancer Cells.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	90-95
30784882-5	2019	More importantly, cRGD target liposomes of the thymidine conjugate markedly promoted the early detection of immunogenic cell death markers including ATP, HMGB1 and calreticulin.	Thymidine	47-56	high mobility group box 1	Homo sapiens	154-159
30871870-4	2019	In NCM460 cells, under the normal glucose state, proliferation increased by overexpression of HMGB1.	Glucose	34-41	high mobility group box 1	Homo sapiens	94-99
30871870-5	2019	Under a high glucose state, increased expression of HMGB1 was accompanied with a release from cell nuclei into the cytoplasm and extracellular matrix.	Glucose	13-20	high mobility group box 1	Homo sapiens	52-57
30871870-7	2019	And overexpression of HMGB1 reversed the suppressing effect of butyrate on abnormally increased proliferation.	Butyrates	63-71	high mobility group box 1	Homo sapiens	22-27
30871870-8	2019	Conclusively, butyrate suppressed the abnormally increased proliferation in colonic epithelial cells under diabetic state by targeting HMGB1.	Butyrates	14-22	high mobility group box 1	Homo sapiens	135-140
30306713-0	2019	High Efficiency Removal of Cytokines and HMGB-1 by Continuous Hemofiltration With a Dual Layered Polyethersulfone Membrane: An Ex Vivo Study.	polyether sulfone	97-113	high mobility group box 1	Homo sapiens	41-47
30306713-2	2019	While hemofiltration has been shown to remove cytokines, removal of cytokines and HMGB-1 by hemofiltration using a polyethersulfone membrane has not been reported.	polyether sulfone	115-131	high mobility group box 1	Homo sapiens	82-88
30306713-11	2019	Continuous hemofiltration with a polyethersulfone membrane achieved high efficiency removal of cytokines and HMGB-1, without excessive removal of albumin.	polyether sulfone	33-49	high mobility group box 1	Homo sapiens	109-115
30871870-0	2019	Butyrate suppresses abnormal proliferation in colonic epithelial cells under diabetic state by targeting HMGB1.	Butyrates	0-8	high mobility group box 1	Homo sapiens	105-110
30832473-4	2019	Glycyrrhizin is a novel pharmacological inhibitor of HMGB1 that may repress prostate cancer metastasis.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	53-58
30832473-5	2019	This research was aimed to investigate the effect of glycyrrhizin on inhibition of HMGB1-induced epithelial-to-mesenchymal transition (EMT), a key step of tumor metastasis, in prostate cancer cells.	Glycyrrhizic Acid	53-65	high mobility group box 1	Homo sapiens	83-88
30912672-11	2021	Stimulation via HMGB1 significantly increased the migration of CPCs.	cpcs	63-67	high mobility group box 1	Homo sapiens	16-21
30832473-8	2019	Furthermore, HMGB1 facilitated cell migration and invasion via downstream signaling, whereas HMGB1 targeting by 10 mM ethyl pyruvate effectively inhibited EMT characteristics.	ethyl pyruvate	118-132	high mobility group box 1	Homo sapiens	93-98
30832473-9	2019	Interestingly, cell migration capacity induced by HMGB1 in DU145 cells was abolished in a dose-dependent effect of 25-200 muM glycyrrhizin treatment.	Glycyrrhizic Acid	126-138	high mobility group box 1	Homo sapiens	50-55
30832473-10	2019	In conclusion, glycyrrhizin successfully inhibited HMGB1-induced EMT phenomenon, which suggested that glycyrrhizin may serves as a therapeutic agent for metastatic prostate cancer.	Glycyrrhizic Acid	15-27	high mobility group box 1	Homo sapiens	51-56
30832473-10	2019	In conclusion, glycyrrhizin successfully inhibited HMGB1-induced EMT phenomenon, which suggested that glycyrrhizin may serves as a therapeutic agent for metastatic prostate cancer.	Glycyrrhizic Acid	102-114	high mobility group box 1	Homo sapiens	51-56
31019652-6	2019	miR-122 expression was downregulated while SBP1 expression was upregulated under TNBS-induced colitis or oxidative stress.	Trinitrobenzenesulfonic Acid	81-85	high mobility group box 1	Homo sapiens	43-47
31019652-7	2019	Pre-miR-122 or siRNA SBP1 (si-SBP1) treatment ameliorated acute TNBS-induced colitis and H2O2-induced oxidative stress.	Hydrogen Peroxide	89-93	high mobility group box 1	Homo sapiens	21-25
31019652-7	2019	Pre-miR-122 or siRNA SBP1 (si-SBP1) treatment ameliorated acute TNBS-induced colitis and H2O2-induced oxidative stress.	Hydrogen Peroxide	89-93	high mobility group box 1	Homo sapiens	30-34
30686534-5	2019	In contrast, genetic ablation (using ATG5-/- or ATG7-/- cells) or pharmacologic inhibition (the administration of bafilomycin A1 or chloroquine) of autophagy was found to block ferroptosis activator-induced HMGB1 release.	bafilomycin A1	114-128	high mobility group box 1	Homo sapiens	207-212
30686534-5	2019	In contrast, genetic ablation (using ATG5-/- or ATG7-/- cells) or pharmacologic inhibition (the administration of bafilomycin A1 or chloroquine) of autophagy was found to block ferroptosis activator-induced HMGB1 release.	Chloroquine	132-143	high mobility group box 1	Homo sapiens	207-212
30686534-4	2019	Both type I and II ferroptosis activators, including erastin, sorafenib, RSL3, and FIN56, induce HMGB1 release in cancer and noncancer cells.	erastin	53-60	high mobility group box 1	Homo sapiens	97-102
30686534-4	2019	Both type I and II ferroptosis activators, including erastin, sorafenib, RSL3, and FIN56, induce HMGB1 release in cancer and noncancer cells.	Sorafenib	62-71	high mobility group box 1	Homo sapiens	97-102
30227219-4	2019	The present study assessed fecal HMGB1 levels in IBD patients and compared the effects of similar doses of Bifidobacterium longum (Bif) versus VSL#3  on HMGB1 levels in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced murine colitis.	Trinitrobenzenesulfonic Acid	169-204	high mobility group box 1	Homo sapiens	153-158
30686534-4	2019	Both type I and II ferroptosis activators, including erastin, sorafenib, RSL3, and FIN56, induce HMGB1 release in cancer and noncancer cells.	RSL3	73-77	high mobility group box 1	Homo sapiens	97-102
30227219-9	2019	In Caco-2 cells, HMGB1 reduced transepithelial electrical resistance, zonula occludins-1 protein expression, and increased paracellular permeability of FITC-dextran; the opposite was found with both probiotic treatments.	fluorescein isothiocyanate dextran	152-164	high mobility group box 1	Homo sapiens	17-22
30260006-10	2019	Treatment with Pingchuanning decoction activated PI3K/Akt/mTOR pathway and inhibited HMGB1/TLR4/NF-kappaB pathway, which could be overturned by LY294002, a PI3K antagonist, or rapamycin (Rapa), an autophagy inducer.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	144-152	high mobility group box 1	Homo sapiens	85-90
30634142-0	2019	Glycyrrhizin attenuates hepatic ischemia-reperfusion injury by suppressing HMGB1-dependent GSDMD-mediated kupffer cells pyroptosis.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	75-80
30634142-3	2019	Glycyrrhizin, a natural anti-inflammatory and antiviral triterpene in clinical use, was recently referred to have ability to prevent I/R induced liver injury by inhibiting HMGB1 expression and activity.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	172-177
30260006-10	2019	Treatment with Pingchuanning decoction activated PI3K/Akt/mTOR pathway and inhibited HMGB1/TLR4/NF-kappaB pathway, which could be overturned by LY294002, a PI3K antagonist, or rapamycin (Rapa), an autophagy inducer.	Sirolimus	187-191	high mobility group box 1	Homo sapiens	85-90
30260006-10	2019	Treatment with Pingchuanning decoction activated PI3K/Akt/mTOR pathway and inhibited HMGB1/TLR4/NF-kappaB pathway, which could be overturned by LY294002, a PI3K antagonist, or rapamycin (Rapa), an autophagy inducer.	Sirolimus	176-185	high mobility group box 1	Homo sapiens	85-90
30716337-0	2019	KLF4 sensitizes the colon cancer cell HCT-15 to cisplatin by altering the expression of HMGB1 and hTERT.	Cisplatin	48-57	high mobility group box 1	Homo sapiens	88-93
30732500-5	2019	RESULTS: High HMGB-1 levels were associated with high cortisol levels.	Hydrocortisone	54-62	high mobility group box 1	Homo sapiens	14-20
30716337-6	2019	Immunoblotting was used to analyze the change in expression hTERT and HMGB1 involved in KLF4 mediated cisplatin resistance.	Cisplatin	102-111	high mobility group box 1	Homo sapiens	70-75
30887719-10	2019	The stimulation study with retenone or LPS suggested that there were mutual regulations between NF-kappaB and HMGB1.	retenone	27-35	high mobility group box 1	Homo sapiens	110-115
30716337-10	2019	Immuno-blotting showed that KLF4 positively regulates expression of the survival proteins hTERT and HMGB1 while in presence of cisplatin, expression of HMGB1 and hTERT is negatively regulated by KLF4.	Cisplatin	127-136	high mobility group box 1	Homo sapiens	152-157
30318858-6	2019	The use of RIPC in recipients only did not allow for reversal of diabetes, with increased serum HMGB1 at day 1; the three other groups demonstrated significantly better outcomes.	ripc	11-15	high mobility group box 1	Homo sapiens	96-101
30891101-4	2019	We conclude that novel strategies targeting HMGB1 may suppress MM cells and interfere with asbestos-induced inflammation.	Asbestos	91-99	high mobility group box 1	Homo sapiens	44-49
31037139-0	2019	H2Se Induces Reductive Stress in HepG2 Cells and Activates Cell Autophagy by Regulating the Redox of HMGB1 Protein under Hypoxia.	hydrogen selenide	0-4	high mobility group box 1	Homo sapiens	101-106
31037139-7	2019	The redox of HMGB1 protein were analyzed by non-reducing sodium dodecyl sulfate polyacrylamide gel electrophoresis.	Sodium Dodecyl Sulfate	57-79	high mobility group box 1	Homo sapiens	13-18
31037139-7	2019	The redox of HMGB1 protein were analyzed by non-reducing sodium dodecyl sulfate polyacrylamide gel electrophoresis.	polyacrylamide	80-94	high mobility group box 1	Homo sapiens	13-18
31037139-11	2019	H2Se could interrupt the disulfide bond in HMGB1 and promote its secretion.	Disulfides	25-34	high mobility group box 1	Homo sapiens	43-48
30796203-0	2019	Tumor-derived exosomal HMGB1 promotes esophageal squamous cell carcinoma progression through inducing PD1+ TAM expansion.	Tamoxifen	107-110	high mobility group box 1	Homo sapiens	23-28
30629986-8	2019	While HMGB1 and ROS production increased with PHMG-P concentration, the addition of anionic compounds with PHMG-P reduced the ROS production and HMGB1 release.	polyhexamethyleneguanidine	46-52	high mobility group box 1	Homo sapiens	6-11
30629986-8	2019	While HMGB1 and ROS production increased with PHMG-P concentration, the addition of anionic compounds with PHMG-P reduced the ROS production and HMGB1 release.	polyhexamethyleneguanidine	107-113	high mobility group box 1	Homo sapiens	145-150
30538136-6	2019	The RAG1 mutation, R401W, places a bulky tryptophan opposite the binding site for HMG Box A at both 12- and 23-spacer recombination signal sequences, disrupting stable binding of HMGB1.	Tryptophan	41-51	high mobility group box 1	Homo sapiens	179-184
30538136-7	2019	Replacement of R401W with leucine and then lysine progressively restores HMGB1 binding, correlating with increased RAG cutting and recombination in vivo.	Leucine	26-33	high mobility group box 1	Homo sapiens	73-78
30538136-7	2019	Replacement of R401W with leucine and then lysine progressively restores HMGB1 binding, correlating with increased RAG cutting and recombination in vivo.	Lysine	43-49	high mobility group box 1	Homo sapiens	73-78
30538129-0	2019	High-mobility group box 1 links sensing of reactive oxygen species by huntingtin to its nuclear entry.	Reactive Oxygen Species	43-66	high mobility group box 1	Homo sapiens	0-25
30859087-6	2019	Results: We found increased staining for HMGB1 in the dermis of psoriatic plaques in comparison to uninvolved skin of patients with PV.	pv	132-134	high mobility group box 1	Homo sapiens	41-46
30744691-0	2019	Cancer-cell-secreted CXCL11 promoted CD8+ T cells infiltration through docetaxel-induced-release of HMGB1 in NSCLC.	Docetaxel	71-80	high mobility group box 1	Homo sapiens	100-105
30744691-4	2019	Functional experiments were carried out to check whether docetaxel (DOC), a chemotherapeutic agent, modifies the expression of HMGB1 and CXCL11, and influences the infiltration properties of CD8+ T cells to the tumor microenvironment.	Docetaxel	57-66	high mobility group box 1	Homo sapiens	127-132
30744691-4	2019	Functional experiments were carried out to check whether docetaxel (DOC), a chemotherapeutic agent, modifies the expression of HMGB1 and CXCL11, and influences the infiltration properties of CD8+ T cells to the tumor microenvironment.	Docetaxel	68-71	high mobility group box 1	Homo sapiens	127-132
30744691-8	2019	DOC treatment significantly increased HMGB1 release in an ROS-dependent manner.	Docetaxel	0-3	high mobility group box 1	Homo sapiens	38-43
30744691-8	2019	DOC treatment significantly increased HMGB1 release in an ROS-dependent manner.	ros	58-61	high mobility group box 1	Homo sapiens	38-43
30744691-12	2019	CONCLUSIONS: Our results demonstrate that DOC induces CD8+ T cell recruitment to the tumor microenvironment by enhancing the secretion of HMGB1 and CXCL11, thus improving the anti-tumor efficacy, indicating that modulating the HMGB1-CXCL11 axis might be helpful for NSCLC treatment.	Docetaxel	42-45	high mobility group box 1	Homo sapiens	138-143
30744691-12	2019	CONCLUSIONS: Our results demonstrate that DOC induces CD8+ T cell recruitment to the tumor microenvironment by enhancing the secretion of HMGB1 and CXCL11, thus improving the anti-tumor efficacy, indicating that modulating the HMGB1-CXCL11 axis might be helpful for NSCLC treatment.	Docetaxel	42-45	high mobility group box 1	Homo sapiens	227-232
30538129-7	2019	We also found that HMGB1 interacts with the huntingtin N17 region and that this interaction is enhanced by the presence of ROS and phosphorylation of critical serine residues in the N17 region.	Reactive Oxygen Species	123-126	high mobility group box 1	Homo sapiens	19-24
30538129-7	2019	We also found that HMGB1 interacts with the huntingtin N17 region and that this interaction is enhanced by the presence of ROS and phosphorylation of critical serine residues in the N17 region.	Serine	159-165	high mobility group box 1	Homo sapiens	19-24
30538129-8	2019	We conclude that HMGB1 is a huntingtin N17/PY-NLS ROS-dependent interactor, and this protein bridging is essential for relaying ROS sensing by huntingtin to its nuclear entry during ROS stress.	Reactive Oxygen Species	50-53	high mobility group box 1	Homo sapiens	17-22
30538129-8	2019	We conclude that HMGB1 is a huntingtin N17/PY-NLS ROS-dependent interactor, and this protein bridging is essential for relaying ROS sensing by huntingtin to its nuclear entry during ROS stress.	Reactive Oxygen Species	128-131	high mobility group box 1	Homo sapiens	17-22
30538129-8	2019	We conclude that HMGB1 is a huntingtin N17/PY-NLS ROS-dependent interactor, and this protein bridging is essential for relaying ROS sensing by huntingtin to its nuclear entry during ROS stress.	Reactive Oxygen Species	128-131	high mobility group box 1	Homo sapiens	17-22
30675709-0	2019	Dexmedetomidine Preconditioning Protects Cardiomyocytes Against Hypoxia/Reoxygenation-Induced Necroptosis by Inhibiting HMGB1-Mediated Inflammation.	Dexmedetomidine	0-15	high mobility group box 1	Homo sapiens	120-125
30728013-0	2019	Ethyl pyruvate reduces organic dust-induced airway inflammation by targeting HMGB1-RAGE signaling.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	77-82
30728013-12	2019	Anti-HMGB1 treatment reduced ODE-induced NF-kappaB p65 expression, IL-6, ROS and RNS but augmented TGF-beta1 and IL-10 levels.	ros	73-76	high mobility group box 1	Homo sapiens	5-10
30728013-12	2019	Anti-HMGB1 treatment reduced ODE-induced NF-kappaB p65 expression, IL-6, ROS and RNS but augmented TGF-beta1 and IL-10 levels.	Radon	81-84	high mobility group box 1	Homo sapiens	5-10
30838095-0	2019	Correction: N-(2 -Hydroxyphenyl)-2-propylpentanamide (OH-VPA), a histone deacetylase inhibitor, induces the release of nuclear HMGB1 and modifies ROS levels in HeLa cells.	N-(2-hydroxyphenyl)-2-propylpentanamide	12-52	high mobility group box 1	Homo sapiens	127-132
30838095-0	2019	Correction: N-(2 -Hydroxyphenyl)-2-propylpentanamide (OH-VPA), a histone deacetylase inhibitor, induces the release of nuclear HMGB1 and modifies ROS levels in HeLa cells.	oh-vpa	54-60	high mobility group box 1	Homo sapiens	127-132
30675709-4	2019	Therefore, we speculated that DEX preconditioning may suppress H/R-induced necroptosis by inhibiting expression of HMGB1 in cardiomyocytes.	Dexmedetomidine	30-33	high mobility group box 1	Homo sapiens	115-120
30675709-4	2019	Therefore, we speculated that DEX preconditioning may suppress H/R-induced necroptosis by inhibiting expression of HMGB1 in cardiomyocytes.	r	65-66	high mobility group box 1	Homo sapiens	115-120
30675709-7	2019	We also found that silencing expression of HMGB1 reinforced the protective effects of DEX preconditioning and overexpression of HMGB1 counteracted the protective effects of DEX preconditioning.	Dexmedetomidine	86-89	high mobility group box 1	Homo sapiens	43-48
30675709-7	2019	We also found that silencing expression of HMGB1 reinforced the protective effects of DEX preconditioning and overexpression of HMGB1 counteracted the protective effects of DEX preconditioning.	Dexmedetomidine	173-176	high mobility group box 1	Homo sapiens	128-133
30675709-8	2019	Thus, we concluded that DEX preconditioning inhibits H/R-induced necroptosis by inhibiting expression of HMGB1 in cardiomyocytes.	Dexmedetomidine	24-27	high mobility group box 1	Homo sapiens	105-110
30675709-8	2019	Thus, we concluded that DEX preconditioning inhibits H/R-induced necroptosis by inhibiting expression of HMGB1 in cardiomyocytes.	r	55-56	high mobility group box 1	Homo sapiens	105-110
30578841-0	2019	Corynoxine B ameliorates HMGB1-dependent autophagy dysfunction during manganese exposure in SH-SY5Y human neuroblastoma cells.	corynoxine B	0-12	high mobility group box 1	Homo sapiens	25-30
30496780-5	2019	SB1 and SB2 significantly reduced the release of HMGB1 in lipopolysaccharide (LPS)-activated primary human umbilical vein endothelial cells (HUVECS) via the SIRT1-mediated deacetylation of HMGB1.	sb2	8-11	high mobility group box 1	Homo sapiens	49-54
30496780-5	2019	SB1 and SB2 significantly reduced the release of HMGB1 in lipopolysaccharide (LPS)-activated primary human umbilical vein endothelial cells (HUVECS) via the SIRT1-mediated deacetylation of HMGB1.	sb2	8-11	high mobility group box 1	Homo sapiens	189-194
30578841-8	2019	Our results showed that Cory B ameliorated Mn-induced autophagic dysregulation and neurotoxicity partly by dissociating HMGB1 from alpha-synuclein and inhibiting mTOR signaling.	corynoxine B	24-30	high mobility group box 1	Homo sapiens	120-125
30578841-0	2019	Corynoxine B ameliorates HMGB1-dependent autophagy dysfunction during manganese exposure in SH-SY5Y human neuroblastoma cells.	Manganese	70-79	high mobility group box 1	Homo sapiens	25-30
30676239-6	2019	DOX suppressed the emission of HMGB1 while Nano-DOX stimulated HMGB1 emission which was attenuated when autophagy was repressed.	Doxorubicin	0-3	high mobility group box 1	Homo sapiens	31-36
30527499-0	2019	Corrigendum to Beneficial Effects of Dantrolene on Sepsis-Induced Diaphragmatic Dysfunction Are Associated With Downregulation of High-Mobility Group Box 1 and Calpain-Caspase-3 Proteolytic Pathway [Journal of Surgical Research 200(2) (2016) 637-647].	Dantrolene	37-47	high mobility group box 1	Homo sapiens	130-155
30732222-11	2019	Correlation analysis showed that serum HMGB1 levels were positive significant correlated with the Birmingham Vasculitis Activity Score, hypersensitive C reactive protein (Hs-CRP), serum creatinine (Scr) and 24-hour proteinuria (all P &lt; .05).	Creatinine	186-196	high mobility group box 1	Homo sapiens	39-44
30676239-6	2019	DOX suppressed the emission of HMGB1 while Nano-DOX stimulated HMGB1 emission which was attenuated when autophagy was repressed.	Doxorubicin	48-51	high mobility group box 1	Homo sapiens	63-68
30676239-7	2019	Blocking of HMGB1 emission mitigated autophagy and enhanced apoptosis in Nano-DOX-treated GC.	Doxorubicin	78-81	high mobility group box 1	Homo sapiens	12-17
30676239-8	2019	Exogenously administered HMGB1 promoted autophagy and protected against apoptosis in both Nano-DOX-treated GC and DOX-treated GC.	Doxorubicin	95-98	high mobility group box 1	Homo sapiens	25-30
30676239-8	2019	Exogenously administered HMGB1 promoted autophagy and protected against apoptosis in both Nano-DOX-treated GC and DOX-treated GC.	Doxorubicin	114-117	high mobility group box 1	Homo sapiens	25-30
30676239-10	2019	Nano-DOX initiates a mutual reinforcement loop between autophagy and HMGB1 in GC and thereby protects GC against apoptosis.	Doxorubicin	5-8	high mobility group box 1	Homo sapiens	69-74
30906660-7	2019	Here, we describe for the first time production of the in vitro hallmarks of immunogenic cell death - ecto-calreticulin and secreted ATP and HMGB1 protein - by cells in response to treatment with antibody-drug conjugates bearing a maytansine payload.	Maytansine	231-241	high mobility group box 1	Homo sapiens	141-146
30782274-12	2019	Glycyrrhizin inhibited the mRNA expression of HMGB1 and the mRNA and protein expression of TLR4 and NF-kappaB and then reduced the mRNA expression of IL-8 (P&lt;0.05).	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	46-51
30782274-14	2019	The HMGB1 blocker glycyrrhizin can inhibit activation of the TLR4/NF-kappaB signaling pathway and the secretion of inflammatory factors.	Glycyrrhizic Acid	18-30	high mobility group box 1	Homo sapiens	4-9
30704538-0	2019	Upregulation of miR-107 expression following hyperbaric oxygen treatment suppresses HMGB1/RAGE signaling in degenerated human nucleus pulposus cells.	Oxygen	56-62	high mobility group box 1	Homo sapiens	84-89
30704538-3	2019	In this study, we investigated the regulation of the miR-107/HMGB1/RAGE pathway in degenerated nucleus pulposus cells (NPCs) after hyperbaric oxygen (HBO) treatment.	Oxygen	142-148	high mobility group box 1	Homo sapiens	61-66
30391318-0	2019	Effect of hyperbaric oxygen therapy on HMGB1/NF-kappaB expression and prognosis of acute spinal cord injury: A randomized clinical trial.	Oxygen	21-27	high mobility group box 1	Homo sapiens	39-44
30502394-0	2019	gamma-Mangostin alleviates liver fibrosis through Sirtuin 3-superoxide-high mobility group box 1 signaling axis.	gamma-mangostin	0-15	high mobility group box 1	Homo sapiens	71-96
30502394-0	2019	gamma-Mangostin alleviates liver fibrosis through Sirtuin 3-superoxide-high mobility group box 1 signaling axis.	Superoxides	59-70	high mobility group box 1	Homo sapiens	71-96
30030153-5	2019	After intermittent UVB exposure, melanocytes treated with the JAK inhibitor ruxolitinib reduced expression of HMGB1 and MX1 as well as activation of JAK1 (pJAK1) and signal transducer and activator of transcription 1 (pSTAT1).	ruxolitinib	76-87	high mobility group box 1	Homo sapiens	110-115
30966773-3	2019	Aloin was administered after LPS or HMGB1 challenge, and the antiseptic activity of aloin was determined from measurements of permeability, activation of pro-inflammatory proteins and production of markers for tissue injury in HMGB1-activated human umbilical vein endothelial cells (HUVECs) and a cecal ligation and puncture (CLP)-induced sepsis mouse model.	alloin	84-89	high mobility group box 1	Homo sapiens	227-232
30474802-6	2019	Elevated plasma HMGB1 concentrations can serve as early and sensitive mechanistic biomarker for clinical acetaminophen hepatotoxicity.	Acetaminophen	105-118	high mobility group box 1	Homo sapiens	16-21
30474802-8	2019	In addition, HMGB1 mediates 80% of gut bacterial translocation (BT) during acetaminophen toxicity.	Acetaminophen	75-88	high mobility group box 1	Homo sapiens	13-18
30502088-0	2019	MiR-216a-5p protects 16HBE cells from H2O2-induced oxidative stress through targeting HMGB1/NF-kB pathway.	mir-216a-5p	0-11	high mobility group box 1	Homo sapiens	86-91
30502088-0	2019	MiR-216a-5p protects 16HBE cells from H2O2-induced oxidative stress through targeting HMGB1/NF-kB pathway.	Hydrogen Peroxide	38-42	high mobility group box 1	Homo sapiens	86-91
30502088-4	2019	A significantly elevation of HMGB1 protein expression and a reduction of miR-216a-5p expression were observed in children with asthma as well as in H2O2 stimulated 16HBE cells.	Hydrogen Peroxide	148-152	high mobility group box 1	Homo sapiens	29-34
30502088-6	2019	MiR-216a-5p repressed HMGB1 protein expression in H2O2 induced 16HBE cells.	mir-216a-5p	0-11	high mobility group box 1	Homo sapiens	22-27
30502088-6	2019	MiR-216a-5p repressed HMGB1 protein expression in H2O2 induced 16HBE cells.	Hydrogen Peroxide	50-54	high mobility group box 1	Homo sapiens	22-27
30502088-9	2019	In conclusion, these results suggested that miR-216a-5p functions as a negative regulator of H2O2 induced 16HBE cell injury through targeting HMGB1/NF-kB pathway, provided a potential therapeutic target for asthma.	Hydrogen Peroxide	93-97	high mobility group box 1	Homo sapiens	142-147
30630344-6	2019	The antiseptic activity of ginsenoside Rh1 was determined by measuring the permeability, leukocyte adhesion and migration, activation of pro-inflammatory proteins in HMGB1-activated human umbilical vein endothelial cells (HUVECs) and mice, and the survival rate in a sepsis mouse model.	ginsenoside Rh1	27-42	high mobility group box 1	Homo sapiens	166-171
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	coenzyme Q10	25-30	high mobility group box 1	Homo sapiens	401-431
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	coenzyme Q10	25-30	high mobility group box 1	Homo sapiens	433-438
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	Adenosine Monophosphate	32-35	high mobility group box 1	Homo sapiens	401-431
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	Adenosine Monophosphate	32-35	high mobility group box 1	Homo sapiens	433-438
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	Methotrexate	37-49	high mobility group box 1	Homo sapiens	401-431
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	Methotrexate	37-49	high mobility group box 1	Homo sapiens	433-438
29895396-5	2019	In the present study, HMGB-1 levels in serum samples collected from six-week-old piglets infected intra-nasally with 2 x 105.75 TCID50/mL of Indian PRRSV (Ind-297221/2013) was estimated by ELISA up to 21 days post infection (dpi).	3-aminodiphenyleneiodium	225-228	high mobility group box 1	Homo sapiens	22-28
29895396-7	2019	Mean HMGB-1 concentration in serum was found to be significantly elevated in PRRSV infected piglets on 6 dpi as compared to uninfected control piglets.	3-aminodiphenyleneiodium	105-108	high mobility group box 1	Homo sapiens	5-11
31266378-0	2019	Curcumin inhibits the lymphangiogenesis of gastric cancer cells by inhibiton of HMGB1/VEGF-D signaling.	Curcumin	0-8	high mobility group box 1	Homo sapiens	80-85
31266378-3	2019	However, the molecular mechanisms by which curcumin regulates HMGB1-mediated lymphangiogenesis in gastric cancer remain unclear.	Curcumin	43-51	high mobility group box 1	Homo sapiens	62-67
31266378-5	2019	The effects of curcumin on HMGB1 and VEGF-D expression were examined by reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis.	Curcumin	15-23	high mobility group box 1	Homo sapiens	27-32
31266378-7	2019	The mRNA and protein expression levels of HMGB1 and VEGF-D were significantly eliminated by curcumin administration.	Curcumin	92-100	high mobility group box 1	Homo sapiens	42-47
31266378-8	2019	Pre-treatment with the recombinant HMGB1 (rHMGB1) markedly abolished curcumin-reduced VEGF-D expression.	Curcumin	69-77	high mobility group box 1	Homo sapiens	35-40
31266378-9	2019	Our findings suggested that curcumin might exert anti-lymphangiogenesis in gastric cancer by inhibition of HMGB1/VEGF-D signaling.	Curcumin	28-36	high mobility group box 1	Homo sapiens	107-112
30954689-6	2019	Moreover, 5-LO expression, accompanied by production of leukotrienes was markedly increased in HMGB1-stimulated VSMCs, which was attenuated in cells deficient of TLR2 or RAGE.	Leukotrienes	56-68	high mobility group box 1	Homo sapiens	95-100
30273982-9	2019	Inhibition of TLR-4 signaling, with TAK-242, completely abrogated HMGB1 induced IL-6 and MMP-1 expression, whereas inhibition of TLR-2, with O-vanillin, or RAGE, with FPS-ZM1, had mild inhibitory effects.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	36-43	high mobility group box 1	Homo sapiens	66-71
31727240-5	2019	Thus, exclusively in the presence of biotin, which liberates HMGB1-SBP-GFP from its nuclear hook, immunogenic cell death (ICD) inducers such as anthracyclines are able to cause the nucleo-cytoplasmic translocation of HMGB1-SBP-GFP.	Biotin	37-43	high mobility group box 1	Homo sapiens	61-66
31727240-5	2019	Thus, exclusively in the presence of biotin, which liberates HMGB1-SBP-GFP from its nuclear hook, immunogenic cell death (ICD) inducers such as anthracyclines are able to cause the nucleo-cytoplasmic translocation of HMGB1-SBP-GFP.	Biotin	37-43	high mobility group box 1	Homo sapiens	217-222
31727240-5	2019	Thus, exclusively in the presence of biotin, which liberates HMGB1-SBP-GFP from its nuclear hook, immunogenic cell death (ICD) inducers such as anthracyclines are able to cause the nucleo-cytoplasmic translocation of HMGB1-SBP-GFP.	Anthracyclines	144-158	high mobility group box 1	Homo sapiens	61-66
31727240-5	2019	Thus, exclusively in the presence of biotin, which liberates HMGB1-SBP-GFP from its nuclear hook, immunogenic cell death (ICD) inducers such as anthracyclines are able to cause the nucleo-cytoplasmic translocation of HMGB1-SBP-GFP.	Anthracyclines	144-158	high mobility group box 1	Homo sapiens	217-222
30954689-5	2019	Both of these effects were markedly attenuated in cells pretreated with zileuton (1-10 muM), a 5-LO inhibitor, as well as in cells transfected with 5-LO siRNA, suggesting a potential involvement of 5-LO signaling in HMGB1-mediated RAGE expression in VSMCs.	zileuton	72-80	high mobility group box 1	Homo sapiens	216-221
29600445-9	2018	Moreover, heat-shock treatment of GBCCLs induced calreticulin translocation and release of HMGB1 and ATP, both known to act as danger signals.	gbccls	34-40	high mobility group box 1	Homo sapiens	91-96
30204458-10	2018	By dividing the distribution of HMGB1 levels into quartiles, serum HMGB1 levels were increased gradually with the increase of testosterone levels (p&lt;0.05), whereas the FMD levels decreased (p&lt;0.05).	Testosterone	126-138	high mobility group box 1	Homo sapiens	32-37
30204458-10	2018	By dividing the distribution of HMGB1 levels into quartiles, serum HMGB1 levels were increased gradually with the increase of testosterone levels (p&lt;0.05), whereas the FMD levels decreased (p&lt;0.05).	Testosterone	126-138	high mobility group box 1	Homo sapiens	67-72
30204458-12	2018	The absolute changes in HMGB1 showed a positive correlation with the changes in testosterone (p&lt;0.05) and negative correlation with the changes in FMD (p&lt;0.05) in patients with PCOS during the course of metformin therapy.	Testosterone	80-92	high mobility group box 1	Homo sapiens	24-29
30204458-12	2018	The absolute changes in HMGB1 showed a positive correlation with the changes in testosterone (p&lt;0.05) and negative correlation with the changes in FMD (p&lt;0.05) in patients with PCOS during the course of metformin therapy.	Metformin	209-218	high mobility group box 1	Homo sapiens	24-29
30481260-9	2018	Furthermore, our study illustrated that atorvastatin played its role in CPC viability and proliferation by modulating the expression of HMGB1 through the MEG3/miR-22 pathway.	Atorvastatin	40-52	high mobility group box 1	Homo sapiens	136-141
30662657-2	2018	Isoliquiritigenin (ISL) as a small molecular from licorice, is able to inhibit the expression of HMGB1.	isoliquiritigenin	0-17	high mobility group box 1	Homo sapiens	97-102
30662657-2	2018	Isoliquiritigenin (ISL) as a small molecular from licorice, is able to inhibit the expression of HMGB1.	isoliquiritigenin	19-22	high mobility group box 1	Homo sapiens	97-102
30587909-4	2018	Glycyrrhizin binds to HMGB1, inhibiting cytokine activities, thus potentially improving DED.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	22-27
30481260-0	2018	Atorvastatin protects cardiac progenitor cells from hypoxia-induced cell growth inhibition via MEG3/miR-22/HMGB1 pathway.	Atorvastatin	0-12	high mobility group box 1	Homo sapiens	107-112
30325653-0	2018	Glycyrrhizin, a Potential Drug for Autoimmune Encephalomyelitis by Inhibiting High-Mobility Group Box 1.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	78-103
30476719-7	2018	Bipartite recognition of heptamer and nonamer, flexibly linked nonamer-binding domain dimer relatively to the heptamer recognition region dimer, and RSS plasticity and bending by HMGB1 together contribute to the molecular basis of the 12/23 rule in the RAG molecular machine.	RSS	149-152	high mobility group box 1	Homo sapiens	179-184
30325653-3	2018	Glycyrrhizin (GL), a major constituent of licorice root, can inhibit the proinflammatory bioactivities of HMGB1.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	106-111
30325653-3	2018	Glycyrrhizin (GL), a major constituent of licorice root, can inhibit the proinflammatory bioactivities of HMGB1.	Glycyrrhizic Acid	14-16	high mobility group box 1	Homo sapiens	106-111
30468092-7	2018	In particular, ONOO- and its derivatives could mediate neurovascular unit damages and induce the BBB disruption and HT possibly through interacting with different cellular signalling pathways including matrix metalloproteinase (MMPs), high mobility group Box 1 (HMGB1), toll-like receptor2/4, poly(ADP-ribose) polymerase, Src, ROCK, and GSK-3beta.	onoo	15-19	high mobility group box 1	Homo sapiens	235-260
30468092-7	2018	In particular, ONOO- and its derivatives could mediate neurovascular unit damages and induce the BBB disruption and HT possibly through interacting with different cellular signalling pathways including matrix metalloproteinase (MMPs), high mobility group Box 1 (HMGB1), toll-like receptor2/4, poly(ADP-ribose) polymerase, Src, ROCK, and GSK-3beta.	onoo	15-19	high mobility group box 1	Homo sapiens	262-267
30328477-0	2018	PKA regulates HMGB1 through activation of IGFBP-3 and SIRT1 in human retinal endothelial cells cultured in high glucose.	Glucose	112-119	high mobility group box 1	Homo sapiens	14-19
30328477-11	2018	High glucose inhibited SIRT1 levels and increased cytoplasmic HMGB1 in REC.	Glucose	5-12	high mobility group box 1	Homo sapiens	62-67
30338917-0	2018	HMGB1 deficiency reduces H2 O2 -induced oxidative damage in human melanocytes via the Nrf2 pathway.	Hydrogen Peroxide	25-30	high mobility group box 1	Homo sapiens	0-5
30338917-7	2018	H2 O2 treatment increased cytoplasmic translocation and extracellular release of HMGB1.	Hydrogen Peroxide	0-5	high mobility group box 1	Homo sapiens	81-86
30338917-10	2018	The expression of Nrf2 and its downstream antioxidant genes was downregulated after the supernatant of H2 O2 -treated NHEMs was added to HMGB1-deficient cells.	Hydrogen Peroxide	103-108	high mobility group box 1	Homo sapiens	137-142
30680297-11	2018	Conclusion: Our results indicated that the levels of IL-17, IL-33, and IL-6 in supernatants from patients" cultured T cells were increased after stimulation with HMGB-1 following employing quercetin.	Quercetin	189-198	high mobility group box 1	Homo sapiens	162-168
30680297-1	2018	Statement of the Problem: Quercetin is a pharmacological flavonoid that can inhibit high mobility group box1 (HMGB1) protein, a non-histone nuclear protein that is implicated in inflammation.	Quercetin	26-35	high mobility group box 1	Homo sapiens	84-108
30118903-2	2018	Here we showed that ALA-PDT significantly upregulated HMGB1 while downregulated miR-34a expression levels in cervical cancer tissues, and the percentages of mature DCs(mDCs) were increased in ALA-PDT treated patients" peripheral blood.	Alanine	20-23	high mobility group box 1	Homo sapiens	54-59
30680297-1	2018	Statement of the Problem: Quercetin is a pharmacological flavonoid that can inhibit high mobility group box1 (HMGB1) protein, a non-histone nuclear protein that is implicated in inflammation.	Quercetin	26-35	high mobility group box 1	Homo sapiens	110-115
30680297-1	2018	Statement of the Problem: Quercetin is a pharmacological flavonoid that can inhibit high mobility group box1 (HMGB1) protein, a non-histone nuclear protein that is implicated in inflammation.	Flavonoids	57-66	high mobility group box 1	Homo sapiens	84-108
30680297-1	2018	Statement of the Problem: Quercetin is a pharmacological flavonoid that can inhibit high mobility group box1 (HMGB1) protein, a non-histone nuclear protein that is implicated in inflammation.	Flavonoids	57-66	high mobility group box 1	Homo sapiens	110-115
30680297-5	2018	Purpose: The current study aimed to compare blocking of HMGB1 function and stimulation of HMGB1 function with quercetin and investigate the effects of the blockage on T helper 17 (Th17) cells and mitogen-activated protein kinase Toll-like receptor 4 (MAPK-TLR4) signaling pathway.	Quercetin	110-119	high mobility group box 1	Homo sapiens	90-95
30680297-9	2018	Results: The level of these cytokines decreased; moreover, western blot data showed that quercetin could decrease MAPK signaling pathway by means of inhibition of HMGB1 on T cells.	Quercetin	89-98	high mobility group box 1	Homo sapiens	163-168
30118903-6	2018	By co-culturing cervical cancer cell lines with immature DCs(imDCs) in the Transwell systems, we found that ALA-PDT induced HMGB1 exosomes could promote DCs maturation, which could be reversed by silencing HMGB1 in HPV-positive cervical cancer cells.	Alanine	108-111	high mobility group box 1	Homo sapiens	124-129
30118903-6	2018	By co-culturing cervical cancer cell lines with immature DCs(imDCs) in the Transwell systems, we found that ALA-PDT induced HMGB1 exosomes could promote DCs maturation, which could be reversed by silencing HMGB1 in HPV-positive cervical cancer cells.	Alanine	108-111	high mobility group box 1	Homo sapiens	206-211
30055307-9	2018	However, HMGB1 overexpression attenuated the protective effect of miR-106 on HUVECs in high glucose conditions.	Glucose	92-99	high mobility group box 1	Homo sapiens	9-14
30591798-7	2018	The results from RT-PCR analysis revealed a significant reduction in the expression of genes involved in inflammation including, HMGB1, IL-6 and IL-8 on treatment of DU-145 cells with crocetin.	crocetin	184-192	high mobility group box 1	Homo sapiens	129-134
30055307-12	2018	Taken together, these data collectively suggested that miR-106 was a potential molecular target for inhibiting high glucose-induced inflammation and apoptosis by targeting HMGB1.	Glucose	116-123	high mobility group box 1	Homo sapiens	172-177
30055307-5	2018	The results showed that the expression of HMGB1 was increased in human umbilical vein endothelial cells (HUVECs) after exposure to high glucose (25 mM).	Glucose	136-143	high mobility group box 1	Homo sapiens	42-47
30055307-6	2018	Downregulation of HMGB1 attenuated the high glucose-induced antiangiogenesis of HUVECs, and the decrease expression of HMGB1 inhibiting HUVEC apoptosis and inflammatory factor expression.	Glucose	44-51	high mobility group box 1	Homo sapiens	18-23
30464464-0	2018	A novel disulfide bond-mediated cleavable RGD-modified PAMAM nanocomplex containing nuclear localization signal HMGB1 for enhancing gene transfection efficiency.	Disulfides	8-17	high mobility group box 1	Homo sapiens	112-117
30464464-0	2018	A novel disulfide bond-mediated cleavable RGD-modified PAMAM nanocomplex containing nuclear localization signal HMGB1 for enhancing gene transfection efficiency.	Poly(amidoamine)	55-60	high mobility group box 1	Homo sapiens	112-117
30464464-7	2018	A pDNA/HMGB1/PAMAM-SS-PEG-RGD (DHP) nanocomplex was prepared via electrostatic interaction and characterized.	pamam-ss-peg-rgd	13-29	high mobility group box 1	Homo sapiens	7-12
30464464-10	2018	Intracellular trafficking and in vitro expression study indicated that the DHP nanocomplex escaped from lysosomes and the disulfide bonds between PAMAM and PEG cleaved due to the high concentration of GSH in the cytoplasm, pDNA consequently became exclusively located in the nucleus under the guidance of HMGB1, thereby promoting the red fluorescence protein (RFP) expression.	Disulfides	122-131	high mobility group box 1	Homo sapiens	305-310
30464464-10	2018	Intracellular trafficking and in vitro expression study indicated that the DHP nanocomplex escaped from lysosomes and the disulfide bonds between PAMAM and PEG cleaved due to the high concentration of GSH in the cytoplasm, pDNA consequently became exclusively located in the nucleus under the guidance of HMGB1, thereby promoting the red fluorescence protein (RFP) expression.	Poly(amidoamine)	146-151	high mobility group box 1	Homo sapiens	305-310
30464464-10	2018	Intracellular trafficking and in vitro expression study indicated that the DHP nanocomplex escaped from lysosomes and the disulfide bonds between PAMAM and PEG cleaved due to the high concentration of GSH in the cytoplasm, pDNA consequently became exclusively located in the nucleus under the guidance of HMGB1, thereby promoting the red fluorescence protein (RFP) expression.	Polyethylene Glycols	156-159	high mobility group box 1	Homo sapiens	305-310
30464464-10	2018	Intracellular trafficking and in vitro expression study indicated that the DHP nanocomplex escaped from lysosomes and the disulfide bonds between PAMAM and PEG cleaved due to the high concentration of GSH in the cytoplasm, pDNA consequently became exclusively located in the nucleus under the guidance of HMGB1, thereby promoting the red fluorescence protein (RFP) expression.	Glutathione	201-204	high mobility group box 1	Homo sapiens	305-310
30307477-5	2018	In this work, we found that the expression of high-mobility group box 1(HMGB1) was upregulated in CPCs under hypoxia conditions.	cpcs	98-102	high mobility group box 1	Homo sapiens	46-71
30307477-5	2018	In this work, we found that the expression of high-mobility group box 1(HMGB1) was upregulated in CPCs under hypoxia conditions.	cpcs	98-102	high mobility group box 1	Homo sapiens	72-77
30307477-7	2018	Additionally, mitogen-activated protein kinase (MAPK) signaling pathway was found to be involved in regulating DNMT1/HMGB1-mediated CPC apoptosis in hypoxia process.	cpc	132-135	high mobility group box 1	Homo sapiens	117-122
30175447-10	2018	RESULTS: Excess glucose triggered a trophoblast sterile inflammatory IL-8 and antimigratory response through HMGB1 activation of TLR4.	Glucose	16-23	high mobility group box 1	Homo sapiens	109-114
29178411-5	2018	Additionally, plasma oleoylethanolamide positively correlated with plasma levels of high mobility group box-1, which is a danger-associated molecular pattern and an endogenous TLR4 agonist, specifically in female alcohol binge drinkers.	oleoylethanolamide	21-39	high mobility group box 1	Homo sapiens	84-109
29178411-5	2018	Additionally, plasma oleoylethanolamide positively correlated with plasma levels of high mobility group box-1, which is a danger-associated molecular pattern and an endogenous TLR4 agonist, specifically in female alcohol binge drinkers.	Alcohols	213-220	high mobility group box 1	Homo sapiens	84-109
30175447-0	2018	Excess glucose induce trophoblast inflammation and limit cell migration through HMGB1 activation of Toll-Like receptor 4.	Glucose	7-14	high mobility group box 1	Homo sapiens	80-85
30214593-5	2018	Therefore, the probable involvement of HMGB1 in the development of carboplatin resistance in ovarian cancer SKOV3 cells was investigated.	Carboplatin	67-78	high mobility group box 1	Homo sapiens	39-44
30257412-0	2018	MiR-1284 enhances sensitivity of cervical cancer cells to cisplatin via downregulating HMGB1.	Cisplatin	58-67	high mobility group box 1	Homo sapiens	87-92
30257412-16	2018	CONCLUSION: miR-1284 enhances sensitivity of cervical cancer cells to cisplatin via targeting HMGB1.	Cisplatin	70-79	high mobility group box 1	Homo sapiens	94-99
30367066-6	2018	SMART in combination with imaging of the release of nuclear DAMPs and Live-Cell Imaging for Secretion activity (LCI-S) reveals two different modes of the release of High Mobility Group Box 1 from necroptotic cells.	lci-s	112-117	high mobility group box 1	Homo sapiens	165-190
30086328-0	2018	High-mobility group box 1 protein-mediated necroptosis contributes to dasatinib-induced cardiotoxicity.	Dasatinib	70-79	high mobility group box 1	Homo sapiens	0-25
30086328-9	2018	What"s more, unlike the inflammation-associated necroptosis, dasatinib-triggered necroptosis was dependent on intracellular instead of secreted High-mobility group box 1 (HMGB1) protein.	Dasatinib	61-70	high mobility group box 1	Homo sapiens	144-169
30086328-9	2018	What"s more, unlike the inflammation-associated necroptosis, dasatinib-triggered necroptosis was dependent on intracellular instead of secreted High-mobility group box 1 (HMGB1) protein.	Dasatinib	61-70	high mobility group box 1	Homo sapiens	171-176
30086328-10	2018	Collectively, our study revealed that dasatinib-induced cardiotoxicity acted via leading cardiomyocytes to HMGB1-mediated necroptosis, indicating a viable strategy for prevention of dasatinib-induced cardiotoxicity.	Dasatinib	38-47	high mobility group box 1	Homo sapiens	107-112
30086328-10	2018	Collectively, our study revealed that dasatinib-induced cardiotoxicity acted via leading cardiomyocytes to HMGB1-mediated necroptosis, indicating a viable strategy for prevention of dasatinib-induced cardiotoxicity.	Dasatinib	182-191	high mobility group box 1	Homo sapiens	107-112
30119194-9	2018	Furthermore, the SH-SY5Y cells were exposed to high glucose stimulation, FMN (2.5, 5 and 10 muM) treatment, and glycyrrhizin, the selective inhibitor of HMGB1.	Glycyrrhizic Acid	112-124	high mobility group box 1	Homo sapiens	153-158
30119194-13	2018	The inhibition of HMGB1 by glycyrrhizin also confirmed the involvement of HMGB1/TLR4/NF-kappaB/NLRP3 pathway in high glucose-induced SH-SY5Y cells.	Glycyrrhizic Acid	27-39	high mobility group box 1	Homo sapiens	18-23
30119194-13	2018	The inhibition of HMGB1 by glycyrrhizin also confirmed the involvement of HMGB1/TLR4/NF-kappaB/NLRP3 pathway in high glucose-induced SH-SY5Y cells.	Glycyrrhizic Acid	27-39	high mobility group box 1	Homo sapiens	74-79
30119194-13	2018	The inhibition of HMGB1 by glycyrrhizin also confirmed the involvement of HMGB1/TLR4/NF-kappaB/NLRP3 pathway in high glucose-induced SH-SY5Y cells.	Glucose	117-124	high mobility group box 1	Homo sapiens	18-23
30119194-13	2018	The inhibition of HMGB1 by glycyrrhizin also confirmed the involvement of HMGB1/TLR4/NF-kappaB/NLRP3 pathway in high glucose-induced SH-SY5Y cells.	Glucose	117-124	high mobility group box 1	Homo sapiens	74-79
30119194-14	2018	In summary, the results suggested that FMN exhibited the protective effect on STZ-induced cognitive impairment possibly via the mediation of HMGB1/TLR4/NF-kappaB signaling and NLRP3 inflammasome.	Streptozocin	78-81	high mobility group box 1	Homo sapiens	141-146
30313098-2	2018	Experimental animal studies suggested that increased extracellular histone and high morbidity group box-1 (HMGB1) levels might contribute to ALI development.	ali	141-144	high mobility group box 1	Homo sapiens	79-105
30313098-2	2018	Experimental animal studies suggested that increased extracellular histone and high morbidity group box-1 (HMGB1) levels might contribute to ALI development.	ali	141-144	high mobility group box 1	Homo sapiens	107-112
30132524-0	2018	Renoprotection of dapagliflozin in human renal proximal tubular cells via the inhibition of the high mobility group box 1-receptor for advanced glycation end products-nuclear factor-kappaB signaling pathway.	dapagliflozin	18-31	high mobility group box 1	Homo sapiens	96-121
30114640-7	2018	In addition, GSK"872 could also decrease the protein levels of RIPK3 and MLKL, and cytoplasmic translocation and expression of HMGB1, an important pro-inflammatory protein.	gsk"872	13-20	high mobility group box 1	Homo sapiens	127-132
30314759-5	2018	Subsequently, HMGB1 permeabilized the phospholipid bilayer in the acidic environment of lysosomes.	Phospholipids	38-50	high mobility group box 1	Homo sapiens	14-19
30405740-10	2018	MAN induced declines of both HMGB1/TLR4/p-p65 and TNF-alpha were substantially reversed by cotreatment with nicotinamide mononucleotide or NAD.	Nicotinamide Mononucleotide	108-135	high mobility group box 1	Homo sapiens	29-34
30405740-10	2018	MAN induced declines of both HMGB1/TLR4/p-p65 and TNF-alpha were substantially reversed by cotreatment with nicotinamide mononucleotide or NAD.	NAD	139-142	high mobility group box 1	Homo sapiens	29-34
30119256-0	2018	Synergy of theophylline reduces necrotic effect of berberine, induces cell cycle arrest and PARP, HMGB1, Bcl-2 family mediated apoptosis in MDA-MB-231 breast cancer cells.	Theophylline	11-23	high mobility group box 1	Homo sapiens	98-103
30119256-6	2018	Combined treatment of Berberine and theophylline reduced extracellular level of HMGB1 and down regulated HMGB1 and MMP-9 mRNA expression.	Berberine	22-31	high mobility group box 1	Homo sapiens	80-85
30119256-6	2018	Combined treatment of Berberine and theophylline reduced extracellular level of HMGB1 and down regulated HMGB1 and MMP-9 mRNA expression.	Berberine	22-31	high mobility group box 1	Homo sapiens	105-110
30119256-6	2018	Combined treatment of Berberine and theophylline reduced extracellular level of HMGB1 and down regulated HMGB1 and MMP-9 mRNA expression.	Theophylline	36-48	high mobility group box 1	Homo sapiens	80-85
30119256-6	2018	Combined treatment of Berberine and theophylline reduced extracellular level of HMGB1 and down regulated HMGB1 and MMP-9 mRNA expression.	Theophylline	36-48	high mobility group box 1	Homo sapiens	105-110
30119256-7	2018	The results of flow cytometry using annexin/PI staining of the cells, HMGB1 release, and poly ADP ribose polymerase cleavage demonstrated that theophylline attenuated necrotic effect of berberine and increased the level of apoptotic cell death.	Theophylline	143-155	high mobility group box 1	Homo sapiens	70-75
30214593-12	2018	Annexin V-fluorescein isothiocyanate/propidium iodide staining demonstrated that HMGB1 silencing enhanced the effects of carboplatin in inducing the apoptosis of SKOV3-Carb cells relative to HMGB1 non-silenced control cells.	Propidium	37-53	high mobility group box 1	Homo sapiens	81-86
30214593-12	2018	Annexin V-fluorescein isothiocyanate/propidium iodide staining demonstrated that HMGB1 silencing enhanced the effects of carboplatin in inducing the apoptosis of SKOV3-Carb cells relative to HMGB1 non-silenced control cells.	Carboplatin	121-132	high mobility group box 1	Homo sapiens	81-86
30214593-13	2018	The results of the present study suggested that HMGB1 may be involved in the development of carboplatin resistance in ovarian cancer SKOV3 cells and that HMGB1 silencing may induce the sensitization of carboplatin-resistant ovarian cancer cells to carboplatin.	Carboplatin	92-103	high mobility group box 1	Homo sapiens	48-53
30214593-13	2018	The results of the present study suggested that HMGB1 may be involved in the development of carboplatin resistance in ovarian cancer SKOV3 cells and that HMGB1 silencing may induce the sensitization of carboplatin-resistant ovarian cancer cells to carboplatin.	Carboplatin	202-213	high mobility group box 1	Homo sapiens	154-159
30214593-13	2018	The results of the present study suggested that HMGB1 may be involved in the development of carboplatin resistance in ovarian cancer SKOV3 cells and that HMGB1 silencing may induce the sensitization of carboplatin-resistant ovarian cancer cells to carboplatin.	Carboplatin	202-213	high mobility group box 1	Homo sapiens	154-159
30214593-14	2018	Therefore, HMGB1 may be considered as a potent therapeutic target for increasing the sensitivity of ovarian cancer cells to carboplatin in order to improve the treatment and prognosis of ovarian cancer.	Carboplatin	124-135	high mobility group box 1	Homo sapiens	11-16
30214593-6	2018	HMGB1 has been reported to be overexpressed in carboplatin-resistant SKOV3-Carb cells compared with control SKOV3 cells.	Carboplatin	47-58	high mobility group box 1	Homo sapiens	0-5
30214593-10	2018	An MTT assay revealed that the proliferation of HMGB1-silenced SKOV3 and SKOV3-Carb cells were decreased compared with the proliferation of non-silenced control cells.	monooxyethylene trimethylolpropane tristearate	3-6	high mobility group box 1	Homo sapiens	48-53
30214593-11	2018	Additionally, HMGB1 protein expression levels in SKOV3 cells, but not in SKOV3-Carb cells, were decreased in response to carboplatin treatment.	Carboplatin	121-132	high mobility group box 1	Homo sapiens	14-19
30283452-2	2018	The alarmin HMGB1, in its reduced form, can complex with CXCL12 enhancing its activity on monocytes via the chemokine receptor CXCR4, while the form containing a disulfide bond, by binding to TLR2 or TLR4, initiates a cascade of events leading to production of cytokines and chemokines.	Disulfides	162-171	high mobility group box 1	Homo sapiens	12-17
28885675-4	2018	In addition, we also investigated the regulatory role of HMGB1 in the sensitivity of NSCLC cells to cisplatin.	Cisplatin	100-109	high mobility group box 1	Homo sapiens	57-62
28885675-7	2018	Then the influence by HMGB1 on the chemosensitivity of lung cancer A549 cells was examined with MTT assay and colony forming assay for the A549 cells post the treatment with cisplatin or (and) HMGB1.	monooxyethylene trimethylolpropane tristearate	96-99	high mobility group box 1	Homo sapiens	22-27
28885675-7	2018	Then the influence by HMGB1 on the chemosensitivity of lung cancer A549 cells was examined with MTT assay and colony forming assay for the A549 cells post the treatment with cisplatin or (and) HMGB1.	Cisplatin	174-183	high mobility group box 1	Homo sapiens	22-27
28885675-10	2018	Recombinant HMGB1 reduced the sensitivity of A549 cells to cisplatin in vitro.	Cisplatin	59-68	high mobility group box 1	Homo sapiens	12-17
28885675-12	2018	HMGB1 reduced the sensitivity of NSCLC A549 cells to cisplatin in vitro.	Cisplatin	53-62	high mobility group box 1	Homo sapiens	0-5
30283452-3	2018	So far, the possibility that the CXCL12/HMGB1 heterocomplex could be maintained in chronic inflammation was debated, due to the release of reactive oxygen species.	Reactive Oxygen Species	139-162	high mobility group box 1	Homo sapiens	40-45
30064906-4	2018	In LPS-induced sepsis model in vivo, administration of KPT330 increased survival rate and ameliorated LPS-induced lung injury, with suppressed levels of TNF-alpha, IL-6 and HMGB1 in the circulation and decreased macrophage and PMN subpopulations in peritoneal cavity.	selinexor	55-61	high mobility group box 1	Homo sapiens	173-178
30166062-0	2018	High-mobility group box 1 is responsible for monosodium urate crystal-induced inflammation in human U937 macrophages.	Uric Acid	45-61	high mobility group box 1	Homo sapiens	0-25
30166062-2	2018	We performed this study to investigate the role of HMGB1 in the pathogenesis of uric acid-induced inflammation in human U937 macrophages.	Uric Acid	80-89	high mobility group box 1	Homo sapiens	51-56
30166062-8	2018	Stimulation of U937 cells with MSU crystals induced translocation of HMGB1 from the nucleus to the cytoplasm and its extracellular release.	Uric Acid	31-34	high mobility group box 1	Homo sapiens	69-74
30166062-10	2018	Antioxidants, such as N-acetyl-l-cysteine and quercetin, markedly inhibited the nuclear-to-cytoplasmic translocation of HMGB1 and its release into the extracellular milieu.	Acetylcysteine	22-41	high mobility group box 1	Homo sapiens	120-125
30166062-10	2018	Antioxidants, such as N-acetyl-l-cysteine and quercetin, markedly inhibited the nuclear-to-cytoplasmic translocation of HMGB1 and its release into the extracellular milieu.	Quercetin	46-55	high mobility group box 1	Homo sapiens	120-125
30166062-11	2018	In conclusion, HMGB1, regulated by the enzymatic activity of caspase-1, is a crucial mediator in uric acid-induced inflammation.	Uric Acid	97-106	high mobility group box 1	Homo sapiens	15-20
30208922-0	2018	Retraction Note: HMGB1: a novel protein that induced platelets active and aggregation via Toll-like receptor-4, NF-kappaB and cGMP dependent mechanisms.	Cyclic GMP	126-130	high mobility group box 1	Homo sapiens	17-22
30064906-5	2018	In vitro investigations showed that KPT330 dose-dependently inhibited LPS-triggered proinflammatory cytokines production including TNF-alpha, IL-6 and HMGB1 in macrophages.	selinexor	36-42	high mobility group box 1	Homo sapiens	151-156
30064906-6	2018	Furthermore, KPT330 treatment significantly suppressed TNF-alpha and IL-6 mRNA expression and inhibited HMGB1 necleocytoplasmic translocation by inhibiting CRM1 distribution.	selinexor	13-19	high mobility group box 1	Homo sapiens	104-109
29901427-8	2018	Ferulic acid significantly ameliorated HUVEC radiation injury, as evidenced by increases in cell viability and angiogenesis and decreases in G2/M cell cycle arrest and levels of high mobility group box 1 protein (HMGB1), interleukin (IL)-6 and IL-8.	ferulic acid	0-12	high mobility group box 1	Homo sapiens	178-203
29947767-0	2018	High linear energy transfer carbon-ion irradiation increases the release of the immune mediator high mobility group box 1 from human cancer cells.	Carbon	28-34	high mobility group box 1	Homo sapiens	96-121
30279967-0	2018	N-(2"-Hydroxyphenyl)-2-propylpentanamide (OH-VPA), a histone deacetylase inhibitor, induces the release of nuclear HMGB1 and modifies ROS levels in HeLa cells.	N-(2-hydroxyphenyl)-2-propylpentanamide	0-40	high mobility group box 1	Homo sapiens	115-120
30279967-0	2018	N-(2"-Hydroxyphenyl)-2-propylpentanamide (OH-VPA), a histone deacetylase inhibitor, induces the release of nuclear HMGB1 and modifies ROS levels in HeLa cells.	oh-vpa	42-48	high mobility group box 1	Homo sapiens	115-120
30279967-6	2018	Our results show that OH-VPA induces nuclear to cytoplasmic translocation of HMGB1, as demonstrated by confocal microscopy observations and infrared spectra that revealed high quantities of acetylated HMGB1 in HeLa cells.	oh-vpa	22-28	high mobility group box 1	Homo sapiens	77-82
30279967-6	2018	Our results show that OH-VPA induces nuclear to cytoplasmic translocation of HMGB1, as demonstrated by confocal microscopy observations and infrared spectra that revealed high quantities of acetylated HMGB1 in HeLa cells.	oh-vpa	22-28	high mobility group box 1	Homo sapiens	201-206
28840951-6	2018	The immune/inflammatory changes were more prominent in female drinkers, who showed elevated levels of alcohol danger-associated molecules, such as high mobility group box 1, indicating that there are sex-related differences in the peripheral inflammatory response to alcohol.	Alcohols	102-109	high mobility group box 1	Homo sapiens	147-172
28840951-6	2018	The immune/inflammatory changes were more prominent in female drinkers, who showed elevated levels of alcohol danger-associated molecules, such as high mobility group box 1, indicating that there are sex-related differences in the peripheral inflammatory response to alcohol.	Alcohols	267-274	high mobility group box 1	Homo sapiens	147-172
29741224-5	2018	Subsequently, HMGB1 inhibitors can reduce the ANG II-elicited polarize of macrophage.	Angiotensin II	46-52	high mobility group box 1	Homo sapiens	14-19
27900730-13	2018	The interactions between DNA and HMGB1 are defined by hydrogen bonds and van der Waals contacts.	Hydrogen	54-62	high mobility group box 1	Homo sapiens	33-38
29901427-8	2018	Ferulic acid significantly ameliorated HUVEC radiation injury, as evidenced by increases in cell viability and angiogenesis and decreases in G2/M cell cycle arrest and levels of high mobility group box 1 protein (HMGB1), interleukin (IL)-6 and IL-8.	ferulic acid	0-12	high mobility group box 1	Homo sapiens	213-218
30157804-13	2018	HMGB1 had good diagnostic ability to differentiate RMPP with AUC of 0.876, sensitivity of 0.833, and specificity of 0.824 compared with TNF-alpha and IL-6.	rmpp	51-55	high mobility group box 1	Homo sapiens	0-5
30157804-17	2018	CONCLUSIONS: HMGB1 is a good diagnostic biomarker for differentiating RMPP and NRMPP.	rmpp	70-74	high mobility group box 1	Homo sapiens	13-18
30157958-7	2018	HMGB1 knockdown in MM cells enhanced the inhibitory effect of chemotherapy with dexamethasone (Dex) via apoptosis induction.	Dexamethasone	80-93	high mobility group box 1	Homo sapiens	0-5
30157958-7	2018	HMGB1 knockdown in MM cells enhanced the inhibitory effect of chemotherapy with dexamethasone (Dex) via apoptosis induction.	Dexamethasone	95-98	high mobility group box 1	Homo sapiens	0-5
30157804-4	2018	The present study aimed to explore the role and clinical significance of HMGB1 in children with RMPP and the potential mechanism of HMGB1 expression.	rmpp	96-100	high mobility group box 1	Homo sapiens	73-78
30157804-12	2018	HMGB1, TNF-alpha, and IL-6 levels were significantly higher in RMPP cases compared with NRMPP cases (all p &lt; 0.05).	rmpp	63-67	high mobility group box 1	Homo sapiens	0-5
30157804-19	2018	Further in vitro and in vivo studies are needed for the development of a new treatment strategy to inhibit the HMGB1 pathway, thereby preventing the inflammation in RMPP.	rmpp	165-169	high mobility group box 1	Homo sapiens	111-116
30157958-8	2018	Furthermore, downregulation of HMGB1 activated the mTOR pathway, inhibited autophagy and increased DNA damage induced by Dex by modulating expression of related genes.	Dexamethasone	121-124	high mobility group box 1	Homo sapiens	31-36
30157958-10	2018	CONCLUSIONS: Our research shows that HMGB1 participates in autophagy and DNA damage repair and that downregulation of HMGB1 enhances the sensitivity of MM cells to Dex, suggesting that HMGB1 may serve as a target for MM treatment.	Dexamethasone	164-167	high mobility group box 1	Homo sapiens	118-123
30096430-0	2018	WITHDRAWN: Paeoniflorin attenuates LPS-induced inflammation in nucleus pulposus cells via Nrf-2/HO-1/HMGB1/NF-kappaB pathway.	peoniflorin	11-23	high mobility group box 1	Homo sapiens	101-106
30157958-10	2018	CONCLUSIONS: Our research shows that HMGB1 participates in autophagy and DNA damage repair and that downregulation of HMGB1 enhances the sensitivity of MM cells to Dex, suggesting that HMGB1 may serve as a target for MM treatment.	Dexamethasone	164-167	high mobility group box 1	Homo sapiens	118-123
30210495-2	2018	In cultured primary bone marrow-derived cells (BMDCs) stimulated with HMGB1, the number of cells with macrophage-like morphology was markedly increased in association with an increased expression of CD11b/Mac-1, which were attenuated in cells pre-treated with Zileuton, a 5-LO inhibitor as well as in 5-LO-deficient BMDCs.	zileuton	260-268	high mobility group box 1	Homo sapiens	70-75
30126243-8	2018	The study on the recognition and binding of the HMGB-1 protein to cisplatin or Pd1 modified DNA probes have shown that HMG proteins are less involved in the palladium agent cytotoxicity.	Cisplatin	66-75	high mobility group box 1	Homo sapiens	48-54
29031614-8	2018	Interfering with disulfide HMGB1-activated cell signaling mediates significant therapeutic effects in epilepsy models.	Disulfides	17-26	high mobility group box 1	Homo sapiens	27-32
30081847-0	2018	Intermittent high glucose-induced oxidative stress modulates retinal pigmented epithelial cell autophagy and promotes cell survival via increased HMGB1.	Glucose	18-25	high mobility group box 1	Homo sapiens	146-151
30081847-7	2018	The expression of HMGB1 was detected by immunohistochemistry.Cells were pre-incubated with HMGB1 inhibitor ethyl pyruvate (EP) ,then detected the expression pattern of autophagic markers and level of cellular ROS.	ethyl pyruvate	107-121	high mobility group box 1	Homo sapiens	91-96
29803174-0	2018	miR-505 enhances doxorubicin-induced cytotoxicity in hepatocellular carcinoma through repressing the Akt pathway by directly targeting HMGB1.	Doxorubicin	17-28	high mobility group box 1	Homo sapiens	135-140
29803174-8	2018	We found that HMGB1 knockdown and miR-505 overexpression exacerbated ADM-induced cell viability inhibition, enhanced ADM-induced apoptosis, and increased caspase-3 activity in ADM-treated HCC cells.	Doxorubicin	69-72	high mobility group box 1	Homo sapiens	14-19
29930000-0	2018	Inorganic Polyphosphate Amplifies High Mobility Group Box 1-Mediated Von Willebrand Factor Release and Platelet String Formation on Endothelial Cells.	inorganic polyphosphate	0-23	high mobility group box 1	Homo sapiens	34-59
29763588-0	2018	Glycyrrhizin ameliorates inflammatory pain by inhibiting microglial activation-mediated inflammatory response via blockage of the HMGB1-TLR4-NF-kB pathway.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	130-135
29704473-8	2018	With regard to cardiovascular risk, levels of serum HMGB1 were positively associated with 10-year CHD risk (beta coefficient 0.506, 95% CI 0.030 to 0.983, p = .037), independent of patients" undiagnosed abnormal glucose regulation.	Glucose	212-219	high mobility group box 1	Homo sapiens	52-57
29763588-8	2018	Furthermore, glycyrrhizin dampened the activation of subsequent TLR4-NF-kappaB pathway in LPS-stimulated microglia, which was abrogated by HMGB1 elevation.	Glycyrrhizic Acid	13-25	high mobility group box 1	Homo sapiens	139-144
29737584-0	2018	Metformin increases the cytotoxicity of oxaliplatin in human DLD-1 colorectal cancer cells through down-regulating HMGB1 expression.	Metformin	0-9	high mobility group box 1	Homo sapiens	115-120
29737584-0	2018	Metformin increases the cytotoxicity of oxaliplatin in human DLD-1 colorectal cancer cells through down-regulating HMGB1 expression.	Oxaliplatin	40-51	high mobility group box 1	Homo sapiens	115-120
29737584-7	2018	In this study, we examined whether HMGB1 plays a role in the OXA- and/or metformin-induced cytotoxic effect on CRC cells.	Metformin	73-82	high mobility group box 1	Homo sapiens	35-40
29737584-8	2018	The results showed that treatment with OXA increased HMGB1 expression in the ERK1/2- and Akt-dependent manners in DLD-1 cells.	Oxaliplatin	39-42	high mobility group box 1	Homo sapiens	53-58
29737584-11	2018	Compared to a single agent, OXA combined with metformin administration resulted in cytotoxicity and cell growth inhibition synergistically, accompanied with reduced HMGB1 level.	Oxaliplatin	28-31	high mobility group box 1	Homo sapiens	165-170
29737584-11	2018	Compared to a single agent, OXA combined with metformin administration resulted in cytotoxicity and cell growth inhibition synergistically, accompanied with reduced HMGB1 level.	Metformin	46-55	high mobility group box 1	Homo sapiens	165-170
29676481-5	2018	Furthermore, therapeutic targeting of HMGB1 with either anti-HMGB1 antibodies or selective inhibitors, such as glycyrrhizin, has been shown to inhibit neurodegeneration in animal models.	Glycyrrhizic Acid	111-123	high mobility group box 1	Homo sapiens	38-43
29997173-3	2018	CD52-Fc bound specifically to the proinflammatory Box B domain of HMGB1, and this in turn promoted binding of the CD52 N-linked glycan, in alpha-2,3 sialic acid linkage with galactose, to Siglec-10.	n-linked glycan	119-134	high mobility group box 1	Homo sapiens	66-71
29715512-0	2018	HMGB1 contributes to adriamycin-induced cardiotoxicity via up-regulating autophagy.	Doxorubicin	21-31	high mobility group box 1	Homo sapiens	0-5
29909245-0	2018	Corrigendum to "Immunosuppressant cytoprotection correlates with HMGB1 suppression in primary astrocyte cultures exposed to combined oxygen-glucose deprivation" [Pharmacol.	oxygen-glucose	133-147	high mobility group box 1	Homo sapiens	65-70
30061484-8	2018	Sulphated K5 carbohydrate fragments inhibited RAGE binding to amyloid beta-peptide and HMGB1.	Carbohydrates	13-25	high mobility group box 1	Homo sapiens	87-92
30061484-11	2018	Further, glycyrrhizin inhibited HMGB1 and HMGB1 A-box binding to heparin.	Glycyrrhizic Acid	9-21	high mobility group box 1	Homo sapiens	32-37
30061484-11	2018	Further, glycyrrhizin inhibited HMGB1 and HMGB1 A-box binding to heparin.	Glycyrrhizic Acid	9-21	high mobility group box 1	Homo sapiens	42-47
30061484-11	2018	Further, glycyrrhizin inhibited HMGB1 and HMGB1 A-box binding to heparin.	Heparin	65-72	high mobility group box 1	Homo sapiens	32-37
30061484-11	2018	Further, glycyrrhizin inhibited HMGB1 and HMGB1 A-box binding to heparin.	Heparin	65-72	high mobility group box 1	Homo sapiens	42-47
30123419-3	2018	In this study we established a representative panel of patient derived xenograft (PDX) mouse models from patients with renal cell carcinomas and determined serum levels of high mobility group B1 (HMGB1) protein under treatment with sunitinib, pazopanib, sorafenib, axitinib, temsirolimus and bevacizumab.	Sorafenib	254-263	high mobility group box 1	Homo sapiens	196-201
30123419-3	2018	In this study we established a representative panel of patient derived xenograft (PDX) mouse models from patients with renal cell carcinomas and determined serum levels of high mobility group B1 (HMGB1) protein under treatment with sunitinib, pazopanib, sorafenib, axitinib, temsirolimus and bevacizumab.	Axitinib	265-273	high mobility group box 1	Homo sapiens	196-201
30123419-3	2018	In this study we established a representative panel of patient derived xenograft (PDX) mouse models from patients with renal cell carcinomas and determined serum levels of high mobility group B1 (HMGB1) protein under treatment with sunitinib, pazopanib, sorafenib, axitinib, temsirolimus and bevacizumab.	temsirolimus	275-287	high mobility group box 1	Homo sapiens	196-201
29997173-3	2018	CD52-Fc bound specifically to the proinflammatory Box B domain of HMGB1, and this in turn promoted binding of the CD52 N-linked glycan, in alpha-2,3 sialic acid linkage with galactose, to Siglec-10.	N-Acetylneuraminic Acid	149-160	high mobility group box 1	Homo sapiens	66-71
29997173-3	2018	CD52-Fc bound specifically to the proinflammatory Box B domain of HMGB1, and this in turn promoted binding of the CD52 N-linked glycan, in alpha-2,3 sialic acid linkage with galactose, to Siglec-10.	Galactose	174-183	high mobility group box 1	Homo sapiens	66-71
29743526-4	2018	It was further shown that HQH administration reduced cisplatin-induced release and nuclear-cytoplasmic translocation of HMGB1 and inactivated its downstream signaling molecules, TLR4 and NFkappaB, in renal tubular cells; as a result, HQH repressed cisplatin-induced TNF-alpha production.	Cisplatin	53-62	high mobility group box 1	Homo sapiens	120-125
29751935-0	2018	Down-Regulation of miR-218-5p Promotes Apoptosis of Human Umbilical Vein Endothelial Cells Through Regulating High-Mobility Group Box-1 in Henoch-Schonlein Purpura.	mir-218-5p	19-29	high mobility group box 1	Homo sapiens	110-135
29751935-6	2018	The association between miR-218-5p and HMGB1 was determined by luciferase assay.	mir-218-5p	24-34	high mobility group box 1	Homo sapiens	39-44
29751935-11	2018	Furthermore, the miR-218-5p mimic demonstrated an inhibitory effect on the apoptosis of HUVECs co-cultured in PBMC supernatant, which was reversed by over expression of HMGB1.	mir-218-5p	17-27	high mobility group box 1	Homo sapiens	169-174
29573352-3	2018	The results showed that administration of 7.5 mg/kg alpha-HMGB1 1 h after IAV (A/Puerto Rico/8/34) inoculation significantly alleviated brain edema at 48 h after IAV inoculation, as confirmed by the suppression of Evans Blue dye leakage and matrix metallopeptidase-9 mRNA expression in the brain.	Evans Blue	214-228	high mobility group box 1	Homo sapiens	58-63
29795370-7	2018	HMGB1 dose-dependently enhanced the expression of CD80 and CD86 on DCs in vitro, and intravenous or oral administration of glycyrrhizin, an HMGB1 inhibitor, significantly suppressed activation of mucosal DCs and induction of intestinal OVA-specific CTLs and IgA by oral CT administration.	Glycyrrhizic Acid	123-135	high mobility group box 1	Homo sapiens	0-5
29795370-7	2018	HMGB1 dose-dependently enhanced the expression of CD80 and CD86 on DCs in vitro, and intravenous or oral administration of glycyrrhizin, an HMGB1 inhibitor, significantly suppressed activation of mucosal DCs and induction of intestinal OVA-specific CTLs and IgA by oral CT administration.	Glycyrrhizic Acid	123-135	high mobility group box 1	Homo sapiens	140-145
29899164-0	2018	miRNA-1284, a regulator of HMGB1, inhibits cell proliferation and migration in osteosarcoma.	mirna-1284	0-10	high mobility group box 1	Homo sapiens	27-32
29773200-0	2018	Lithium chloride attenuates mitomycin C induced necrotic cell death in MDA-MB-231 breast cancer cells via HMGB1 and Bax signaling.	Lithium Chloride	0-16	high mobility group box 1	Homo sapiens	106-111
29773200-0	2018	Lithium chloride attenuates mitomycin C induced necrotic cell death in MDA-MB-231 breast cancer cells via HMGB1 and Bax signaling.	Mitomycin	28-39	high mobility group box 1	Homo sapiens	106-111
29773200-8	2018	LiCl combined with mitomycin C significantly down-regulated HMGB1, MMP9 and Bcl-2 gene expression but significantly increased the level of Bax protein.	Lithium Chloride	0-4	high mobility group box 1	Homo sapiens	60-65
29773200-8	2018	LiCl combined with mitomycin C significantly down-regulated HMGB1, MMP9 and Bcl-2 gene expression but significantly increased the level of Bax protein.	Mitomycin	19-30	high mobility group box 1	Homo sapiens	60-65
29773200-9	2018	In addition, the content of HMGB1 in the nuclei decreased and pretreatment with LiCl reduced the content of HMGB1 release induced by MMC.	Lithium Chloride	80-84	high mobility group box 1	Homo sapiens	108-113
29773200-9	2018	In addition, the content of HMGB1 in the nuclei decreased and pretreatment with LiCl reduced the content of HMGB1 release induced by MMC.	Mitomycin	133-136	high mobility group box 1	Homo sapiens	108-113
29791130-10	2018	The concentration of HMGB1 in citrated and EDTA-treated plasma from the same healthy control subjects was below the limit of detection of our assay (1 ng/mL), confirming that HMGB1 in serum arises when blood is allowed to clot.	Edetic Acid	43-47	high mobility group box 1	Homo sapiens	21-26
29791130-10	2018	The concentration of HMGB1 in citrated and EDTA-treated plasma from the same healthy control subjects was below the limit of detection of our assay (1 ng/mL), confirming that HMGB1 in serum arises when blood is allowed to clot.	Edetic Acid	43-47	high mobility group box 1	Homo sapiens	175-180
29292841-6	2018	In vitro, the exposure of normal human bronchial epithelial cells to HMGB1 resulted in the upregulation of GRP75, proinflammatory cytokine production, enhanced ER-Mitochondrial Ca2+ transfer, and enhancement of reactive oxygen species (ROS).	Reactive Oxygen Species	236-239	high mobility group box 1	Homo sapiens	69-74
29356044-9	2018	High expression levels of HMGB1 as total (P = 0.0011) and cytoplasmic score (P = 0.0462) were related to a worse disease-specific survival (DSS) in the entire cohort and in the clinicopathological subgroups.	dss	140-143	high mobility group box 1	Homo sapiens	26-31
29292841-6	2018	In vitro, the exposure of normal human bronchial epithelial cells to HMGB1 resulted in the upregulation of GRP75, proinflammatory cytokine production, enhanced ER-Mitochondrial Ca2+ transfer, and enhancement of reactive oxygen species (ROS).	Reactive Oxygen Species	211-234	high mobility group box 1	Homo sapiens	69-74
29292841-8	2018	Sequentially, pretreatment with 2-APB, SKF960365 (SKF) and Ru360 which inhibit ER-Mitochondrial Ca2+ transfer significantly lowered HMGB1-induced the generation of ROS and the release of Th2 cytokines in 16HBE cells.	2-aminoethoxydiphenyl borate	32-37	high mobility group box 1	Homo sapiens	132-137
29292841-8	2018	Sequentially, pretreatment with 2-APB, SKF960365 (SKF) and Ru360 which inhibit ER-Mitochondrial Ca2+ transfer significantly lowered HMGB1-induced the generation of ROS and the release of Th2 cytokines in 16HBE cells.	Reactive Oxygen Species	164-167	high mobility group box 1	Homo sapiens	132-137
29329282-3	2018	The role of HMGB1 in RSV infection was explored using glycyrrhizin, a selective HMGB1 inhibitor.ResultsRSV infection strongly induced HMGB1 expression both in vitro and in vivo.	Glycyrrhizic Acid	54-66	high mobility group box 1	Homo sapiens	80-85
29395576-3	2018	OBJECTIVE: To evaluate the effect of reduced-HMGB1 (previously termed chemoattractive-HMGB1) on polyinosine-polycytidylic acid [poly(I:C)]-induced inflammation in normal human keratinocytes (NHKs).	polyinosine-polycytidylic acid	96-126	high mobility group box 1	Homo sapiens	86-91
29395576-5	2018	An immunoprecipitation was performed to know whether HMGB1 could bind to poly(I:C), and immunofluorescence staining and flow cytometric analysis were performed to check whether reduced-HMGB interferes with cellular uptake of poly(I:C) translocation (possibly by endocytosis).	Poly I-C	73-81	high mobility group box 1	Homo sapiens	53-58
29395576-5	2018	An immunoprecipitation was performed to know whether HMGB1 could bind to poly(I:C), and immunofluorescence staining and flow cytometric analysis were performed to check whether reduced-HMGB interferes with cellular uptake of poly(I:C) translocation (possibly by endocytosis).	Poly I-C	73-82	high mobility group box 1	Homo sapiens	53-58
29395576-6	2018	RESULTS: Application of exogenous HMGB1 before, but not after, exerted a suppressive effect on poly(I:C)-induced inflammation in NHKs.	Poly I-C	95-104	high mobility group box 1	Homo sapiens	34-39
29395576-7	2018	In addition, reduced-HMGB1, but not disulfide-HMGB1, exerted a suppressive effect on poly(I:C)-induced inflammation in NHKs, suggesting the importance of the redox status of exogenous HMGB1.	Poly I-C	85-94	high mobility group box 1	Homo sapiens	21-26
29395576-9	2018	Disulfide-HMGB1 formed a complex with poly(I:C), as did reduced- and oxidized-HMGB1, albeit to a lesser extent.	Disulfides	0-9	high mobility group box 1	Homo sapiens	10-15
29395576-11	2018	CONCLUSION: These findings suggest that pre-treatment with reduced-HMGB1 ameliorates poly(I:C)-mediated inflammation in NHKs.	Poly I-C	85-94	high mobility group box 1	Homo sapiens	67-72
29395576-0	2018	Reduced-HMGB1 suppresses poly(I:C)-induced inflammation in keratinocytes.	Poly I-C	25-34	high mobility group box 1	Homo sapiens	8-13
29395576-3	2018	OBJECTIVE: To evaluate the effect of reduced-HMGB1 (previously termed chemoattractive-HMGB1) on polyinosine-polycytidylic acid [poly(I:C)]-induced inflammation in normal human keratinocytes (NHKs).	polyinosine-polycytidylic acid	96-126	high mobility group box 1	Homo sapiens	45-50
29329282-3	2018	The role of HMGB1 in RSV infection was explored using glycyrrhizin, a selective HMGB1 inhibitor.ResultsRSV infection strongly induced HMGB1 expression both in vitro and in vivo.	Glycyrrhizic Acid	54-66	high mobility group box 1	Homo sapiens	80-85
29329282-4	2018	Glycyrrhizin dose-dependently inhibited HMGB1 upregulation in both RSV-infected immortalized and primary human bronchial epithelial cells, and this effect was associated with significant reduction of viral replication.ConclusionOur data suggest that HMGB1 expression increases during RSV replication.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	40-45
29329282-4	2018	Glycyrrhizin dose-dependently inhibited HMGB1 upregulation in both RSV-infected immortalized and primary human bronchial epithelial cells, and this effect was associated with significant reduction of viral replication.ConclusionOur data suggest that HMGB1 expression increases during RSV replication.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	250-255
29531138-4	2018	In vitro analysis indicated that HMGB1, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interleukin-1beta (IL-1beta) were secreted in response to tumor necrosis factor-alpha (TNF-alpha) stimuli in human gingival epithelial cells (HGECs) and human monocytic leukemia cells (THP-1) treated with phorbol myristate acetate.	Tetradecanoylphorbol Acetate	308-333	high mobility group box 1	Homo sapiens	33-38
29922279-0	2018	Staphylococcus aureus Phenol-Soluble Modulins alpha1-alpha3 Act as Novel Toll-Like Receptor (TLR) 4 Antagonists to Inhibit HMGB1/TLR4/NF-kappaB Signaling Pathway.	Phenol	22-28	high mobility group box 1	Homo sapiens	123-128
29853785-6	2018	The plasma high-mobility group box 1 level decreased significantly from 51.7 (58.1) to 33.9 (45.0) ng.ml-1 (p &lt; 0.05) in the dexmedetomidine group, which was not observed in the saline group.	Dexmedetomidine	128-143	high mobility group box 1	Homo sapiens	11-36
29850505-7	2018	The matrix metalloproteinase-2 (MMP-2) expression and activity were upregulated after treatment with HMGB1, while the upregulated expression of MMP-2 stimulated by HMGB1 in lung cancer cells was significantly reduced with the blockage of si-p65.	Silicon	45-47	high mobility group box 1	Homo sapiens	101-106
29850505-7	2018	The matrix metalloproteinase-2 (MMP-2) expression and activity were upregulated after treatment with HMGB1, while the upregulated expression of MMP-2 stimulated by HMGB1 in lung cancer cells was significantly reduced with the blockage of si-p65.	Silicon	45-47	high mobility group box 1	Homo sapiens	164-169
29330155-0	2018	Amlexanox Inhibits Cerebral Ischemia-Induced Delayed Astrocytic High-Mobility Group Box 1 Release and Subsequent Brain Damage.	amlexanox	0-9	high mobility group box 1	Homo sapiens	64-89
29436639-6	2018	GL suppressed HMGB1-induced monocyte migration and increased HMGB1-inhibited monocyte apoptosis.	Glycyrrhizic Acid	0-2	high mobility group box 1	Homo sapiens	61-66
29393419-0	2018	HMGB1 mediates microglia activation via the TLR4/NF-kappaB pathway in coriaria lactone induced epilepsy.	coriaria lactone	70-86	high mobility group box 1	Homo sapiens	0-5
29393419-8	2018	The potential toxic effect of HMGB1 on HM cells was evaluated by MTT and 5-ethynyl-2-deoxyuridine assays.	monooxyethylene trimethylolpropane tristearate	65-68	high mobility group box 1	Homo sapiens	30-35
29393419-8	2018	The potential toxic effect of HMGB1 on HM cells was evaluated by MTT and 5-ethynyl-2-deoxyuridine assays.	5-ethynyl-2'-deoxyuridine	73-97	high mobility group box 1	Homo sapiens	30-35
29436639-0	2018	Glycyrrhizin affects monocyte migration and apoptosis by blocking HMGB1 signaling.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	66-71
29436639-3	2018	Glycyrrhizin (GL), an effective component of licorice, weakens the proinflammatory effect of HMGB1.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	93-98
29436639-3	2018	Glycyrrhizin (GL), an effective component of licorice, weakens the proinflammatory effect of HMGB1.	Glycyrrhizic Acid	14-16	high mobility group box 1	Homo sapiens	93-98
29436639-4	2018	The present study investigated the effect of GL on the migration and apoptosis of monocytes associated with HMGB1 signaling.	Glycyrrhizic Acid	45-47	high mobility group box 1	Homo sapiens	108-113
29436639-6	2018	GL suppressed HMGB1-induced monocyte migration and increased HMGB1-inhibited monocyte apoptosis.	Glycyrrhizic Acid	0-2	high mobility group box 1	Homo sapiens	14-19
29330155-4	2018	HMGB1 depletion from neuronal nuclei was observed within 3 hours after transient middle cerebral artery occlusion (tMCAO), whereas the intracerebroventricular (i.c.v.)	tmcao	115-120	high mobility group box 1	Homo sapiens	0-5
29330155-5	2018	pretreatment with amlexanox blocked HMGB1 release from neurons, resulting in HMGB1 redistribution in the nuclei and cytoplasm.	amlexanox	18-27	high mobility group box 1	Homo sapiens	36-41
29330155-5	2018	pretreatment with amlexanox blocked HMGB1 release from neurons, resulting in HMGB1 redistribution in the nuclei and cytoplasm.	amlexanox	18-27	high mobility group box 1	Homo sapiens	77-82
29330155-6	2018	HMGB1 was selectively released from astrocytes 27 hours after tMCAO and this HMGB1 release was blocked by late treatment with amlexanox (i.c.v.)	tmcao	62-67	high mobility group box 1	Homo sapiens	0-5
29330155-6	2018	HMGB1 was selectively released from astrocytes 27 hours after tMCAO and this HMGB1 release was blocked by late treatment with amlexanox (i.c.v.)	amlexanox	126-135	high mobility group box 1	Homo sapiens	0-5
29330155-6	2018	HMGB1 was selectively released from astrocytes 27 hours after tMCAO and this HMGB1 release was blocked by late treatment with amlexanox (i.c.v.)	amlexanox	126-135	high mobility group box 1	Homo sapiens	77-82
29330155-8	2018	Proximity extension assay revealed that the HMGB1 level was elevated in the CSF at 3 and 27 hours after tMCAO.	tmcao	104-109	high mobility group box 1	Homo sapiens	44-49
29330155-11	2018	with anti-HMGB1 antibody 24 hours after tMCAO also ameliorated ischemic brain damage 48 hours after tMCAO.	tmcao	40-45	high mobility group box 1	Homo sapiens	10-15
29330155-11	2018	with anti-HMGB1 antibody 24 hours after tMCAO also ameliorated ischemic brain damage 48 hours after tMCAO.	tmcao	100-105	high mobility group box 1	Homo sapiens	10-15
29330155-12	2018	Thus, the inhibition of brain damage by late treatment with amlexanox or anti-HMGB1 antibody indicates that late HMGB1 release plays a role in the maintenance of stroke-induced brain damage, and the inhibition of this release would be a novel therapeutic target for protection of ischemic brain damage.	amlexanox	60-69	high mobility group box 1	Homo sapiens	113-118
29541234-3	2018	Papaverine significantly inhibited RAGE-dependent nuclear factor kappa-B activation driven by high mobility group box-1, a RAGE ligand.	Papaverine	0-10	high mobility group box 1	Homo sapiens	94-119
29673663-9	2018	(3) HMGB1 and RAGE immunoreactivity in pPROM placenta TMA were increased in the cytoplasm of syncytiotrophoblast (STB), extravillous trophoblast (EVT) and mesenchymal cells, while NF-kappaBp65 was enhanced in the nucleus of STB and EVT.	EVT	146-149	high mobility group box 1	Homo sapiens	4-9
29673663-9	2018	(3) HMGB1 and RAGE immunoreactivity in pPROM placenta TMA were increased in the cytoplasm of syncytiotrophoblast (STB), extravillous trophoblast (EVT) and mesenchymal cells, while NF-kappaBp65 was enhanced in the nucleus of STB and EVT.	EVT	232-235	high mobility group box 1	Homo sapiens	4-9
29665925-5	2018	Meanwhile, the protein expression levels of HMGB1 in peripheral blood serum and mononuclear cells(PBMNC) of 25 patients with chronic and refractory ITP were detected by ELISA and Western blot.	Inosine Triphosphate	148-151	high mobility group box 1	Homo sapiens	44-49
29665925-10	2018	The HMGB1 expression positive rate in spleen of ITP patients was significantly higher than that in control group (85.0% vs 15.0%)(P&lt;0.001).	Inosine Triphosphate	48-51	high mobility group box 1	Homo sapiens	4-9
29665925-13	2018	CONCLUSION: The splenectomy has been found to be effective therapeutic method for patients with ITP, the HMGB1 highly express in the spleen of the patients with chronic refractory ITP, but negatively correlats with the therapeutic outcome after splenectomy.	Inosine Triphosphate	96-99	high mobility group box 1	Homo sapiens	105-110
29540727-7	2018	In addition, 1 ng/ml HMGB1 increased the percentage of filopodia formation using phalloidin staining.	Phalloidine	81-91	high mobility group box 1	Homo sapiens	21-26
29599781-13	2018	Finally, we detected several subunits of the proteasome (PSMB9, PSMB10) as well as the danger signal HMGB1 exclusively within apoptotic cell-released LEVs.	levs	150-154	high mobility group box 1	Homo sapiens	101-106
29588304-7	2018	Nevertheless, according to fluorescence-activated cell sorter analysis, VLD rivaroxaban treatment resulted in a significantly reduced expression of platelet HMGB-1, whereas P-selectin exposure was not affected.	Rivaroxaban	76-87	high mobility group box 1	Homo sapiens	157-163
29535197-14	2018	Towards development of a new therapeutic modality, we show herein that blocking serum HMGB1 levels by Eritoran improves lung pathology in influenza B virus-infected cotton rats.	eritoran	102-110	high mobility group box 1	Homo sapiens	86-91
29361549-3	2018	In this study, we studied the effect of inflachromene (ICM), a novel HMGB1 secretion inhibitor, on autophagy.	inflachromene	40-53	high mobility group box 1	Homo sapiens	69-74
29316268-9	2018	Pharmacological inhibition of HMGB1 Cyt translocation with ethyl pyruvate prevented HBx-induced autophagy.	ethyl pyruvate	59-73	high mobility group box 1	Homo sapiens	30-35
29197622-4	2018	Mechanistic study showed that dioscin significantly up-regulated the expression levels of Sirt3, SOD2, and then suppressed inflammation by decreasing the expression levels of NF-kB, HMGB1, c-Jun, c-Fos, COX2, TNF-alpha, IL-1beta and IL-6.	dioscin	30-37	high mobility group box 1	Homo sapiens	182-187
29536989-0	2018	Corrigendum: 1,25-Dihydroxyvitamin D Inhibits LPS-Induced High-Mobility Group Box 1 (HMGB1) Secretion via Targeting the NF-E2-Related Factor 2-Hemeoxygenase-1-HMGB1 Pathway in Macrophages.	1,25-dihydroxyvitamin D	13-36	high mobility group box 1	Homo sapiens	58-83
29536989-0	2018	Corrigendum: 1,25-Dihydroxyvitamin D Inhibits LPS-Induced High-Mobility Group Box 1 (HMGB1) Secretion via Targeting the NF-E2-Related Factor 2-Hemeoxygenase-1-HMGB1 Pathway in Macrophages.	1,25-dihydroxyvitamin D	13-36	high mobility group box 1	Homo sapiens	85-90
29536989-0	2018	Corrigendum: 1,25-Dihydroxyvitamin D Inhibits LPS-Induced High-Mobility Group Box 1 (HMGB1) Secretion via Targeting the NF-E2-Related Factor 2-Hemeoxygenase-1-HMGB1 Pathway in Macrophages.	1,25-dihydroxyvitamin D	13-36	high mobility group box 1	Homo sapiens	159-164
29447008-7	2018	Expert opinion: Blocking excessive amounts of extracellular HMGB1, particularly the disulfide isoform, offers an attractive clinical opportunity to ameliorate systemic inflammatory diseases.	Disulfides	84-93	high mobility group box 1	Homo sapiens	60-65
29328447-2	2018	Western blot analysis revealed that vincristine (VCR), etoposide (ETO) and carboplatin (CBP) significantly increased the expression of HMGB1 in Weri-Rb-1 and Y79 cells compared with the untreated control (P&lt;0.01).	Vincristine	36-47	high mobility group box 1	Homo sapiens	135-140
29328447-2	2018	Western blot analysis revealed that vincristine (VCR), etoposide (ETO) and carboplatin (CBP) significantly increased the expression of HMGB1 in Weri-Rb-1 and Y79 cells compared with the untreated control (P&lt;0.01).	Etoposide	55-64	high mobility group box 1	Homo sapiens	135-140
29328447-2	2018	Western blot analysis revealed that vincristine (VCR), etoposide (ETO) and carboplatin (CBP) significantly increased the expression of HMGB1 in Weri-Rb-1 and Y79 cells compared with the untreated control (P&lt;0.01).	Etoposide	66-69	high mobility group box 1	Homo sapiens	135-140
29328447-2	2018	Western blot analysis revealed that vincristine (VCR), etoposide (ETO) and carboplatin (CBP) significantly increased the expression of HMGB1 in Weri-Rb-1 and Y79 cells compared with the untreated control (P&lt;0.01).	Carboplatin	75-86	high mobility group box 1	Homo sapiens	135-140
29197515-6	2018	In addition, Fingolimod treatment reduced serum levels of HMGB1 by 71.6% (P = 0.02) and pentosidine serum levels by 41.3% (P = 0.12).	Fingolimod Hydrochloride	13-23	high mobility group box 1	Homo sapiens	58-63
29448108-3	2018	In this study, glycyrrhizin (GL), an inhibitor of HMGB1, was used to investigate whether the inhibition of HMGB1 could modulate microglia/macrophage polarization after TBI.	Glycyrrhizic Acid	15-27	high mobility group box 1	Homo sapiens	50-55
29448108-3	2018	In this study, glycyrrhizin (GL), an inhibitor of HMGB1, was used to investigate whether the inhibition of HMGB1 could modulate microglia/macrophage polarization after TBI.	Glycyrrhizic Acid	15-27	high mobility group box 1	Homo sapiens	107-112
29448108-3	2018	In this study, glycyrrhizin (GL), an inhibitor of HMGB1, was used to investigate whether the inhibition of HMGB1 could modulate microglia/macrophage polarization after TBI.	Glycyrrhizic Acid	29-31	high mobility group box 1	Homo sapiens	50-55
29448108-4	2018	The results showed that treatment with GL improved the neurological function recovery, reduced the lesion volume, and inhibited the release and expression of HMGB1 after TBI.	Glycyrrhizic Acid	39-41	high mobility group box 1	Homo sapiens	158-163
29448108-6	2018	In conclusion, the results suggested that GL attenuated TBI by inhibiting M1 phenotype while inducing M2 phenotype activation of microglia/macrophages, at least partly through inhibiting HMGB1.	Glycyrrhizic Acid	42-44	high mobility group box 1	Homo sapiens	187-192
28816009-4	2018	After atazanavir sulphate treatment, in A549 cells and HPMECs, the expression of vimentin, HMGB1, Toll-like receptor 4 (TLR-4) and p-NF-kappaB decreased, while the expression of E-cadherin and VE-cadherin increased.	Atazanavir Sulfate	6-25	high mobility group box 1	Homo sapiens	91-96
29447234-0	2018	Folic acid derived-P5779 mimetics regulate DAMP-mediated inflammation through disruption of HMGB1:TLR4:MD-2 axes.	Folic Acid	0-10	high mobility group box 1	Homo sapiens	92-97
28816009-6	2018	Proliferation of HLF-1 was reduced after atazanavir treatment, meanwhile the expression of hypoxia-inducible factor-1alpha (HIF-1alpha), prolyl hydroxylase domain protein 2 (PHD-2), HMGB1, TLR-9, p-NF-kappaB, collagen I and collagen III was decreased.	Atazanavir Sulfate	41-51	high mobility group box 1	Homo sapiens	182-187
28816009-8	2018	In summary, our study supports the proposal that atazanavir sulphate may have a therapeutic potential in reducing the progression of pulmonary fibrosis by suppressing HMGB1/TLR signalling.	Atazanavir Sulfate	49-68	high mobility group box 1	Homo sapiens	167-172
28033959-0	2018	Assessment of binding properties of Actinomycin-D to 21nt DNA segment of hmgb1 gene promoter using spectroscopic and calorimetric techniques.	Dactinomycin	36-49	high mobility group box 1	Homo sapiens	73-78
29366441-7	2018	Furthermore, hypoxia-induced inflammation by HMGB1 translocation into the cytoplasm results in the release of IL-8 through a ROS-dependent mechanism in upper airway epithelium.	ros	125-128	high mobility group box 1	Homo sapiens	45-50
29191973-9	2018	The combined inhibition of IL6R and HMGB1 may serve as a new treatment for enzalutamide resistance in patients with advanced or metastatic prostate cancer.	enzalutamide	75-87	high mobility group box 1	Homo sapiens	36-41
29083089-7	2018	Furthermore, both U0126 (ErK inhibitor) and SP600125 (JNK inhibitor) significantly suppressed the enhanced production of HIF-1alpha and VEGF induced by HMGB1.	pyrazolanthrone	44-52	high mobility group box 1	Homo sapiens	152-157
29083089-7	2018	Furthermore, both U0126 (ErK inhibitor) and SP600125 (JNK inhibitor) significantly suppressed the enhanced production of HIF-1alpha and VEGF induced by HMGB1.	U 0126	18-23	high mobility group box 1	Homo sapiens	152-157
29375570-0	2017	From Human Megakaryocytes to Platelets: Effects of Aspirin on High-Mobility Group Box 1/Receptor for Advanced Glycation End Products Axis.	Aspirin	51-58	high mobility group box 1	Homo sapiens	62-87
29241031-0	2018	The protective effect of dexmedetomidine on LPS-induced acute lung injury through the HMGB1-mediated TLR4/NF-kappaB and PI3K/Akt/mTOR pathways.	Dexmedetomidine	25-40	high mobility group box 1	Homo sapiens	86-91
29241031-9	2018	Additionally, treatment with DEX inhibited the expression of HMGB1, TLR4, MyD88, p-IkappaB, p-NF-kappaB, p-PI3K, p-Akt and p-mTOR in vivo and in vitro.	Dexmedetomidine	29-32	high mobility group box 1	Homo sapiens	61-66
29241031-11	2018	Treatment with glycyrrhizin, an inhibitor of HMGB1, confirmed that HMGB1 was involved in the mechanism of DEX on LPS-induced ALI.	Glycyrrhizic Acid	15-27	high mobility group box 1	Homo sapiens	45-50
29241031-11	2018	Treatment with glycyrrhizin, an inhibitor of HMGB1, confirmed that HMGB1 was involved in the mechanism of DEX on LPS-induced ALI.	Glycyrrhizic Acid	15-27	high mobility group box 1	Homo sapiens	67-72
29241031-11	2018	Treatment with glycyrrhizin, an inhibitor of HMGB1, confirmed that HMGB1 was involved in the mechanism of DEX on LPS-induced ALI.	Dexmedetomidine	106-109	high mobility group box 1	Homo sapiens	45-50
29241031-11	2018	Treatment with glycyrrhizin, an inhibitor of HMGB1, confirmed that HMGB1 was involved in the mechanism of DEX on LPS-induced ALI.	Dexmedetomidine	106-109	high mobility group box 1	Homo sapiens	67-72
29386662-6	2018	DHA-treated breast cancer cells triggered increased caspase-1and gasdermin D activation, enhanced IL-1beta secretion, translocated HMGB1 towards the cytoplasm, and membrane pore formation when compared to untreated cells, suggesting DHA induces pyroptosis programmed cell death in breast cancer cells.	Docosahexaenoic Acids	0-3	high mobility group box 1	Homo sapiens	131-136
30154286-1	2018	OBJECTIVE: To determine mechanisms for the role of high mobility group box-1 (HMGB1) to platinum based chemo-sensitivity in cervical cancer.	Platinum	88-96	high mobility group box 1	Homo sapiens	51-76
30154286-1	2018	OBJECTIVE: To determine mechanisms for the role of high mobility group box-1 (HMGB1) to platinum based chemo-sensitivity in cervical cancer.	Platinum	88-96	high mobility group box 1	Homo sapiens	78-83
29568761-0	2018	Glycyrrhizin Suppresses the Growth of Human NSCLC Cell Line HCC827 by Downregulating HMGB1 Level.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	85-90
29568761-4	2018	And high level of HMGB1 promoted the migration and invasion of lung cancer cells, which was suppressed by glycyrrhizin.	Glycyrrhizic Acid	106-118	high mobility group box 1	Homo sapiens	18-23
29568761-5	2018	Moreover, glycyrrhizin reduced the activity of JAK/STAT signaling pathway, which is the upstream regulator of HMGB1.	Glycyrrhizic Acid	10-22	high mobility group box 1	Homo sapiens	110-115
29375570-4	2017	Aspirin "in vivo" and "in vitro" not only reduces HMGB1 and receptor for advanced glycation end products expression on MKs and PLTs but also drives the movement of HMGB1 from MKs into PLTs and PLT-derived MV.	Aspirin	0-7	high mobility group box 1	Homo sapiens	50-55
29375570-4	2017	Aspirin "in vivo" and "in vitro" not only reduces HMGB1 and receptor for advanced glycation end products expression on MKs and PLTs but also drives the movement of HMGB1 from MKs into PLTs and PLT-derived MV.	Aspirin	0-7	high mobility group box 1	Homo sapiens	164-169
29203538-3	2018	We previously showed that HMGB1 with reduced cysteines is a chemoattractant, whereas a disulfide bond makes it a proinflammatory cytokine.	Cysteine	45-54	high mobility group box 1	Homo sapiens	26-31
29317708-5	2018	By screening a panel of Cx43 mimetic peptides, we discovered that one cysteine-containing peptide, P5 (ENVCYD), effectively attenuated hemichannel activities, and significantly suppressed endotoxin-induced release of ATP and HMGB1 in vitro.	Cysteine	70-78	high mobility group box 1	Homo sapiens	225-230
29203538-4	2018	Here we report that fully reduced HMGB1 orchestrates muscle and liver regeneration via CXCR4, whereas disulfide HMGB1 and its receptors TLR4/MD-2 and RAGE (receptor for advanced glycation end products) are not involved.	Disulfides	102-111	high mobility group box 1	Homo sapiens	112-117
29203538-6	2018	The nonoxidizable HMGB1 mutant 3S, in which serines replace cysteines, promotes muscle and liver regeneration more efficiently than the wild-type protein and without exacerbating inflammation by selectively interacting with CXCR4.	Serine	44-51	high mobility group box 1	Homo sapiens	18-23
29203538-6	2018	The nonoxidizable HMGB1 mutant 3S, in which serines replace cysteines, promotes muscle and liver regeneration more efficiently than the wild-type protein and without exacerbating inflammation by selectively interacting with CXCR4.	Cysteine	60-69	high mobility group box 1	Homo sapiens	18-23
30198432-0	2018	miR-142-3p Inhibits the Metastasis of Hepatocellular Carcinoma Cells by Regulating HMGB1 Gene Expression.	mir-142-3p	0-10	high mobility group box 1	Homo sapiens	83-88
30205729-0	2018	HMGB1 represses the anti-cancer activity of sunitinib by governing TP53 autophagic degradation via its nucleus-to-cytoplasm transport.	Sunitinib	44-53	high mobility group box 1	Homo sapiens	0-5
30205729-7	2018	The inhibition of HMGB1 sensitized cancer cells to sunitinib.	Sunitinib	51-60	high mobility group box 1	Homo sapiens	18-23
30205729-9	2018	In conclusion, our data identify an alternative HMGB1-mediated TP53 protein turnover mechanism that participates in the resistance of sunitinib and suggest HMGB1 as a potential therapeutic target for improving clinical outcomes of sunitinib.	Sunitinib	134-143	high mobility group box 1	Homo sapiens	48-53
30205729-9	2018	In conclusion, our data identify an alternative HMGB1-mediated TP53 protein turnover mechanism that participates in the resistance of sunitinib and suggest HMGB1 as a potential therapeutic target for improving clinical outcomes of sunitinib.	Sunitinib	231-240	high mobility group box 1	Homo sapiens	48-53
30205729-9	2018	In conclusion, our data identify an alternative HMGB1-mediated TP53 protein turnover mechanism that participates in the resistance of sunitinib and suggest HMGB1 as a potential therapeutic target for improving clinical outcomes of sunitinib.	Sunitinib	231-240	high mobility group box 1	Homo sapiens	156-161
29719300-0	2018	Unfractionated Heparin Alleviates Human Lung Endothelial Barrier Dysfunction Induced by High Mobility Group Box 1 Through Regulation of P38-GSK3beta-Snail Signaling Pathway.	Heparin	15-22	high mobility group box 1	Homo sapiens	88-113
29719300-12	2018	Moreover, HMGB1 activated p38/GSK3beta/Snail signaling pathway and treatment with p38 inhibitor SB203580 abolished its biological effects.	SB 203580	96-104	high mobility group box 1	Homo sapiens	10-15
29719300-13	2018	In addition, we found that UFH was able to reverse the effect of HMGB1 on EndoMT and endothelial permeability through inhibition of p38 signaling in a dose-dependent manner.	Heparin	27-30	high mobility group box 1	Homo sapiens	65-70
29244233-5	2018	RESULTS: DAB caused neuronal pannexin-1 large pore opening and activation of the downstream inflammatory pathway as shown by procaspase-1 cleavage and HMGB1 release from neurons.	1,4-dideoxy-1,4-iminoarabinitol	9-12	high mobility group box 1	Homo sapiens	151-156
30497069-6	2018	HMGB1 activated p38 mitogen-activated protein kinase (p38 MAPK) and ADAM17, while HMGB1-induced ADAM17 activation was inhibited by SB203580, a p38 MAPK inhibitor.	SB 203580	131-139	high mobility group box 1	Homo sapiens	82-87
30497069-7	2018	HMGB1-induced ectodomain shedding of RAGE and TLR4 was prevented by siRNA depletion of ADAM17 as well as TAPI-2, an inhibitor of ADAM family, and SB203580.	TAPI-2	105-111	high mobility group box 1	Homo sapiens	0-5
30497069-7	2018	HMGB1-induced ectodomain shedding of RAGE and TLR4 was prevented by siRNA depletion of ADAM17 as well as TAPI-2, an inhibitor of ADAM family, and SB203580.	SB 203580	146-154	high mobility group box 1	Homo sapiens	0-5
29138861-3	2018	In the present study, the expression of HMGB1 and calreticulin was evaluated by immunohistochemistry in pre-treatment biopsy specimens and surgically resected specimens, which were obtained from patients with breast cancer (n=52) and esophageal squamous cell carcinoma (ESCC) (n=8) who had been treated with neoadjuvant chemotherapy (NAC).	nac	334-337	high mobility group box 1	Homo sapiens	40-45
28555325-0	2018	Erratum to: Serum HMGB1 concentrations at 4 weeks is a useful predictor of extreme poor prognosis for advanced hepatocellular carcinoma treated with sorafenib and hepatic arterial infusion chemotherapy.	Sorafenib	149-158	high mobility group box 1	Homo sapiens	18-23
28474222-0	2018	Serum HMGB1 concentrations at 4 weeks is a useful predictor of extreme poor prognosis for advanced hepatocellular carcinoma treated with sorafenib and hepatic arterial infusion chemotherapy.	Sorafenib	137-146	high mobility group box 1	Homo sapiens	6-11
28474222-4	2018	METHODS: Serum HMGB1 concentrations were measured in 71 and 72 patients with advanced HCC treated with sorafenib and HAIC, respectively, to assess their usefulness for prediction of the response to the treatment and prognosis.	Sorafenib	103-112	high mobility group box 1	Homo sapiens	15-20
28474222-8	2018	CONCLUSIONS: These results suggest that serum HMGB1 at 4 weeks after the start of treatment might be a useful biomarker with added value to the conventional tumor marker and radiologic responses to predict poor overall survival in patients with advanced HCC treated with sorafenib or HAIC.	Sorafenib	271-280	high mobility group box 1	Homo sapiens	46-51
29138861-5	2018	As a result, both HMGB1 and calreticulin expression levels were significantly upregulated after NAC in both breast cancer and ESCC tissues.	nac	96-99	high mobility group box 1	Homo sapiens	18-23
29283384-4	2017	Treatment of the HMGB1 inhibitor glycyrrhizic acid (GA) showed an opposing effect on both activities.	Glycyrrhizic Acid	33-50	high mobility group box 1	Homo sapiens	17-22
28986506-4	2018	Furthermore, methylation of arginines in the RGG domain abolishes the protein-protein interaction and the inhibitory effect of Sbp1 on translation initiation of Pab1 mRNA.	Arginine	28-37	high mobility group box 1	Homo sapiens	127-131
32476912-8	2018	HMGB1 level varied in different diagnoses: the highest level was detected in QuantiFERON TB-positive subjects (median: 30.2) and hypersensitivity pneumonitis (median: 33.2), followed by pulmonary sarcoidosis (median: 16.8) and idiopathic pulmonary fibrosis (median: 8.8).	quantiferon tb	77-91	high mobility group box 1	Homo sapiens	0-5
29283384-4	2017	Treatment of the HMGB1 inhibitor glycyrrhizic acid (GA) showed an opposing effect on both activities.	Glycyrrhizic Acid	52-54	high mobility group box 1	Homo sapiens	17-22
29258482-4	2017	Thus, this study aimed to investigate the dose- and time-dependent effects of herbal medicines to protect against AKI in cisplatin-induced human kidney 2 (HK-2) cells by assessing the activities of high-mobility group box protein 1 (HMGB1), neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1).	Cisplatin	121-130	high mobility group box 1	Homo sapiens	233-238
29246127-0	2017	High mobility group box 1 promotes sorafenib resistance in HepG2 cells and in vivo.	Sorafenib	35-44	high mobility group box 1	Homo sapiens	0-25
29246127-7	2017	This study investigated the association between HMGB1 and sorafenib resistance in HCC.	Sorafenib	58-67	high mobility group box 1	Homo sapiens	48-53
29246127-10	2017	The subcellular localization of HMGB1 in HepG2 cells following sorafenib treatment was measured by western blotting and confocal microscopy.	Sorafenib	63-72	high mobility group box 1	Homo sapiens	32-37
29246127-12	2017	RESULTS: The HMGB1 knockdown cells exhibited a significantly higher apoptotic level and lower cell viability than the normal HMGB1 expressing cells following the sorafenib treatment.	Sorafenib	162-171	high mobility group box 1	Homo sapiens	13-18
29246127-12	2017	RESULTS: The HMGB1 knockdown cells exhibited a significantly higher apoptotic level and lower cell viability than the normal HMGB1 expressing cells following the sorafenib treatment.	Sorafenib	162-171	high mobility group box 1	Homo sapiens	125-130
29246127-13	2017	In addition, the cell viability observed in the HMGB1 overexpressing cells was higher than that observed in the control cells following the sorafenib intervention.	Sorafenib	140-149	high mobility group box 1	Homo sapiens	48-53
29246127-14	2017	Sorafenib had a better tumour inhibition effect in the HMGB1 knockdown group in vivo.	Sorafenib	0-9	high mobility group box 1	Homo sapiens	55-60
29246127-15	2017	The amount of mitochondrial HMGB1 decreased, while the amount of cytosolic HMGB1 increased following the exposure to sorafenib.	Sorafenib	117-126	high mobility group box 1	Homo sapiens	28-33
29246127-15	2017	The amount of mitochondrial HMGB1 decreased, while the amount of cytosolic HMGB1 increased following the exposure to sorafenib.	Sorafenib	117-126	high mobility group box 1	Homo sapiens	75-80
29246127-16	2017	Altogether, HMGB1 translocated from the mitochondria to the cytoplasm outside the mitochondria following the exposure of HepG2 cells to sorafenib.	Sorafenib	136-145	high mobility group box 1	Homo sapiens	12-17
29246127-17	2017	CONCLUSIONS: A novel potential role of HMGB1 in the regulation of sorafenib therapy resistance in HCC was observed.	Sorafenib	66-75	high mobility group box 1	Homo sapiens	39-44
29246127-18	2017	The knockdown of HMGB1 restores sensitivity to sorafenib and enhances HepG2 cell death, while HMGB1 overexpression blunts these effects.	Sorafenib	47-56	high mobility group box 1	Homo sapiens	17-22
29246127-19	2017	The translocation of HMGB1 from the mitochondria to the cytosol following sorafenib treatment provides new insight into sorafenib resistance in HCC.	Sorafenib	74-83	high mobility group box 1	Homo sapiens	21-26
29246127-19	2017	The translocation of HMGB1 from the mitochondria to the cytosol following sorafenib treatment provides new insight into sorafenib resistance in HCC.	Sorafenib	120-129	high mobility group box 1	Homo sapiens	21-26
29259392-7	2017	Significant positive correlations were observed between the levels of HMGB1 and the levels of 8-OHdG (r = 0.422; p = 0.001) and sVAP-1 (r = 0.354; p = 0.004) and between the levels of 8-OHdG and the levels of sVAP-1 (r = 0.598; p&lt;0.0001).	8-ohdg	94-100	high mobility group box 1	Homo sapiens	70-75
29259392-7	2017	Significant positive correlations were observed between the levels of HMGB1 and the levels of 8-OHdG (r = 0.422; p = 0.001) and sVAP-1 (r = 0.354; p = 0.004) and between the levels of 8-OHdG and the levels of sVAP-1 (r = 0.598; p&lt;0.0001).	8-ohdg	184-190	high mobility group box 1	Homo sapiens	70-75
29259392-13	2017	Treatment of HRMECs with HMGB1 increased leukocyte adhesion and induced the upregulation of 8-OHdG and HO-1 and the membranous translocation of VAP-1.	8-ohdg	92-98	high mobility group box 1	Homo sapiens	25-30
28970183-3	2017	A chemical hypoxia mimetic agent, cobalt chloride, induced SIRT1 downregulation, HMGB1 nucleocytoplasmic relocation and extracellular release from ARPE-19 cells, implicating its autocrine function.	cobaltous chloride	34-49	high mobility group box 1	Homo sapiens	81-86
28970183-4	2017	Resveratrol treatment significantly reduced secretion of HMGB1 from ARPE-19 cells exposed to hypoxia.	Resveratrol	0-11	high mobility group box 1	Homo sapiens	57-62
29285170-7	2017	The results of western blot analysis indicated that the expression levels of HMGB1, TGF-beta1 and NF-kappaB were significantly higher in the CAN group, compared with the normal group (P&lt;0.05), and the expression levels increased with the progression of CAN grade.	can	141-144	high mobility group box 1	Homo sapiens	77-82
29285170-11	2017	HMGB1, TGF-beta1 and NF-kappaB may form a signaling pathway that leads to the occurrence of CAN, which induces renal interstitial fibrosis.	can	92-95	high mobility group box 1	Homo sapiens	0-5
29113279-6	2017	Meanwhile, administration of gemcitabine to HIPC cells increased the expression of high mobility group box1 (HMGB1).	gemcitabine	29-40	high mobility group box 1	Homo sapiens	109-114
29181774-6	2017	Two of the most commonly used ABAs in pharmaceutical vaccine formulations, aluminium oxyhydroxide and aluminium hydroxyphosphate, induced a vigorous extracellular expression of the two DAMP molecules calreticulin and HMGB1.	abas	30-34	high mobility group box 1	Homo sapiens	217-222
29181774-6	2017	Two of the most commonly used ABAs in pharmaceutical vaccine formulations, aluminium oxyhydroxide and aluminium hydroxyphosphate, induced a vigorous extracellular expression of the two DAMP molecules calreticulin and HMGB1.	aluminium oxyhydroxide	75-97	high mobility group box 1	Homo sapiens	217-222
29181774-6	2017	Two of the most commonly used ABAs in pharmaceutical vaccine formulations, aluminium oxyhydroxide and aluminium hydroxyphosphate, induced a vigorous extracellular expression of the two DAMP molecules calreticulin and HMGB1.	aluminium hydroxyphosphate	102-128	high mobility group box 1	Homo sapiens	217-222
29149067-0	2017	The HMGB1/RAGE Pro-Inflammatory Axis in the Human Placenta: Modulating Effect of Low Molecular Weight Heparin.	Heparin	102-109	high mobility group box 1	Homo sapiens	4-9
29149067-2	2017	Moreover, we investigated, in physiological placental tissue, the ability of Low Molecular Weight Heparin (LMWH) to modify HMGB1 structural conformation thus inhibiting RAGE binding and HMGB1/RAGE axis inflammatory activity.	Heparin	98-105	high mobility group box 1	Homo sapiens	123-128
29149067-2	2017	Moreover, we investigated, in physiological placental tissue, the ability of Low Molecular Weight Heparin (LMWH) to modify HMGB1 structural conformation thus inhibiting RAGE binding and HMGB1/RAGE axis inflammatory activity.	Heparin	98-105	high mobility group box 1	Homo sapiens	186-191
29149067-2	2017	Moreover, we investigated, in physiological placental tissue, the ability of Low Molecular Weight Heparin (LMWH) to modify HMGB1 structural conformation thus inhibiting RAGE binding and HMGB1/RAGE axis inflammatory activity.	Heparin, Low-Molecular-Weight	107-111	high mobility group box 1	Homo sapiens	123-128
29149067-2	2017	Moreover, we investigated, in physiological placental tissue, the ability of Low Molecular Weight Heparin (LMWH) to modify HMGB1 structural conformation thus inhibiting RAGE binding and HMGB1/RAGE axis inflammatory activity.	Heparin, Low-Molecular-Weight	107-111	high mobility group box 1	Homo sapiens	186-191
29149067-5	2017	Physiological term placental explants were treated by 0.5 U LMWH for 24 or 48 h. HMGB1 and RAGE expression and association were evaluated in LMWH explants by RAGE immunoprecipitation followed by HMGB1 immunoblot.	Heparin, Low-Molecular-Weight	141-145	high mobility group box 1	Homo sapiens	81-86
29149067-8	2017	24 h LMWH treatment significantly up-regulated HMGB1 expression but inhibited HMGB1/RAGE complex formation in physiological explants.	Heparin, Low-Molecular-Weight	5-9	high mobility group box 1	Homo sapiens	47-52
29149067-8	2017	24 h LMWH treatment significantly up-regulated HMGB1 expression but inhibited HMGB1/RAGE complex formation in physiological explants.	Heparin, Low-Molecular-Weight	5-9	high mobility group box 1	Homo sapiens	78-83
29149067-11	2017	Our data depicted a new molecular mechanism through which LMWH exerts its anti-inflammatory effect on PE placentae, underlying the importance of HMGB1/RAGE axis in PE inflammatory response.	Heparin, Low-Molecular-Weight	58-62	high mobility group box 1	Homo sapiens	145-150
29296182-0	2017	MicroRNA-410-3p attenuates gemcitabine resistance in pancreatic ductal adenocarcinoma by inhibiting HMGB1-mediated autophagy.	gemcitabine	27-38	high mobility group box 1	Homo sapiens	100-105
29296182-6	2017	We also found that miR-410-3p attenuated the gemcitabine resistance of PDAC by targeting the 3"-UTR of HMGB1.	gemcitabine	45-56	high mobility group box 1	Homo sapiens	103-108
29296182-6	2017	We also found that miR-410-3p attenuated the gemcitabine resistance of PDAC by targeting the 3"-UTR of HMGB1.	pdac	71-75	high mobility group box 1	Homo sapiens	103-108
29296182-7	2017	Moreover, our study clearly demonstrated that miR-410-3p enhanced chemosensitivity to gemcitabine via inhibiting HMGB1-induced autophagy during chemotherapy in PDAC cells.	gemcitabine	86-97	high mobility group box 1	Homo sapiens	113-118
29201182-0	2017	The efficacy of gastrodin in combination with folate and vitamin B12 on patients with epilepsy after stroke and its effect on HMGB-1, IL-2 and IL-6 serum levels.	gastrodin	16-25	high mobility group box 1	Homo sapiens	126-132
29201182-1	2017	This study evaluated the efficacy of gastrodin in combination with folate (FOL) and vitamin-B12 (V-B12) on patients with epilepsy after stroke (EAS) and its effect on high-mobility group protein B1 (HMGB-1), interleukin-1 (IL-1), and IL-6 serum levels.	gastrodin	37-46	high mobility group box 1	Homo sapiens	167-197
29201182-1	2017	This study evaluated the efficacy of gastrodin in combination with folate (FOL) and vitamin-B12 (V-B12) on patients with epilepsy after stroke (EAS) and its effect on high-mobility group protein B1 (HMGB-1), interleukin-1 (IL-1), and IL-6 serum levels.	gastrodin	37-46	high mobility group box 1	Homo sapiens	199-205
29113279-0	2017	HMGB1-mediated autophagy confers resistance to gemcitabine in hormone-independent prostate cancer cells.	gemcitabine	47-58	high mobility group box 1	Homo sapiens	0-5
29113279-6	2017	Meanwhile, administration of gemcitabine to HIPC cells increased the expression of high mobility group box1 (HMGB1).	gemcitabine	29-40	high mobility group box 1	Homo sapiens	83-107
29113279-7	2017	Furthermore, the gemcitabine-induced autophagy response was attenuated in stable HIPC cells harboring HMGB1 shRNA.	gemcitabine	17-28	high mobility group box 1	Homo sapiens	102-107
29113279-8	2017	Notably, the HIPC cells stably transfected with HMGB1 shRNA or treated with autophagy inhibitors were more sensitive to gemcitabine compared with the control group.	gemcitabine	120-131	high mobility group box 1	Homo sapiens	48-53
29113279-9	2017	These data suggested that inhibition of HMGB1 increased the sensitivity to gemcitabine by decreasing autophagy response in HIPC cells.	gemcitabine	75-86	high mobility group box 1	Homo sapiens	40-45
29085368-0	2017	1,25-Dihydroxyvitamin D Inhibits LPS-Induced High-Mobility Group Box 1 (HMGB1) Secretion via Targeting the NF-E2-Related Factor 2-Hemeoxygenase-1-HMGB1 Pathway in Macrophages.	1,25-dihydroxyvitamin D	0-23	high mobility group box 1	Homo sapiens	45-70
29085368-0	2017	1,25-Dihydroxyvitamin D Inhibits LPS-Induced High-Mobility Group Box 1 (HMGB1) Secretion via Targeting the NF-E2-Related Factor 2-Hemeoxygenase-1-HMGB1 Pathway in Macrophages.	1,25-dihydroxyvitamin D	0-23	high mobility group box 1	Homo sapiens	72-77
29085368-0	2017	1,25-Dihydroxyvitamin D Inhibits LPS-Induced High-Mobility Group Box 1 (HMGB1) Secretion via Targeting the NF-E2-Related Factor 2-Hemeoxygenase-1-HMGB1 Pathway in Macrophages.	1,25-dihydroxyvitamin D	0-23	high mobility group box 1	Homo sapiens	146-151
28975966-2	2017	MATERIALS AND METHODS: The effect of HMGB1 on the proliferation of the two cell types was examined using the MTT assay under environmental hypoxia (incubation with 1.5% oxygen) to simulate the condition of pulmonary arterial hypertension in the body.	monooxyethylene trimethylolpropane tristearate	109-112	high mobility group box 1	Homo sapiens	37-42
29085368-6	2017	When siHO-1 or an HO-1 inhibitor are used, the effect of 1,25(OH)2D3 on inhibition of HMGB1 secretion is suppressed.	Calcitriol	57-68	high mobility group box 1	Homo sapiens	86-91
29018504-2	2017	We also report data on the use of 18-beta-glycyrrhetic acid (GA), which has been shown able to inhibit the pro-inflammatory activities of HMGB1, in young patients affected by allergic rhinitis and complaining of nasal obstruction as main symptom.	Glycyrrhetinic Acid	34-59	high mobility group box 1	Homo sapiens	138-143
29018504-2	2017	We also report data on the use of 18-beta-glycyrrhetic acid (GA), which has been shown able to inhibit the pro-inflammatory activities of HMGB1, in young patients affected by allergic rhinitis and complaining of nasal obstruction as main symptom.	Glycyrrhetinic Acid	61-63	high mobility group box 1	Homo sapiens	138-143
29018504-8	2017	GA inhibits HMGB1 chemotactic and mitogenic function by a scavenger mechanism on extracellular HMGB1 accumulation stimulated by lipopolysaccharides in vitro.	Glycyrrhetinic Acid	0-2	high mobility group box 1	Homo sapiens	12-17
29018504-8	2017	GA inhibits HMGB1 chemotactic and mitogenic function by a scavenger mechanism on extracellular HMGB1 accumulation stimulated by lipopolysaccharides in vitro.	Glycyrrhetinic Acid	0-2	high mobility group box 1	Homo sapiens	95-100
27501713-7	2017	The biphasic biological property of extracellular HMGB1 may be related to the redox modifications of its cysteine residues.	Cysteine	105-113	high mobility group box 1	Homo sapiens	50-55
28474284-5	2017	This review focuses on the interactions and contribution to the pathogenesis and progression of OA through the DAMPs: high-mobility group box 1 (HMGB-1), the receptor for advanced glycation end-products (RAGE), the alarmin proteins S100A8 and S100A9, and heparan sulfate.	Heparitin Sulfate	255-270	high mobility group box 1	Homo sapiens	145-151
28474284-9	2017	Heparan sulfate has been shown to facilitate the binding of HMGB-1 to RAGE and could play a role in the progression of OA.	Heparitin Sulfate	0-15	high mobility group box 1	Homo sapiens	60-66
28741799-5	2017	RESULT: Baseline HMGB-1 was significantly higher in the BHT (+) group than in the BHT (-) group.	Butylated Hydroxytoluene	56-59	high mobility group box 1	Homo sapiens	17-23
28741799-5	2017	RESULT: Baseline HMGB-1 was significantly higher in the BHT (+) group than in the BHT (-) group.	Butylated Hydroxytoluene	82-85	high mobility group box 1	Homo sapiens	17-23
28741799-6	2017	Thereafter, HMGB-1 in the BHT (+) group significantly decreased at 24 h intervals, reaching the reference range by 2 days of age.	Butylated Hydroxytoluene	26-29	high mobility group box 1	Homo sapiens	12-18
28741799-7	2017	In the BHT (+) group, when patients were classified into clinically significant neurological disorder due to HIE (+) and (-) according to MRI, the neurological disorder (+) group had higher mean HMGB-1.	Butylated Hydroxytoluene	7-10	high mobility group box 1	Homo sapiens	195-201
28741799-8	2017	CONCLUSIONS: In HIE, HMGB-1 differs according to the presence of BHT, suggesting that HMGB-1 measurement soon after birth might be useful for determining BHT necessity and short-term outcome.	Butylated Hydroxytoluene	65-68	high mobility group box 1	Homo sapiens	21-27
28741799-8	2017	CONCLUSIONS: In HIE, HMGB-1 differs according to the presence of BHT, suggesting that HMGB-1 measurement soon after birth might be useful for determining BHT necessity and short-term outcome.	Butylated Hydroxytoluene	65-68	high mobility group box 1	Homo sapiens	86-92
28741799-8	2017	CONCLUSIONS: In HIE, HMGB-1 differs according to the presence of BHT, suggesting that HMGB-1 measurement soon after birth might be useful for determining BHT necessity and short-term outcome.	Butylated Hydroxytoluene	154-157	high mobility group box 1	Homo sapiens	21-27
28741799-8	2017	CONCLUSIONS: In HIE, HMGB-1 differs according to the presence of BHT, suggesting that HMGB-1 measurement soon after birth might be useful for determining BHT necessity and short-term outcome.	Butylated Hydroxytoluene	154-157	high mobility group box 1	Homo sapiens	86-92
29033853-0	2017	Proinflammatory Effect of High Glucose Concentrations on HMrSV5 Cells via the Autocrine Effect of HMGB1.	Glucose	31-38	high mobility group box 1	Homo sapiens	98-103
29033853-5	2017	Aim: In this study, we aimed to explore the effect and underlying mechanism of endogenous HMGB1 in high-glucose-induced MC injury.	Glucose	104-111	high mobility group box 1	Homo sapiens	90-95
29033853-9	2017	Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways.	mcs	56-59	high mobility group box 1	Homo sapiens	69-74
29033853-9	2017	Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways.	Glucose	116-123	high mobility group box 1	Homo sapiens	69-74
28692534-7	2017	NDE from neuropsychologically impaired study participants had significantly higher levels of high-mobility group box 1 (HMGB1), NF-L, and amyloid beta proteins compared with neuropsychologically normal individuals.	NDE	0-3	high mobility group box 1	Homo sapiens	93-118
28692534-7	2017	NDE from neuropsychologically impaired study participants had significantly higher levels of high-mobility group box 1 (HMGB1), NF-L, and amyloid beta proteins compared with neuropsychologically normal individuals.	NDE	0-3	high mobility group box 1	Homo sapiens	120-125
28741799-1	2017	BACKGROUND: We measured changes in the blood level of high-mobility group box-1 (HMGB-1) at 24 h intervals in neonates treated with brain/body hypothermia (body hypothermia therapy: BHT) for hypoxic-ischemic encephalopathy (HIE), to evaluate the usefulness of HMGB-1 level for determining outcomes.	Butylated Hydroxytoluene	182-185	high mobility group box 1	Homo sapiens	54-79
28741799-1	2017	BACKGROUND: We measured changes in the blood level of high-mobility group box-1 (HMGB-1) at 24 h intervals in neonates treated with brain/body hypothermia (body hypothermia therapy: BHT) for hypoxic-ischemic encephalopathy (HIE), to evaluate the usefulness of HMGB-1 level for determining outcomes.	Butylated Hydroxytoluene	182-185	high mobility group box 1	Homo sapiens	81-87
29033853-9	2017	Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways.	mcs	175-178	high mobility group box 1	Homo sapiens	132-137
29033853-9	2017	Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways.	mcs	175-178	high mobility group box 1	Homo sapiens	132-137
29033853-9	2017	Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways.	mcs	175-178	high mobility group box 1	Homo sapiens	132-137
29033853-9	2017	Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways.	Glucose	260-267	high mobility group box 1	Homo sapiens	132-137
29033853-9	2017	Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways.	Glucose	260-267	high mobility group box 1	Homo sapiens	132-137
29033853-9	2017	Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways.	Glucose	260-267	high mobility group box 1	Homo sapiens	132-137
29033853-9	2017	Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways.	mcs	175-178	high mobility group box 1	Homo sapiens	132-137
29033853-9	2017	Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways.	mcs	175-178	high mobility group box 1	Homo sapiens	132-137
29033853-9	2017	Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways.	mcs	175-178	high mobility group box 1	Homo sapiens	132-137
29033853-10	2017	In conclusion, endogenous HMGB1 plays an important role in the inflammatory reaction induced by high glucose on MCs via mitogen-activated protein kinase (MAPK) signaling pathways, but it seems to have little effect on high-glucose-induced apoptosis.	Glucose	101-108	high mobility group box 1	Homo sapiens	26-31
29033853-10	2017	In conclusion, endogenous HMGB1 plays an important role in the inflammatory reaction induced by high glucose on MCs via mitogen-activated protein kinase (MAPK) signaling pathways, but it seems to have little effect on high-glucose-induced apoptosis.	mcs	112-115	high mobility group box 1	Homo sapiens	26-31
28514198-6	2017	The current study further indicated that piceatannol decreased the expression of sbp-1 (encodes an ortholog of mammalian sterol regulatory element-binding protein) and its target gene fasn-1 (encodes an ortholog of fatty acid synthase) as well as increased the expression of hosl-1 (encodes an ortholog of hormone-sensitive lipase) in glucose-treated worms.	3,3',4,5'-tetrahydroxystilbene	41-52	high mobility group box 1	Homo sapiens	81-86
28185215-10	2017	Importantly, SA up-regulated a series of apoptosis-related gene expression and reduced the mRNA level of HMGB1.	Salicylic Acid	13-15	high mobility group box 1	Homo sapiens	105-110
28514198-6	2017	The current study further indicated that piceatannol decreased the expression of sbp-1 (encodes an ortholog of mammalian sterol regulatory element-binding protein) and its target gene fasn-1 (encodes an ortholog of fatty acid synthase) as well as increased the expression of hosl-1 (encodes an ortholog of hormone-sensitive lipase) in glucose-treated worms.	Glucose	335-342	high mobility group box 1	Homo sapiens	81-86
28161237-5	2017	Here we report that LMWHs induce a profound change in the ability of human neutrophils to generate NETs and to mobilize the content of the primary granules in response to unrelated inflammatory stimuli, such as IL-8, PMA and HMGB1.	Heparin, Low-Molecular-Weight	20-25	high mobility group box 1	Homo sapiens	225-230
28858636-9	2017	OS and senescence caused the translocation of HMGB1 and cffTF from AECs" nuclei to cytoplasm compared to untreated cells, which was inhibited by antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	157-174	high mobility group box 1	Homo sapiens	46-51
28858636-9	2017	OS and senescence caused the translocation of HMGB1 and cffTF from AECs" nuclei to cytoplasm compared to untreated cells, which was inhibited by antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	176-179	high mobility group box 1	Homo sapiens	46-51
28677786-8	2017	Furthermore, LPS-stimulation significantly upregulated HMGB-1 secretion via the c-Jun N-terminal kinase (JNK) signaling pathway in RAW264.7 macrophages, whereas pretreatment with the JNK inhibitor SP600125 markedly downregulated LPS-induced HMGB-1 levels.	pyrazolanthrone	197-205	high mobility group box 1	Homo sapiens	55-61
29798353-3	2017	The effect of HMGB1 on fluorescein isothiocyanatedextran 4 kDa (FD4) permeability of NECs was measured.	fluorescein isothiocyanatedextran 4 kda	23-62	high mobility group box 1	Homo sapiens	14-19
28912678-6	2017	These findings demonstrated that ROS might be located upstream of IL-17A and HMGB1 so that ROS can regulate HMGB1/IL-17A expression to affect the p53 and PI3K/Akt signaling pathways and therefore promote the occurrence of apoptosis in microglial cells.	ros	33-36	high mobility group box 1	Homo sapiens	77-82
28912678-6	2017	These findings demonstrated that ROS might be located upstream of IL-17A and HMGB1 so that ROS can regulate HMGB1/IL-17A expression to affect the p53 and PI3K/Akt signaling pathways and therefore promote the occurrence of apoptosis in microglial cells.	ros	33-36	high mobility group box 1	Homo sapiens	108-113
28912678-6	2017	These findings demonstrated that ROS might be located upstream of IL-17A and HMGB1 so that ROS can regulate HMGB1/IL-17A expression to affect the p53 and PI3K/Akt signaling pathways and therefore promote the occurrence of apoptosis in microglial cells.	ros	91-94	high mobility group box 1	Homo sapiens	77-82
28912678-6	2017	These findings demonstrated that ROS might be located upstream of IL-17A and HMGB1 so that ROS can regulate HMGB1/IL-17A expression to affect the p53 and PI3K/Akt signaling pathways and therefore promote the occurrence of apoptosis in microglial cells.	ros	91-94	high mobility group box 1	Homo sapiens	108-113
28732809-8	2017	RESULTS: Oleacein at the concentrations of 10 and 20 microM significantly (P &lt; 0.001) decreased secretion of HMGB1 (up 90%), MMP-9 (up to 80%), MMP-9/NGAL complex (up to 80%) and TF (more than 90%) from the treated plaque, as compared to control.	oleacein	9-17	high mobility group box 1	Homo sapiens	112-117
28677729-13	2017	In-depth IPA analysis revealed that CENPU was associated with the HMGB1 signaling pathway.	ipa	9-12	high mobility group box 1	Homo sapiens	66-71
28167116-3	2017	anti-HMGB1 mAb attenuated both acute seizure models (maximal electroshock seizure, pentylenetetrazole-induced and kindling-induced), and chronic epilepsy model (kainic acid-induced) in a dose-dependent manner.	Pentylenetetrazole	83-101	high mobility group box 1	Homo sapiens	5-10
28167116-3	2017	anti-HMGB1 mAb attenuated both acute seizure models (maximal electroshock seizure, pentylenetetrazole-induced and kindling-induced), and chronic epilepsy model (kainic acid-induced) in a dose-dependent manner.	Kainic Acid	161-172	high mobility group box 1	Homo sapiens	5-10
28912641-6	2017	Moreover, we also discuss our recent findings that its endogenous ligand, high-mobility group box 1 (HMGB1), is released from dying OLs and exerts autocrine trophic effects on OLs and myelin sheath under ischemic condition.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	132-135	high mobility group box 1	Homo sapiens	74-99
28912641-6	2017	Moreover, we also discuss our recent findings that its endogenous ligand, high-mobility group box 1 (HMGB1), is released from dying OLs and exerts autocrine trophic effects on OLs and myelin sheath under ischemic condition.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	132-135	high mobility group box 1	Homo sapiens	101-106
28912641-6	2017	Moreover, we also discuss our recent findings that its endogenous ligand, high-mobility group box 1 (HMGB1), is released from dying OLs and exerts autocrine trophic effects on OLs and myelin sheath under ischemic condition.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	176-179	high mobility group box 1	Homo sapiens	74-99
28912641-6	2017	Moreover, we also discuss our recent findings that its endogenous ligand, high-mobility group box 1 (HMGB1), is released from dying OLs and exerts autocrine trophic effects on OLs and myelin sheath under ischemic condition.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	176-179	high mobility group box 1	Homo sapiens	101-106
28652214-4	2017	Serum concentrations of vWF and HMGB1 were significantly higher in all the patients than in the healthy controls, both prior to doxycycline treatment and on day 7 of doxycycline treatment (p&lt;0.01).	Doxycycline	166-177	high mobility group box 1	Homo sapiens	32-37
28159648-2	2017	Microglia, the innate immune cells of the brain, and neurons respond to alcohol, signaling through Toll-like receptors (TLRs), high-mobility group box 1 (HMGB1), miRNAs, pro-inflammatory cytokines and their associated receptors involved in signaling between microglia, other glia and neurons.	Alcohols	72-79	high mobility group box 1	Homo sapiens	127-152
28159648-2	2017	Microglia, the innate immune cells of the brain, and neurons respond to alcohol, signaling through Toll-like receptors (TLRs), high-mobility group box 1 (HMGB1), miRNAs, pro-inflammatory cytokines and their associated receptors involved in signaling between microglia, other glia and neurons.	Alcohols	72-79	high mobility group box 1	Homo sapiens	154-159
28159648-3	2017	Repeated cycles of alcohol and stress cause a progressive, persistent induction of HMGB1, miRNA and TLR receptors in brain that appear to underlie the progressive and persistent loss of behavioral control, increased impulsivity and anxiety, as well as craving, coupled with increasing ventral striatal responses that promote reward seeking behavior and increase risk of developing alcohol use disorders.	Alcohols	19-26	high mobility group box 1	Homo sapiens	83-88
28159648-3	2017	Repeated cycles of alcohol and stress cause a progressive, persistent induction of HMGB1, miRNA and TLR receptors in brain that appear to underlie the progressive and persistent loss of behavioral control, increased impulsivity and anxiety, as well as craving, coupled with increasing ventral striatal responses that promote reward seeking behavior and increase risk of developing alcohol use disorders.	Alcohols	381-388	high mobility group box 1	Homo sapiens	83-88
28575153-11	2017	Oxidative stress during epileptogenesis was associated with de novo brain and blood generation of disulfide high mobility group box 1 (HMGB1), a neuroinflammatory molecule implicated in seizure mechanisms.	Disulfides	98-107	high mobility group box 1	Homo sapiens	108-133
29089150-0	2017	Hemin Reduces HMGB1 Release by UVB in an AMPK/HO-1-dependent Pathway in Human Keratinocytes HaCaT Cells.	Hemin	0-5	high mobility group box 1	Homo sapiens	14-19
29089150-2	2017	We hypothesized that hemin might reduce HMGB1 release through the induction of HO-1 in UVB-induced HaCaTs.	Hemin	21-26	high mobility group box 1	Homo sapiens	40-45
29089150-3	2017	METHODS: The effects of hemin on the release of HMGB1 in UVB exposure were evaluated.	Hemin	24-29	high mobility group box 1	Homo sapiens	48-53
29089150-6	2017	HMGB1 release by UVB was significantly reduced by hemin, N-acetyl-cysteine and DPI (NADPH oxidase inhibitor).	Hemin	50-55	high mobility group box 1	Homo sapiens	0-5
29089150-6	2017	HMGB1 release by UVB was significantly reduced by hemin, N-acetyl-cysteine and DPI (NADPH oxidase inhibitor).	Acetylcysteine	57-74	high mobility group box 1	Homo sapiens	0-5
29089150-6	2017	HMGB1 release by UVB was significantly reduced by hemin, N-acetyl-cysteine and DPI (NADPH oxidase inhibitor).	3-aminodiphenyleneiodium	79-82	high mobility group box 1	Homo sapiens	0-5
29089150-9	2017	The inhibitory effects of UVB-induced HMGB1 release by hemin were significantly reversed not only with pharmacological inhibitors of AMPK (compound c) or HO-1 (ZnPPIX) but also through transfection of small interfering RNAs (siRNAs) for AMPK or HO-1.	zinc protoporphyrin	160-166	high mobility group box 1	Homo sapiens	38-43
29089150-12	2017	CONCLUSIONS: It is concluded that the increased activity of HO-1/AMPK and scavenging ROS are, at least in part, responsible for the inhibition of UVB-induced HMGB1 release in keratinocyte HaCaTs.	Reactive Oxygen Species	85-88	high mobility group box 1	Homo sapiens	158-163
28575153-11	2017	Oxidative stress during epileptogenesis was associated with de novo brain and blood generation of disulfide high mobility group box 1 (HMGB1), a neuroinflammatory molecule implicated in seizure mechanisms.	Disulfides	98-107	high mobility group box 1	Homo sapiens	135-140
28575153-12	2017	Drug-induced reduction of oxidative stress prevented disulfide HMGB1 generation, thus highlighting a potential novel mechanism contributing to therapeutic effects.	Disulfides	53-62	high mobility group box 1	Homo sapiens	63-68
28216372-3	2017	HBx triggered an increase of cytoplasmic calcium and activated CAMKK/CAMKIV pathway, leading to subsequent translocation and release of HMGB1.	Calcium	41-48	high mobility group box 1	Homo sapiens	136-141
28294475-0	2017	Sodium tanshinone IIA sulfonate prevents hypoxic trophoblast-induced endothelial cell dysfunction via targeting HMGB1 release.	tanshinone II A sodium sulfonate	0-31	high mobility group box 1	Homo sapiens	112-117
28294475-3	2017	In the present study, we investigated the protective effect of sodium tanshinone IIA sulfonate (STS), the soluble form of tanshinone IIA isolated from danshen, against hypoxic trophoblast HMGB1-induced human umbilical vein endothelial cell (HUVEC) dysfunction.	tanshinone II A sodium sulfonate	63-94	high mobility group box 1	Homo sapiens	188-193
28294475-3	2017	In the present study, we investigated the protective effect of sodium tanshinone IIA sulfonate (STS), the soluble form of tanshinone IIA isolated from danshen, against hypoxic trophoblast HMGB1-induced human umbilical vein endothelial cell (HUVEC) dysfunction.	tanshinone II A sodium sulfonate	96-99	high mobility group box 1	Homo sapiens	188-193
28294475-6	2017	In conclusion, our study suggests that STS is an effective agent against hypoxic trophoblast-induced cell injury of HUVEC via targeting HMGB1 release and forms the basis of the development of such a compound in treating PE.	tanshinone II A sodium sulfonate	39-42	high mobility group box 1	Homo sapiens	136-141
28504645-6	2017	The pathologic disulfide HMGB1 isoform progressively increased in blood before epilepsy onset and prospectively identified animals that developed the disease.	Disulfides	15-24	high mobility group box 1	Homo sapiens	25-30
28504645-7	2017	Consistent with animal data, we observed early expression of disulfide HMGB1 in patients with newly diagnosed epilepsy, and its persistence was associated with subsequent seizures.	Disulfides	61-70	high mobility group box 1	Homo sapiens	71-76
28504645-8	2017	In contrast with patients with well-controlled epilepsy, patients with chronic, drug-refractory epilepsy persistently expressed the acetylated, disulfide HMGB1 isoforms.	Disulfides	144-153	high mobility group box 1	Homo sapiens	154-159
28251435-7	2017	Moreover, HMGB1-mediated EPC apoptosis and CHOP expression were dramatically suppressed by PERK shRNA or a specific eIF2alpha inhibitor (salubrinal).	salubrinal	137-147	high mobility group box 1	Homo sapiens	10-15
28444390-6	2017	High-mobility group box 1 protein (HMGB1) and lactate dehydrogenase release as well as adenosine triphosphate depletion occurred in a drug-, time-, and concentration-dependent manner with SMX-NO and flucloxacillin, whereas isoniazid and amoxicillin were nontoxic.	4-nitrososulfamethoxazole	188-194	high mobility group box 1	Homo sapiens	0-25
28444390-6	2017	High-mobility group box 1 protein (HMGB1) and lactate dehydrogenase release as well as adenosine triphosphate depletion occurred in a drug-, time-, and concentration-dependent manner with SMX-NO and flucloxacillin, whereas isoniazid and amoxicillin were nontoxic.	4-nitrososulfamethoxazole	188-194	high mobility group box 1	Homo sapiens	35-40
28444390-6	2017	High-mobility group box 1 protein (HMGB1) and lactate dehydrogenase release as well as adenosine triphosphate depletion occurred in a drug-, time-, and concentration-dependent manner with SMX-NO and flucloxacillin, whereas isoniazid and amoxicillin were nontoxic.	Floxacillin	199-213	high mobility group box 1	Homo sapiens	0-25
28444390-6	2017	High-mobility group box 1 protein (HMGB1) and lactate dehydrogenase release as well as adenosine triphosphate depletion occurred in a drug-, time-, and concentration-dependent manner with SMX-NO and flucloxacillin, whereas isoniazid and amoxicillin were nontoxic.	Floxacillin	199-213	high mobility group box 1	Homo sapiens	35-40
28444390-6	2017	High-mobility group box 1 protein (HMGB1) and lactate dehydrogenase release as well as adenosine triphosphate depletion occurred in a drug-, time-, and concentration-dependent manner with SMX-NO and flucloxacillin, whereas isoniazid and amoxicillin were nontoxic.	Isoniazid	223-232	high mobility group box 1	Homo sapiens	0-25
28444390-6	2017	High-mobility group box 1 protein (HMGB1) and lactate dehydrogenase release as well as adenosine triphosphate depletion occurred in a drug-, time-, and concentration-dependent manner with SMX-NO and flucloxacillin, whereas isoniazid and amoxicillin were nontoxic.	Isoniazid	223-232	high mobility group box 1	Homo sapiens	35-40
28444390-6	2017	High-mobility group box 1 protein (HMGB1) and lactate dehydrogenase release as well as adenosine triphosphate depletion occurred in a drug-, time-, and concentration-dependent manner with SMX-NO and flucloxacillin, whereas isoniazid and amoxicillin were nontoxic.	Amoxicillin	237-248	high mobility group box 1	Homo sapiens	0-25
28444390-6	2017	High-mobility group box 1 protein (HMGB1) and lactate dehydrogenase release as well as adenosine triphosphate depletion occurred in a drug-, time-, and concentration-dependent manner with SMX-NO and flucloxacillin, whereas isoniazid and amoxicillin were nontoxic.	Amoxicillin	237-248	high mobility group box 1	Homo sapiens	35-40
28444390-8	2017	The disulfide isoform of HMGB1 stimulated dendritic cell cytokine release and enhanced the priming of naive T-cells.	Disulfides	4-13	high mobility group box 1	Homo sapiens	25-30
28584116-7	2017	Knockdown of HMGB1 or application of glycyrrhizin, a specific HMGB1 inhibitor, aggravated OGD-induced OL death, and recombinant HMGB1 application reduced the extent of OL death in a TLR2-dependent manner.	Glycyrrhizic Acid	37-49	high mobility group box 1	Homo sapiens	62-67
28584116-7	2017	Knockdown of HMGB1 or application of glycyrrhizin, a specific HMGB1 inhibitor, aggravated OGD-induced OL death, and recombinant HMGB1 application reduced the extent of OL death in a TLR2-dependent manner.	Glycyrrhizic Acid	37-49	high mobility group box 1	Homo sapiens	62-67
28216372-7	2017	CONCLUSION: HBx promotes the progression of HCC through translocation and secretion of HMGB1 from tumor cells via calcium dependent cascades.	Calcium	114-121	high mobility group box 1	Homo sapiens	87-92
28373282-0	2017	Metformin directly binds the alarmin HMGB1 and inhibits its proinflammatory activity.	Metformin	0-9	high mobility group box 1	Homo sapiens	37-42
28373282-4	2017	Here we identified HMGB1 as a novel metformin-binding protein by affinity purification using a biotinylated metformin analogue.	Metformin	36-45	high mobility group box 1	Homo sapiens	19-24
28373282-5	2017	Metformin directly bound to the C-terminal acidic tail of HMGB1.	Metformin	0-9	high mobility group box 1	Homo sapiens	58-63
28373282-6	2017	Both in vitro and in vivo, metformin inhibited inflammatory responses induced by full-length HMGB1 but not by HMGB1 lacking the acidic tail.	Metformin	27-36	high mobility group box 1	Homo sapiens	93-98
28373282-7	2017	In an acetaminophen-induced acute liver injury model in which HMGB1 released from injured cells exacerbates the initial injury, metformin effectively reduced liver injury and had no additional inhibitory effects when the extracellular HMGB1 was blocked by anti-HMGB1-neutralizing antibody.	Metformin	128-137	high mobility group box 1	Homo sapiens	235-240
28373282-7	2017	In an acetaminophen-induced acute liver injury model in which HMGB1 released from injured cells exacerbates the initial injury, metformin effectively reduced liver injury and had no additional inhibitory effects when the extracellular HMGB1 was blocked by anti-HMGB1-neutralizing antibody.	Metformin	128-137	high mobility group box 1	Homo sapiens	235-240
28373282-8	2017	In summary, we report for the first time that metformin suppresses inflammation by inhibiting the extracellular activity of HMGB1.	Metformin	46-55	high mobility group box 1	Homo sapiens	124-129
29069735-0	2017	HMGB1-mediated autophagy attenuates gemcitabine-induced apoptosis in bladder cancer cells involving JNK and ERK activation.	gemcitabine	36-47	high mobility group box 1	Homo sapiens	0-5
28426082-0	2017	Deciphering of interactions between platinated DNA and HMGB1 by hydrogen/deuterium exchange mass spectrometry.	Hydrogen	64-72	high mobility group box 1	Homo sapiens	55-60
28426082-0	2017	Deciphering of interactions between platinated DNA and HMGB1 by hydrogen/deuterium exchange mass spectrometry.	Deuterium	73-82	high mobility group box 1	Homo sapiens	55-60
28426082-1	2017	A high mobility group box 1 (HMGB1) protein has been reported to recognize both 1,2-intrastrand crosslinked DNA by cisplatin (1,2-cis-Pt-DNA) and monofunctional platinated DNA using trans-[PtCl2(NH3)(thiazole)] (1-trans-PtTz-DNA).	Cisplatin	115-124	high mobility group box 1	Homo sapiens	2-27
28426082-1	2017	A high mobility group box 1 (HMGB1) protein has been reported to recognize both 1,2-intrastrand crosslinked DNA by cisplatin (1,2-cis-Pt-DNA) and monofunctional platinated DNA using trans-[PtCl2(NH3)(thiazole)] (1-trans-PtTz-DNA).	Cisplatin	115-124	high mobility group box 1	Homo sapiens	29-34
28426082-1	2017	A high mobility group box 1 (HMGB1) protein has been reported to recognize both 1,2-intrastrand crosslinked DNA by cisplatin (1,2-cis-Pt-DNA) and monofunctional platinated DNA using trans-[PtCl2(NH3)(thiazole)] (1-trans-PtTz-DNA).	ptcl2(nh3)	189-199	high mobility group box 1	Homo sapiens	2-27
28426082-1	2017	A high mobility group box 1 (HMGB1) protein has been reported to recognize both 1,2-intrastrand crosslinked DNA by cisplatin (1,2-cis-Pt-DNA) and monofunctional platinated DNA using trans-[PtCl2(NH3)(thiazole)] (1-trans-PtTz-DNA).	ptcl2(nh3)	189-199	high mobility group box 1	Homo sapiens	29-34
28426082-1	2017	A high mobility group box 1 (HMGB1) protein has been reported to recognize both 1,2-intrastrand crosslinked DNA by cisplatin (1,2-cis-Pt-DNA) and monofunctional platinated DNA using trans-[PtCl2(NH3)(thiazole)] (1-trans-PtTz-DNA).	Thiazoles	200-208	high mobility group box 1	Homo sapiens	2-27
28426082-1	2017	A high mobility group box 1 (HMGB1) protein has been reported to recognize both 1,2-intrastrand crosslinked DNA by cisplatin (1,2-cis-Pt-DNA) and monofunctional platinated DNA using trans-[PtCl2(NH3)(thiazole)] (1-trans-PtTz-DNA).	Thiazoles	200-208	high mobility group box 1	Homo sapiens	29-34
28426082-3	2017	In the present work, we described a hydrogen/deuterium exchange mass spectrometry (HDX-MS) method in combination with docking simulation to decipher the interactions of platinated DNA with domain A of HMGB1.	Hydrogen	36-44	high mobility group box 1	Homo sapiens	201-206
28426082-3	2017	In the present work, we described a hydrogen/deuterium exchange mass spectrometry (HDX-MS) method in combination with docking simulation to decipher the interactions of platinated DNA with domain A of HMGB1.	Deuterium	45-54	high mobility group box 1	Homo sapiens	201-206
29069735-8	2017	Interestingly, suppressing HMGB1 expression attenuated gemcitabine-induced ERK and JNK activation and Bcl-2 phosphorylation.	gemcitabine	55-66	high mobility group box 1	Homo sapiens	27-32
29069735-9	2017	Thus, our results suggest that while gemcitabine kills bladder cancer cells through apoptosis, a cytoprotective autophagy is also induced involving HMGB1-mediated JNK and ERK to counteract the cytotoxicity of gemcitabine, and intervention targeting this pathway may improve the anticancer efficacy of gemcitabine against bladder cancer.	gemcitabine	209-220	high mobility group box 1	Homo sapiens	148-153
29069735-9	2017	Thus, our results suggest that while gemcitabine kills bladder cancer cells through apoptosis, a cytoprotective autophagy is also induced involving HMGB1-mediated JNK and ERK to counteract the cytotoxicity of gemcitabine, and intervention targeting this pathway may improve the anticancer efficacy of gemcitabine against bladder cancer.	gemcitabine	209-220	high mobility group box 1	Homo sapiens	148-153
29069735-4	2017	While gemcitabine induced apoptotic cell death, it also induced HMGB1 expression and autophagy in bladder cancer T24 and BIU-87 cells.	gemcitabine	6-17	high mobility group box 1	Homo sapiens	64-69
29069735-5	2017	Suppressing HMGB1 expression with siRNA strongly potentiated gemcitabine-induced apoptosis.	gemcitabine	61-72	high mobility group box 1	Homo sapiens	12-17
29069735-6	2017	HMGB1 siRNA or autophagy inhibitors suppressed gemcitabine-induced autophagy.	gemcitabine	47-58	high mobility group box 1	Homo sapiens	0-5
28210782-6	2017	Multiple TLRs, HMGB1, and miRNAs are induced in the brain by stress, alcohol, and other drugs of abuse and are increased in the postmortem human alcoholic brain.	Alcohols	69-76	high mobility group box 1	Homo sapiens	15-20
27908811-12	2017	CONCLUSIONS: Removal or isolation of AL via surgical intervention significantly decreases serum HMGB-1 levels.	Aluminum	37-39	high mobility group box 1	Homo sapiens	96-102
28407046-4	2017	Methods and results: Expression of RAGE and its activating ligands, S100/calgranulins and high mobility group box 1 (HMGB1), were increased in both human and mouse pulmonary arterial smooth muscle cells (PASMCs) under hypoxic conditions and were also strikingly upregulated in pulmonary arteries in hypoxia plus SU5416 (HySu)-induced PAH in mice.	pasmcs	204-210	high mobility group box 1	Homo sapiens	90-115
28407046-4	2017	Methods and results: Expression of RAGE and its activating ligands, S100/calgranulins and high mobility group box 1 (HMGB1), were increased in both human and mouse pulmonary arterial smooth muscle cells (PASMCs) under hypoxic conditions and were also strikingly upregulated in pulmonary arteries in hypoxia plus SU5416 (HySu)-induced PAH in mice.	pasmcs	204-210	high mobility group box 1	Homo sapiens	117-122
27943400-5	2017	The injection of HMGB1 into the IMQ-treated skin further aggravated the psoriasis-like disease, enhanced the infiltration of CD3+ T cells, myeloperoxidase+ neutrophils and CD11c+ dendritic cells, increased the number of gammadelta T cells, and upregulated the mRNA expression of interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma and IL-17 compared with the PBS injection.	Imiquimod	32-35	high mobility group box 1	Homo sapiens	17-22
27943400-5	2017	The injection of HMGB1 into the IMQ-treated skin further aggravated the psoriasis-like disease, enhanced the infiltration of CD3+ T cells, myeloperoxidase+ neutrophils and CD11c+ dendritic cells, increased the number of gammadelta T cells, and upregulated the mRNA expression of interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma and IL-17 compared with the PBS injection.	pbs	385-388	high mobility group box 1	Homo sapiens	17-22
27624778-0	2017	ROS-dependent HMGB1 secretion upregulates IL-8 in upper airway epithelial cells under hypoxic condition.	Reactive Oxygen Species	0-3	high mobility group box 1	Homo sapiens	14-19
27624778-4	2017	Reactive oxygen species (ROS) level was evaluated to estimate the translocation mechanism of HMGB1.	Reactive Oxygen Species	0-23	high mobility group box 1	Homo sapiens	93-98
27624778-4	2017	Reactive oxygen species (ROS) level was evaluated to estimate the translocation mechanism of HMGB1.	Reactive Oxygen Species	25-28	high mobility group box 1	Homo sapiens	93-98
27624778-7	2017	Hypoxia induced translocation of HMGB1 into the extracellular area and it was dependent on ROS produced by dual oxidase 2.	Reactive Oxygen Species	91-94	high mobility group box 1	Homo sapiens	33-38
27624778-11	2017	We suggest that HMGB1 is secreted in hypoxic condition via ROS-dependent mechanism and secreted HMGB1 participates in IL-8 upregulation mediating inflammatory response.	Reactive Oxygen Species	59-62	high mobility group box 1	Homo sapiens	16-21
28404891-3	2017	HMGB1 and the pro-inflammatory cytokines IL-1beta and TNF-alpha were gradually released from NB4 and HL-60 cells treated with ATRA and/or ATO.	Tretinoin	126-130	high mobility group box 1	Homo sapiens	0-5
28404891-3	2017	HMGB1 and the pro-inflammatory cytokines IL-1beta and TNF-alpha were gradually released from NB4 and HL-60 cells treated with ATRA and/or ATO.	Arsenic Trioxide	138-141	high mobility group box 1	Homo sapiens	0-5
28404891-8	2017	Treatment with a HMGB1-neutralizing antibody reduced secretion of TNF-alpha and IL-1beta, arrested the elevation of ICAM-1 and blunted the activation of ERK1/2 in ATRA-induced NB4 cells.	Tretinoin	163-167	high mobility group box 1	Homo sapiens	17-22
28616398-7	2017	We also found that PDT with G-chlorin induced immunogenic cell death which is characterized by the secretion, release, or surface exposure of damage-associated molecular patterns (DAMPs), including calreticulin (CRT) and the high-mobility group box 1 (HMGB1) protein.	g-chlorin	28-37	high mobility group box 1	Homo sapiens	225-250
28469775-0	2017	Melatonin promoted renal regeneration in folic acid-induced acute kidney injury via inhibiting nucleocytoplasmic translocation of HMGB1 in tubular epithelial cells.	Melatonin	0-9	high mobility group box 1	Homo sapiens	130-135
28469775-0	2017	Melatonin promoted renal regeneration in folic acid-induced acute kidney injury via inhibiting nucleocytoplasmic translocation of HMGB1 in tubular epithelial cells.	Folic Acid	41-51	high mobility group box 1	Homo sapiens	130-135
28469775-2	2017	High-mobility group box 1 (HMGB1) is a novel member of the damage-associated molecular pattern (DAMP) family, and has been verified to be an inflammatory cytokine mediating AKI induced by I/R and cisplatin.	Cisplatin	196-205	high mobility group box 1	Homo sapiens	0-25
28469775-2	2017	High-mobility group box 1 (HMGB1) is a novel member of the damage-associated molecular pattern (DAMP) family, and has been verified to be an inflammatory cytokine mediating AKI induced by I/R and cisplatin.	Cisplatin	196-205	high mobility group box 1	Homo sapiens	27-32
28469775-4	2017	In this study, we sought to identify the role of melatonin on folic acid induced AKI and its association with HMGB1.	Melatonin	49-58	high mobility group box 1	Homo sapiens	110-115
28469775-7	2017	This protective role of melatonin was closely related to the inhibition of nucleocytoplasmic translocation of HMGB1 in TECs.	Melatonin	24-33	high mobility group box 1	Homo sapiens	110-115
28186988-0	2017	HMGB1 targeting by ethyl pyruvate suppresses malignant phenotype of human mesothelioma.	ethyl pyruvate	19-33	high mobility group box 1	Homo sapiens	0-5
28186988-4	2017	Ethyl pyruvate (EP), the ethyl ester of pyruvic acid, has been shown to be an effective HMGB1 inhibitor in inflammation-related diseases and several cancers.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	88-93
28186988-4	2017	Ethyl pyruvate (EP), the ethyl ester of pyruvic acid, has been shown to be an effective HMGB1 inhibitor in inflammation-related diseases and several cancers.	ethyl pyruvate	16-18	high mobility group box 1	Homo sapiens	88-93
28186988-4	2017	Ethyl pyruvate (EP), the ethyl ester of pyruvic acid, has been shown to be an effective HMGB1 inhibitor in inflammation-related diseases and several cancers.	Pyruvic Acid	40-52	high mobility group box 1	Homo sapiens	88-93
28616398-7	2017	We also found that PDT with G-chlorin induced immunogenic cell death which is characterized by the secretion, release, or surface exposure of damage-associated molecular patterns (DAMPs), including calreticulin (CRT) and the high-mobility group box 1 (HMGB1) protein.	g-chlorin	28-37	high mobility group box 1	Homo sapiens	252-257
28089782-9	2017	In the supernatant of co-cultured, but not single-cultured HepG2 and Huh-7 cells, o-anisidine caused increases of damage-associated proteins, such as HMGB1 (high mobility group box-1) protein.	2-anisidine	82-93	high mobility group box 1	Homo sapiens	150-155
28685526-0	2017	Glycyrrhetinic acid suppressed hmgb1 release by up-regulation of Sirt6 in nasal inflammation.	Glycyrrhetinic Acid	0-19	high mobility group box 1	Homo sapiens	31-36
28685526-7	2017	In an in vitro study we used the 18-beta-stereoisomer of GTA to enhance Sirt6 expression levels, inhibiting through this mechanism the translocation of HMGB1 protein from nucleus and reversing its extracellular accumulation stimulated by lipopolysaccharides.	Glycyrrhetinic Acid	57-60	high mobility group box 1	Homo sapiens	152-157
28089782-9	2017	In the supernatant of co-cultured, but not single-cultured HepG2 and Huh-7 cells, o-anisidine caused increases of damage-associated proteins, such as HMGB1 (high mobility group box-1) protein.	2-anisidine	82-93	high mobility group box 1	Homo sapiens	157-182
28024939-11	2017	RAGE or ER stress knockdown reduced the up-regulation of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) in human AVICs exposed to HMGB1.These novel findings demonstrate that RAGE deficiency protects against aortic valve calcification in high cholesterol diet-fed ApoE-/- mice via inhibition of ER stress.	Cholesterol	282-293	high mobility group box 1	Homo sapiens	170-175
28443467-3	2017	In this study, the effect of irinotecan on high-mobility group protein B1 and MMP9 content, gene expression, cell cycle, and cell growth in human breast cancer cells (MCF-7) was investigated.	Irinotecan	29-39	high mobility group box 1	Homo sapiens	43-73
28443467-11	2017	From the results, it is concluded that overexpression of high-mobility group protein B1 in the presence of irinotecan precedes breast cancer cells into apoptosis and in this response the binding of irinotecan to chromatin or high-mobility group protein B1 may condense/aggregate chromatin, preventing high-mobility group protein B1 release from chromatin.	Irinotecan	107-117	high mobility group box 1	Homo sapiens	57-87
28443467-11	2017	From the results, it is concluded that overexpression of high-mobility group protein B1 in the presence of irinotecan precedes breast cancer cells into apoptosis and in this response the binding of irinotecan to chromatin or high-mobility group protein B1 may condense/aggregate chromatin, preventing high-mobility group protein B1 release from chromatin.	Irinotecan	198-208	high mobility group box 1	Homo sapiens	57-87
28396833-11	2017	HMGB1, sRAGE, IL6 and TGFbeta1 levels in BALF were also reduced by baicalin treatment.	baicalin	67-75	high mobility group box 1	Homo sapiens	0-5
28396833-13	2017	Furthermore, expression levels of HMGB1, RAGE, IL6 and TGFbeta1 in lung tissue were dramatically decreased by baicalin in a dosage-dependent manner.	baicalin	110-118	high mobility group box 1	Homo sapiens	34-39
28049065-4	2017	Herein, we demonstrated that nucleic acid binding polymers, e.g., polyethylenimine (PEI) and polyamidoamine dendrimers, immobilized onto electrospun microfiber mesh can effectively capture various DAMPs, such as extracellular DNAs and high mobility group box 1 (HMGB1).	Polymers	50-58	high mobility group box 1	Homo sapiens	235-260
28049065-4	2017	Herein, we demonstrated that nucleic acid binding polymers, e.g., polyethylenimine (PEI) and polyamidoamine dendrimers, immobilized onto electrospun microfiber mesh can effectively capture various DAMPs, such as extracellular DNAs and high mobility group box 1 (HMGB1).	Polymers	50-58	high mobility group box 1	Homo sapiens	262-267
28049065-4	2017	Herein, we demonstrated that nucleic acid binding polymers, e.g., polyethylenimine (PEI) and polyamidoamine dendrimers, immobilized onto electrospun microfiber mesh can effectively capture various DAMPs, such as extracellular DNAs and high mobility group box 1 (HMGB1).	Polyethyleneimine	66-82	high mobility group box 1	Homo sapiens	235-260
28049065-4	2017	Herein, we demonstrated that nucleic acid binding polymers, e.g., polyethylenimine (PEI) and polyamidoamine dendrimers, immobilized onto electrospun microfiber mesh can effectively capture various DAMPs, such as extracellular DNAs and high mobility group box 1 (HMGB1).	Polyethyleneimine	66-82	high mobility group box 1	Homo sapiens	262-267
28049065-4	2017	Herein, we demonstrated that nucleic acid binding polymers, e.g., polyethylenimine (PEI) and polyamidoamine dendrimers, immobilized onto electrospun microfiber mesh can effectively capture various DAMPs, such as extracellular DNAs and high mobility group box 1 (HMGB1).	Polyethyleneimine	84-87	high mobility group box 1	Homo sapiens	235-260
28049065-4	2017	Herein, we demonstrated that nucleic acid binding polymers, e.g., polyethylenimine (PEI) and polyamidoamine dendrimers, immobilized onto electrospun microfiber mesh can effectively capture various DAMPs, such as extracellular DNAs and high mobility group box 1 (HMGB1).	Polyethyleneimine	84-87	high mobility group box 1	Homo sapiens	262-267
27393275-0	2017	Urinary MCP-1 HMGB1 increased in calcium nephrolithiasis patients and the influence of hypercalciuria on the production of the two cytokines.	Calcium	33-40	high mobility group box 1	Homo sapiens	14-19
27393275-9	2017	Results showed that urinary MCP-1 and HMGB1 increased in calcium nephrolithiasis patients and hypercalciuria might affect the identical pathways (through the reactive oxygen species) with other factors in stimulating the production of MCP-1 and HMGB1 in vivo.	Calcium	57-64	high mobility group box 1	Homo sapiens	38-43
27393275-9	2017	Results showed that urinary MCP-1 and HMGB1 increased in calcium nephrolithiasis patients and hypercalciuria might affect the identical pathways (through the reactive oxygen species) with other factors in stimulating the production of MCP-1 and HMGB1 in vivo.	Reactive Oxygen Species	158-181	high mobility group box 1	Homo sapiens	245-250
28218519-2	2017	Herein, a simple and sensitive sensor system was tailored for real-time probing of the dynamic molecular recognition between cisplatin-damaged-DNA (cisPt-DNA) and a cellular responsive protein, high-mobility-group box 1 (HMGB1).	Cisplatin	125-134	high mobility group box 1	Homo sapiens	194-219
28218519-2	2017	Herein, a simple and sensitive sensor system was tailored for real-time probing of the dynamic molecular recognition between cisplatin-damaged-DNA (cisPt-DNA) and a cellular responsive protein, high-mobility-group box 1 (HMGB1).	Cisplatin	125-134	high mobility group box 1	Homo sapiens	221-226
28049065-4	2017	Herein, we demonstrated that nucleic acid binding polymers, e.g., polyethylenimine (PEI) and polyamidoamine dendrimers, immobilized onto electrospun microfiber mesh can effectively capture various DAMPs, such as extracellular DNAs and high mobility group box 1 (HMGB1).	Poly(amidoamine)	93-107	high mobility group box 1	Homo sapiens	235-260
28012970-0	2017	Isoliquiritigenin inhibits TNF-alpha-induced release of high-mobility group box 1 through activation of HDAC in human intestinal epithelial HT-29 cells.	isoliquiritigenin	0-17	high mobility group box 1	Homo sapiens	56-81
28049065-4	2017	Herein, we demonstrated that nucleic acid binding polymers, e.g., polyethylenimine (PEI) and polyamidoamine dendrimers, immobilized onto electrospun microfiber mesh can effectively capture various DAMPs, such as extracellular DNAs and high mobility group box 1 (HMGB1).	Poly(amidoamine)	93-107	high mobility group box 1	Homo sapiens	262-267
28012822-12	2017	Pharmacological inhibition of HMGB1 cytoplasmic translocation by agents such as ethyl pyruvate limits starvation-induced autophagy.	ethyl pyruvate	80-94	high mobility group box 1	Homo sapiens	30-35
28216608-8	2017	The multivariate statistical analysis indicated an iron-related 10-protein panel effective in separating non-cancerous from cancerous lesions including STAT5, STAT5_pY694, myeloid differentiation factor 88 (MYD88), CD74, iron exporter ferroportin (FPN), high mobility group box 1 (HMGB1), STAT3_pS727, TFRC, ferritin heavy chain (FTH), and ferritin light chain (FTL).	Iron	51-55	high mobility group box 1	Homo sapiens	254-279
28216608-8	2017	The multivariate statistical analysis indicated an iron-related 10-protein panel effective in separating non-cancerous from cancerous lesions including STAT5, STAT5_pY694, myeloid differentiation factor 88 (MYD88), CD74, iron exporter ferroportin (FPN), high mobility group box 1 (HMGB1), STAT3_pS727, TFRC, ferritin heavy chain (FTH), and ferritin light chain (FTL).	Iron	51-55	high mobility group box 1	Homo sapiens	281-286
27579780-9	2017	Additionally, pretreatment with resveratrol, a selective SIRT1 activator, abrogated IFN-gamma-induced HMGB1 translocation and its release.	Resveratrol	32-43	high mobility group box 1	Homo sapiens	102-107
27579780-11	2017	In contrast, blocking HMGB1 release or activity by resveratrol and HMGB1-neutralizing antibody prevents IFN-gamma-induced phenotypic modulation of VSMCs.	Resveratrol	51-62	high mobility group box 1	Homo sapiens	22-27
27579780-11	2017	In contrast, blocking HMGB1 release or activity by resveratrol and HMGB1-neutralizing antibody prevents IFN-gamma-induced phenotypic modulation of VSMCs.	vsmcs	147-152	high mobility group box 1	Homo sapiens	22-27
27579780-11	2017	In contrast, blocking HMGB1 release or activity by resveratrol and HMGB1-neutralizing antibody prevents IFN-gamma-induced phenotypic modulation of VSMCs.	vsmcs	147-152	high mobility group box 1	Homo sapiens	67-72
28118842-0	2017	Microglial-derived miRNA let-7 and HMGB1 contribute to ethanol-induced neurotoxicity via TLR7.	Ethanol	55-62	high mobility group box 1	Homo sapiens	35-40
27838489-9	2017	HMGB1 inhibition by ethyl pyruvate or blockade by neutralizing antibodies significantly decreased the phosphorylation of STAT3, p38 and IkappaBalpha, the production of IL-1beta and TNF-alpha, and the islet injury in wild-type islets after exposure to H/R and significantly improved early islet graft failure.	ethyl pyruvate	20-34	high mobility group box 1	Homo sapiens	0-5
28000879-11	2017	Treatment with NF-kappaB inhibitor (BAY11-7082) and receptor for advanced glycation end products (RAGE) antagonist (anti-RAGE) significantly suppressed HMGB1-mediated epithelial-to-mesenchymal transition in the HeLa cervical cancer cells.	3-(4-methylphenylsulfonyl)-2-propenenitrile	36-46	high mobility group box 1	Homo sapiens	152-157
28197072-4	2017	Here in this study, we investigated the interaction between HMGB1 and alpha-synuclein in rotenone-induced PD cell models and their roles in autophagy flux.	Rotenone	89-97	high mobility group box 1	Homo sapiens	60-65
28197072-5	2017	Results revealed elevated expression and cytosolic translocation of endogenous HMGB1 upon rotenone exposure.	Rotenone	90-98	high mobility group box 1	Homo sapiens	79-84
28197072-8	2017	Based on these findings, we propose that HMGB1 is involved in rotenone-induced dopaminergic cell death via interacting with alpha-synuclein, perturbing the autophagy process, aggravating protein aggregation and finally propelling dopaminergic neurons to move from morbidity to mortality.	Rotenone	62-70	high mobility group box 1	Homo sapiens	41-46
27840243-5	2017	Further investigation found that simvastatin reversed the TAM-mediated down-regulation of Gfi-1 and up-regulation of CTGF and HMGB1.	Simvastatin	33-44	high mobility group box 1	Homo sapiens	126-131
27840243-5	2017	Further investigation found that simvastatin reversed the TAM-mediated down-regulation of Gfi-1 and up-regulation of CTGF and HMGB1.	tam	58-61	high mobility group box 1	Homo sapiens	126-131
28118842-10	2017	Further, ethanol increased let-7b binding to the danger signaling molecule high mobility group box-1 (HMGB1) in MVs, while reducing let-7 binding to classical chaperone protein argonaute (Ago2).	Ethanol	9-16	high mobility group box 1	Homo sapiens	75-100
28118842-10	2017	Further, ethanol increased let-7b binding to the danger signaling molecule high mobility group box-1 (HMGB1) in MVs, while reducing let-7 binding to classical chaperone protein argonaute (Ago2).	Ethanol	9-16	high mobility group box 1	Homo sapiens	102-107
28118842-10	2017	Further, ethanol increased let-7b binding to the danger signaling molecule high mobility group box-1 (HMGB1) in MVs, while reducing let-7 binding to classical chaperone protein argonaute (Ago2).	let-7	27-32	high mobility group box 1	Homo sapiens	75-100
28118842-10	2017	Further, ethanol increased let-7b binding to the danger signaling molecule high mobility group box-1 (HMGB1) in MVs, while reducing let-7 binding to classical chaperone protein argonaute (Ago2).	let-7	27-32	high mobility group box 1	Homo sapiens	102-107
28118842-12	2017	CONCLUSIONS: Our results identify that ethanol induces neuroimmune pathology involving the release of let-7b/HMGB1 complexes in microglia-derived microvesicles.	Ethanol	39-46	high mobility group box 1	Homo sapiens	109-114
28116308-0	2017	Uric Acid Induces Endothelial Dysfunction by Activating the HMGB1/RAGE Signaling Pathway.	Uric Acid	0-9	high mobility group box 1	Homo sapiens	60-65
28270074-4	2017	OBJECTIVE: In the present study, we have mobilized a proximal twenty one base pair nucleotide (21RY) which is in the promoter region (-55 to-75) of hmgb1 gene and targeted it with triplex forming oligonucleotide (TFO) in combination with two widely used chemotherapeutic drugs, actinomycin (ACT) and adriamycin (ADM).	triplex forming oligonucleotide	180-211	high mobility group box 1	Homo sapiens	148-153
28270074-4	2017	OBJECTIVE: In the present study, we have mobilized a proximal twenty one base pair nucleotide (21RY) which is in the promoter region (-55 to-75) of hmgb1 gene and targeted it with triplex forming oligonucleotide (TFO) in combination with two widely used chemotherapeutic drugs, actinomycin (ACT) and adriamycin (ADM).	tfo	213-216	high mobility group box 1	Homo sapiens	148-153
28270074-4	2017	OBJECTIVE: In the present study, we have mobilized a proximal twenty one base pair nucleotide (21RY) which is in the promoter region (-55 to-75) of hmgb1 gene and targeted it with triplex forming oligonucleotide (TFO) in combination with two widely used chemotherapeutic drugs, actinomycin (ACT) and adriamycin (ADM).	Dactinomycin	278-289	high mobility group box 1	Homo sapiens	148-153
28270074-4	2017	OBJECTIVE: In the present study, we have mobilized a proximal twenty one base pair nucleotide (21RY) which is in the promoter region (-55 to-75) of hmgb1 gene and targeted it with triplex forming oligonucleotide (TFO) in combination with two widely used chemotherapeutic drugs, actinomycin (ACT) and adriamycin (ADM).	Doxorubicin	300-310	high mobility group box 1	Homo sapiens	148-153
28270074-4	2017	OBJECTIVE: In the present study, we have mobilized a proximal twenty one base pair nucleotide (21RY) which is in the promoter region (-55 to-75) of hmgb1 gene and targeted it with triplex forming oligonucleotide (TFO) in combination with two widely used chemotherapeutic drugs, actinomycin (ACT) and adriamycin (ADM).	Doxorubicin	312-315	high mobility group box 1	Homo sapiens	148-153
28241714-0	2017	[Molecular mechanisms of HMGB1 extracellular secretion in asbestos-induced malignant mesothelioma].	Asbestos	58-66	high mobility group box 1	Homo sapiens	25-30
28059131-7	2017	Our in vivo and in vitro studies show dioscin protects hippocampus from endotoxemia induced cascade neuro-inflammation through neurotransmitter 5-HT and HMGB-1/TLR4 signaling pathway, which accounts for the dioscin therapeutic effect in behavioral tests.	dioscin	38-45	high mobility group box 1	Homo sapiens	153-159
28059131-7	2017	Our in vivo and in vitro studies show dioscin protects hippocampus from endotoxemia induced cascade neuro-inflammation through neurotransmitter 5-HT and HMGB-1/TLR4 signaling pathway, which accounts for the dioscin therapeutic effect in behavioral tests.	dioscin	207-214	high mobility group box 1	Homo sapiens	153-159
27585400-0	2017	2-O, 3-O Desulfated Heparin Blocks High Mobility Group Box 1 Release by Inhibition of p300 Acetyltransferase Activity.	2-o, 3-o desulfated heparin	0-27	high mobility group box 1	Homo sapiens	35-60
28116308-2	2017	UA increases high mobility group box chromosomal protein 1 (HMGB1) expression and extracellular release in endothelial cells.	Uric Acid	0-2	high mobility group box 1	Homo sapiens	60-65
28116308-5	2017	UA inhibited endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) production in HUVECs, increased intracellular HMGB1 expression and extracellular HMGB1 secretion, and upregulated RAGE expression.	Uric Acid	0-2	high mobility group box 1	Homo sapiens	133-138
28116308-5	2017	UA inhibited endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) production in HUVECs, increased intracellular HMGB1 expression and extracellular HMGB1 secretion, and upregulated RAGE expression.	Uric Acid	0-2	high mobility group box 1	Homo sapiens	168-173
28116308-9	2017	Our results suggest that high concentrations of UA cause endothelial dysfunction via the HMGB1/RAGE signaling pathway.	Uric Acid	48-50	high mobility group box 1	Homo sapiens	89-94
28478444-4	2017	Lipofectamine 2000 was used to transfect with miR-34a mimics, miR-34a inhibitor, si-HMGB1, pcDNA 3.1-HMGB1, and corresponding controls.	Lipofectamine	0-18	high mobility group box 1	Homo sapiens	84-89
28478444-4	2017	Lipofectamine 2000 was used to transfect with miR-34a mimics, miR-34a inhibitor, si-HMGB1, pcDNA 3.1-HMGB1, and corresponding controls.	Lipofectamine	0-18	high mobility group box 1	Homo sapiens	101-106
28052268-5	2017	Once mucosal barrier function is disrupted due to NSAID-induced prostaglandin deficiency and mitochondrial malfunction, lipopolysaccharide from luminal gram-negative bacteria and high mobility group box 1 from the injured epithelial cells activate toll-like receptor 4-signaling pathway and nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 inflammasome; this leads to the release of proinflammatory cytokines such as tumor necrosis factor-alpha and interleukin-1beta.	Prostaglandins	64-77	high mobility group box 1	Homo sapiens	179-204
27488419-0	2017	Every Cloud Has a Silver Lining: Proneurogenic Effects of Abeta Oligomers and HMGB-1 via Activation of the RAGE-NF-kappaB Axis.	Silver	18-24	high mobility group box 1	Homo sapiens	78-84
27931589-6	2016	The serum levels of high-mobility group box 1 protein showed a peak at 8 hours after occlusion in control group, and this elevation was significantly blunted by 4.5 mg/kg NecroX-7 treatment.	necrox-7	171-179	high mobility group box 1	Homo sapiens	20-45
27908419-5	2017	The selenium levels in the tissues were correlated to the genotype of the SELENOP selenium carrier protein, but not to other proteins whose levels have been reported to be responsive to selenium availability, including GPX1, SELENOF and SBP1.	Selenium	4-12	high mobility group box 1	Homo sapiens	237-241
29249869-7	2017	The patients with POCD had higher serum interleukin 1beta (IL-1beta), serum amyloid A (SAA), S100 calcium-binding protein beta (S-100beta), and high mobility group box-1 protein (HMGB-1) levels at 1 and 24 h postoperatively than patients without POCD.	pocd	18-22	high mobility group box 1	Homo sapiens	144-169
29249869-7	2017	The patients with POCD had higher serum interleukin 1beta (IL-1beta), serum amyloid A (SAA), S100 calcium-binding protein beta (S-100beta), and high mobility group box-1 protein (HMGB-1) levels at 1 and 24 h postoperatively than patients without POCD.	pocd	18-22	high mobility group box 1	Homo sapiens	179-185
27560926-7	2017	High glucose induced a significant upregulation of HMGB1 and pSTAT-3 upregulation and nuclear translocation in retinal Muller cells.	Glucose	5-12	high mobility group box 1	Homo sapiens	51-56
27560926-8	2017	GA co-treatment normalized the high-glucose-induced upregulation of HMGB1 and pSTAT-3 upregulation and nuclear translocation in Muller cells.	Gallium	0-2	high mobility group box 1	Homo sapiens	68-73
27560926-8	2017	GA co-treatment normalized the high-glucose-induced upregulation of HMGB1 and pSTAT-3 upregulation and nuclear translocation in Muller cells.	Glucose	36-43	high mobility group box 1	Homo sapiens	68-73
26239884-3	2017	Here, we examined the effects of methylthiouracil (MTU), used as antithyroid drug, by monitoring the effects on lipopolysaccharide (LPS)- or cecal ligation and puncture (CLP)-mediated release of HMGB1, and on the modulation of HMGB1-mediated inflammatory responses.	Methylthiouracil	33-49	high mobility group box 1	Homo sapiens	195-200
26239884-3	2017	Here, we examined the effects of methylthiouracil (MTU), used as antithyroid drug, by monitoring the effects on lipopolysaccharide (LPS)- or cecal ligation and puncture (CLP)-mediated release of HMGB1, and on the modulation of HMGB1-mediated inflammatory responses.	Methylthiouracil	33-49	high mobility group box 1	Homo sapiens	227-232
26239884-3	2017	Here, we examined the effects of methylthiouracil (MTU), used as antithyroid drug, by monitoring the effects on lipopolysaccharide (LPS)- or cecal ligation and puncture (CLP)-mediated release of HMGB1, and on the modulation of HMGB1-mediated inflammatory responses.	Methylthiouracil	51-54	high mobility group box 1	Homo sapiens	195-200
26239884-3	2017	Here, we examined the effects of methylthiouracil (MTU), used as antithyroid drug, by monitoring the effects on lipopolysaccharide (LPS)- or cecal ligation and puncture (CLP)-mediated release of HMGB1, and on the modulation of HMGB1-mediated inflammatory responses.	Methylthiouracil	51-54	high mobility group box 1	Homo sapiens	227-232
26239884-5	2017	MTU inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses in human endothelial cells.	Methylthiouracil	0-3	high mobility group box 1	Homo sapiens	29-34
26239884-5	2017	MTU inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses in human endothelial cells.	Methylthiouracil	0-3	high mobility group box 1	Homo sapiens	53-58
26239884-7	2017	In addition, treatment with MTU reduced CLP-induced release of HMGB1 and sepsis-related mortality and pulmonary injury.	Methylthiouracil	28-31	high mobility group box 1	Homo sapiens	63-68
27983705-6	2016	Our results indicated an efficient reduction in pro-inflammatory factors (TNFalpha, IL-6, MCP-1, HMGB1) upon culture with riboflavin supplementation (500-1000 nM), accompanied by elevation in anti-inflammatory adiponectin and IL-10.	Riboflavin	122-132	high mobility group box 1	Homo sapiens	97-102
27075010-8	2016	Urine protein to urine creatinine ratio (P/C) correlated with urinary HMGB-1 (r = 0.52, p &lt; 0.001), but across the classes this was true only for membranous disease (r = 0.71, p = 0.022, proliferative, p = 0.63; mixed, p = 0.34).	Creatinine	23-33	high mobility group box 1	Homo sapiens	70-76
27959427-0	2017	Inhibiting the cytoplasmic location of HMGB1 reverses cisplatin resistance in human cervical cancer cells.	Cisplatin	54-63	high mobility group box 1	Homo sapiens	39-44
27959427-3	2017	When human cervical cancer cells were treated with 10 microg/ml of cisplatin for 24 and 48 h, high mobility group box 1 (HMGB1) protein expression levels significantly increased in a time-dependent manner.	Cisplatin	67-76	high mobility group box 1	Homo sapiens	94-119
27959427-3	2017	When human cervical cancer cells were treated with 10 microg/ml of cisplatin for 24 and 48 h, high mobility group box 1 (HMGB1) protein expression levels significantly increased in a time-dependent manner.	Cisplatin	67-76	high mobility group box 1	Homo sapiens	121-126
27959427-4	2017	Comparisons between cisplatin-sensitive HeLa cells and cisplatin-resistant HeLa/DDP cells revealed higher levels of HMGB1 in HeLa/DDP cells than in HeLa cells.	Cisplatin	20-29	high mobility group box 1	Homo sapiens	116-121
27959427-4	2017	Comparisons between cisplatin-sensitive HeLa cells and cisplatin-resistant HeLa/DDP cells revealed higher levels of HMGB1 in HeLa/DDP cells than in HeLa cells.	Cisplatin	55-64	high mobility group box 1	Homo sapiens	116-121
27959427-6	2017	Analysis of the distribution of cellular components revealed that HMGB1 translocation from the nucleus to cytoplasm contributed to cisplatin resistance.	Cisplatin	131-140	high mobility group box 1	Homo sapiens	66-71
27959427-7	2017	This was further confirmed by demonstration that ethyl pyruvate treatment suppressed the cytoplasmic translocation of HMGB1, resulting in inhibition of HeLa cell proliferation.	ethyl pyruvate	49-63	high mobility group box 1	Homo sapiens	118-123
27959427-8	2017	Furthermore, endogenous HMGB1 was inhibited with HMGB1-specific short hairpin (sh)RNA, and MTT assay results showed that interference with HMGB1 expression reduced cell viability and potentially reversed cisplatin resistance in HeLa cells.	Cisplatin	204-213	high mobility group box 1	Homo sapiens	24-29
27959427-11	2017	Thus, cytoplasmic HMGB1 translocation and HMGB1-induced cell autophagy are proposed to contribute to cisplatin resistance by inhibiting apoptosis of cervical cancer cells.	Cisplatin	101-110	high mobility group box 1	Homo sapiens	18-23
27959427-11	2017	Thus, cytoplasmic HMGB1 translocation and HMGB1-induced cell autophagy are proposed to contribute to cisplatin resistance by inhibiting apoptosis of cervical cancer cells.	Cisplatin	101-110	high mobility group box 1	Homo sapiens	42-47
27717108-6	2016	The augmenting effects of glycyrrhizin were also observed in other synthetic HMGB1 inhibitors, gabexate mesilate, nafamostat, and sivelestat.	Glycyrrhizic Acid	26-38	high mobility group box 1	Homo sapiens	77-82
27779688-0	2016	[Retracted] Inhibitory effects of ethyl pyruvate administration on human gastric cancer growth via regulation of the HMGB1-RAGE and Akt pathways in vitro and in vivo.	ethyl pyruvate	34-48	high mobility group box 1	Homo sapiens	117-122
28024504-5	2016	RESULTS: Before treatment, the plasma HMGB1 level in ITP group was significantly higher than that in control group (t=4.259, P&lt;0.01), while after treatment it significantly decreased and close to level in control group (t=1.267, P&gt;0.05).	Inosine Triphosphate	53-56	high mobility group box 1	Homo sapiens	38-43
27836008-8	2016	The degree of TAM infiltration was higher in peritumoral tissues with high HMGB1 expression than in peritumoral tissues with low HMGB1 expression (p &lt; 0.001).	tam	14-17	high mobility group box 1	Homo sapiens	75-80
27897164-0	2016	HMGB1-mediated autophagy decreases sensitivity to oxymatrine in SW982 human synovial sarcoma cells.	oxymatrine	50-60	high mobility group box 1	Homo sapiens	0-5
27897164-10	2016	Therefore, we believe that combining OMT with an inhibitor of autophagy or HMGB1 may make OMT more effective in the treatment of human synovial sarcoma.	oxymatrine	90-93	high mobility group box 1	Homo sapiens	75-80
27771306-3	2016	We found that the overexpression of HMGB1 A-box significantly decreased the IL-1beta-stimulated the production of MMP-1, MMP-3 and MMP-9, and also reduced the elevated levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) associated with the inhibition of prostaglandin E2 (PGE2) and nitric oxide (NO) production in IL-1beta-stimulated chondrocytes.	Dinoprostone	280-296	high mobility group box 1	Homo sapiens	36-41
27771306-3	2016	We found that the overexpression of HMGB1 A-box significantly decreased the IL-1beta-stimulated the production of MMP-1, MMP-3 and MMP-9, and also reduced the elevated levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) associated with the inhibition of prostaglandin E2 (PGE2) and nitric oxide (NO) production in IL-1beta-stimulated chondrocytes.	Dinoprostone	298-302	high mobility group box 1	Homo sapiens	36-41
27771306-3	2016	We found that the overexpression of HMGB1 A-box significantly decreased the IL-1beta-stimulated the production of MMP-1, MMP-3 and MMP-9, and also reduced the elevated levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) associated with the inhibition of prostaglandin E2 (PGE2) and nitric oxide (NO) production in IL-1beta-stimulated chondrocytes.	Nitric Oxide	188-200	high mobility group box 1	Homo sapiens	36-41
27836008-8	2016	The degree of TAM infiltration was higher in peritumoral tissues with high HMGB1 expression than in peritumoral tissues with low HMGB1 expression (p &lt; 0.001).	tam	14-17	high mobility group box 1	Homo sapiens	129-134
27826297-8	2016	In contrast to the effects of LPS treatment, the alarmin high-mobility group protein B1 acts in synergy with polyI:C to promote TSLP and IL33 expression.	Poly I-C	109-116	high mobility group box 1	Homo sapiens	57-87
27911399-7	2016	Here, we use a TFO covalently conjugated on the 5" end to a 4"-hydroxymethyl-4,5",8-trimethylpsoralen (HMT) psoralen to generate a site-specific ICL on a mutation-reporter plasmid to use as a tool to study the architectural modification, processing, and repair of complex DNA lesions by HMGB1 in human cells.	tfo	15-18	high mobility group box 1	Homo sapiens	287-292
27911399-7	2016	Here, we use a TFO covalently conjugated on the 5" end to a 4"-hydroxymethyl-4,5",8-trimethylpsoralen (HMT) psoralen to generate a site-specific ICL on a mutation-reporter plasmid to use as a tool to study the architectural modification, processing, and repair of complex DNA lesions by HMGB1 in human cells.	hydroxymethyltrioxsalen	60-101	high mobility group box 1	Homo sapiens	287-292
27911399-7	2016	Here, we use a TFO covalently conjugated on the 5" end to a 4"-hydroxymethyl-4,5",8-trimethylpsoralen (HMT) psoralen to generate a site-specific ICL on a mutation-reporter plasmid to use as a tool to study the architectural modification, processing, and repair of complex DNA lesions by HMGB1 in human cells.	hydroxymethyltrioxsalen	103-106	high mobility group box 1	Homo sapiens	287-292
27911399-8	2016	We describe experimental techniques to prepare TFO-directed ICLs on reporter plasmids, and to interrogate the association of HMGB1 with the TFO-directed ICLs in a cellular context using chromatin immunoprecipitation assays.	tfo	140-143	high mobility group box 1	Homo sapiens	125-130
26431816-0	2016	HMGB1 is responsible for Amitriptyline-mediated cardiac protection from ischemic-reperfusion injury.	Amitriptyline	25-38	high mobility group box 1	Homo sapiens	0-5
27899980-0	2016	Treatment effects of oxaliplatin combined with gemcitabine on colorectal cancer and its influence on HMGB1 expression.	Oxaliplatin	21-32	high mobility group box 1	Homo sapiens	101-106
27899980-0	2016	Treatment effects of oxaliplatin combined with gemcitabine on colorectal cancer and its influence on HMGB1 expression.	gemcitabine	47-58	high mobility group box 1	Homo sapiens	101-106
27899980-1	2016	In the present study, we analyzed the supra-additive effect of oxaliplatin in combination with gemcitabine on terminal colorectal cancer and its influence on high-mobility group box 1 (HMGB1) expression.	Oxaliplatin	63-74	high mobility group box 1	Homo sapiens	158-183
27899980-1	2016	In the present study, we analyzed the supra-additive effect of oxaliplatin in combination with gemcitabine on terminal colorectal cancer and its influence on high-mobility group box 1 (HMGB1) expression.	Oxaliplatin	63-74	high mobility group box 1	Homo sapiens	185-190
27899980-12	2016	We conclude that the reduced expression rate of HMGB1 in terminal colorectal cancer cases was probably related to the effects of oxaliplatin combined with gemcitabine.	Oxaliplatin	129-140	high mobility group box 1	Homo sapiens	48-53
27899980-12	2016	We conclude that the reduced expression rate of HMGB1 in terminal colorectal cancer cases was probably related to the effects of oxaliplatin combined with gemcitabine.	gemcitabine	155-166	high mobility group box 1	Homo sapiens	48-53
27807322-8	2016	:  Results: Compared with the control group, the cell activity was significantly decreased and the level of serum HMGB1 was significantly increased in the chemotherapeutic (VCR, VP-16, Ara-C, ADM and As2O3) groups (all P&lt;0.05).	Cytarabine	185-190	high mobility group box 1	Homo sapiens	114-119
27807322-8	2016	:  Results: Compared with the control group, the cell activity was significantly decreased and the level of serum HMGB1 was significantly increased in the chemotherapeutic (VCR, VP-16, Ara-C, ADM and As2O3) groups (all P&lt;0.05).	Doxorubicin	192-195	high mobility group box 1	Homo sapiens	114-119
27807322-8	2016	:  Results: Compared with the control group, the cell activity was significantly decreased and the level of serum HMGB1 was significantly increased in the chemotherapeutic (VCR, VP-16, Ara-C, ADM and As2O3) groups (all P&lt;0.05).	Arsenic Trioxide	200-205	high mobility group box 1	Homo sapiens	114-119
27899819-0	2016	4-cholesten-3-one suppresses lung adenocarcinoma metastasis by regulating translocation of HMGB1, HIF1alpha and Caveolin-1.	cholest-4-en-3-one	0-17	high mobility group box 1	Homo sapiens	91-96
27704361-5	2016	Our results found that the risk of susceptibility to cervical invasive cancer was 1.85 (95 % CI 1.12-3.04; p = 0.016) in women with TC and 1.99 (95 % CI 1.24-3.23; p = 0.005) in women with TC/CC after adjusting for age, using TT as a comparison reference in HMGB1 SNP rs1412125.	Technetium	132-134	high mobility group box 1	Homo sapiens	258-263
27704361-8	2016	In conclusion, Taiwanese women with TC or TC/CC in HMGB1 SNP rs1412125 as well as CG or CG/GG in rs2249825 were susceptible to the development of cervical invasive cancer.	Technetium	36-38	high mobility group box 1	Homo sapiens	51-56
27704361-8	2016	In conclusion, Taiwanese women with TC or TC/CC in HMGB1 SNP rs1412125 as well as CG or CG/GG in rs2249825 were susceptible to the development of cervical invasive cancer.	Technetium	42-44	high mobility group box 1	Homo sapiens	51-56
27451951-0	2016	DNA-HMGB1 interaction: The nuclear aggregates of polyamine mediation.	Polyamines	49-58	high mobility group box 1	Homo sapiens	4-9
27383136-5	2016	Interestingly, with the increasing concentration of DDP, HMGB1 was gradually located into cytoplasm in cisplatin-sensitive A549 cells.	Cisplatin	103-112	high mobility group box 1	Homo sapiens	57-62
27383136-6	2016	Moreover, interference with endogenous HMGB1 sensitized the effects of chemotherapeutic drugs, including 5-Fu, DDP, and OXA.	Fluorouracil	105-109	high mobility group box 1	Homo sapiens	39-44
27473010-9	2016	CONCLUSION: MCZ may have preventive roles in the clinical management of IP in ELBWI by the suppression of IL-8 and HMGB-1.	Miconazole	12-15	high mobility group box 1	Homo sapiens	115-121
27413111-0	2016	From the Cover: Tetrachlorobenzoquinone Exerts Neurological Proinflammatory Activity by Promoting HMGB1 Release, Which Induces TLR4 Clustering within the Lipid Raft.	tetrachlorobenzoquinone	16-39	high mobility group box 1	Homo sapiens	98-103
27413111-5	2016	Indeed, this study demonstrated that TCBQ induces the secretion/translocation of HMGB1, which in turn activates its receptors, TLR family gene (especially TLR4) and receptor for advanced glycation end-products (RAGE) expressions.	tetrachlorobenzoquinone	37-41	high mobility group box 1	Homo sapiens	81-86
27413111-9	2016	In summary, our current findings revealed a previously unknown mechanism of TCBQ-induced neurological inflammation related to HMGB1-TLR4 signaling.	tetrachlorobenzoquinone	76-80	high mobility group box 1	Homo sapiens	126-131
27924158-0	2016	Lycorine Downregulates HMGB1 to Inhibit Autophagy and Enhances Bortezomib Activity in Multiple Myeloma.	lycorine	0-8	high mobility group box 1	Homo sapiens	23-28
27924158-4	2016	We identified High mobility group box 1 (HMGB1), an important regulator of autophagy, as the most aberrantly expressed protein after lycorine treatment and as a critical mediator of lycorine activity.	lycorine	133-141	high mobility group box 1	Homo sapiens	14-39
27924158-4	2016	We identified High mobility group box 1 (HMGB1), an important regulator of autophagy, as the most aberrantly expressed protein after lycorine treatment and as a critical mediator of lycorine activity.	lycorine	133-141	high mobility group box 1	Homo sapiens	41-46
27924158-4	2016	We identified High mobility group box 1 (HMGB1), an important regulator of autophagy, as the most aberrantly expressed protein after lycorine treatment and as a critical mediator of lycorine activity.	lycorine	182-190	high mobility group box 1	Homo sapiens	14-39
27924158-4	2016	We identified High mobility group box 1 (HMGB1), an important regulator of autophagy, as the most aberrantly expressed protein after lycorine treatment and as a critical mediator of lycorine activity.	lycorine	182-190	high mobility group box 1	Homo sapiens	41-46
27924158-7	2016	Mechanistically, proteasomal degradation of HMGB1 by lycorine inhibits the activation of MEK-ERK thereby decreases phosphorylation of Bcl-2 resulting in constitutive association of Bcl-2 with Beclin-1.	lycorine	53-61	high mobility group box 1	Homo sapiens	44-49
27924158-8	2016	In addition, we observed higher HMGB1 expression in bortezomib resistant cells and the combination of bortezomib plus lycorine was highly efficient in vitro and in vivo myeloma models as well as in re-sensitizing resistant cells to bortezomib.	Bortezomib	52-62	high mobility group box 1	Homo sapiens	32-37
27924158-8	2016	In addition, we observed higher HMGB1 expression in bortezomib resistant cells and the combination of bortezomib plus lycorine was highly efficient in vitro and in vivo myeloma models as well as in re-sensitizing resistant cells to bortezomib.	Bortezomib	102-112	high mobility group box 1	Homo sapiens	32-37
27924158-8	2016	In addition, we observed higher HMGB1 expression in bortezomib resistant cells and the combination of bortezomib plus lycorine was highly efficient in vitro and in vivo myeloma models as well as in re-sensitizing resistant cells to bortezomib.	lycorine	118-126	high mobility group box 1	Homo sapiens	32-37
27924158-8	2016	In addition, we observed higher HMGB1 expression in bortezomib resistant cells and the combination of bortezomib plus lycorine was highly efficient in vitro and in vivo myeloma models as well as in re-sensitizing resistant cells to bortezomib.	Bortezomib	102-112	high mobility group box 1	Homo sapiens	32-37
27568461-8	2016	HMGB1 levels were significantly decreased after sildenafil therapy for 6months (P&lt;0.01).	Sildenafil Citrate	48-58	high mobility group box 1	Homo sapiens	0-5
27568461-9	2016	CONCLUSIONS: Our study suggests that serum HMGB1 level may be used as a biomarker to identify PAH in CHD patients, assess pulmonary vascular remodeling, and evaluate the treatment response to sildenafil.	Sildenafil Citrate	192-202	high mobility group box 1	Homo sapiens	43-48
27198223-0	2016	PKCalpha and HMGB1 antagonistically control hydrogen peroxide-induced poly-ADP-ribose formation.	Hydrogen Peroxide	44-61	high mobility group box 1	Homo sapiens	13-18
27198223-0	2016	PKCalpha and HMGB1 antagonistically control hydrogen peroxide-induced poly-ADP-ribose formation.	poly-adp	70-78	high mobility group box 1	Homo sapiens	13-18
27198223-8	2016	Together, these results identify PKCalpha and HMGB1 as important co-regulators involved in H2O2-induced PAR formation, a finding that may have important relevance for oxidative stress-associated pathophysiological conditions.	Hydrogen Peroxide	91-95	high mobility group box 1	Homo sapiens	46-51
27512095-6	2016	Results demonstrated that either IL-1beta or HMGB1 promoted the release of the inflammatory cytokines such as prostaglandin E2 (PGE2), TNF-alpha, IL-6 and IL-8 in human IVD cells.	Dinoprostone	110-126	high mobility group box 1	Homo sapiens	45-50
27512095-6	2016	Results demonstrated that either IL-1beta or HMGB1 promoted the release of the inflammatory cytokines such as prostaglandin E2 (PGE2), TNF-alpha, IL-6 and IL-8 in human IVD cells.	Dinoprostone	128-132	high mobility group box 1	Homo sapiens	45-50
27725858-5	2016	The targeting effect of HMGB1 by miR-218 was measured with luciferase reporter assay.	mir-218	33-40	high mobility group box 1	Homo sapiens	24-29
27899819-8	2016	4-cholesten-3-one-induced autophagy facilitated the release of HMGB1 from nuclei to cytoplasm, blocking nuclear translocation of HIF1alpha and activation of MMP2 and MMP9.	cholest-4-en-3-one	0-17	high mobility group box 1	Homo sapiens	63-68
27285673-5	2016	The aim of this study was to investigate whether the expression of HMGB1differed between early onset and late onset preeclampsia or severe and mild preeclampsia and whether its expression correlated with the levels of uric acid.	Uric Acid	218-227	high mobility group box 1	Homo sapiens	67-72
27093475-7	2016	Moreover, CS extract induced cellular senescence in cultured human airway epithelial cells, represented by induced senescence-associated beta-galactosidase activity, inhibited cell proliferation, increased p21 expression, and increased release of high-mobility group box 1 and IL-6.	Cesium	10-12	high mobility group box 1	Homo sapiens	247-272
27457217-3	2016	We showed recently that an epirubicin/docetaxel therapy is associated with an increase in the cell death marker high-mobility group box 1 protein (HMGB1) in the circulation.	Epirubicin	27-37	high mobility group box 1	Homo sapiens	112-137
27457217-3	2016	We showed recently that an epirubicin/docetaxel therapy is associated with an increase in the cell death marker high-mobility group box 1 protein (HMGB1) in the circulation.	Epirubicin	27-37	high mobility group box 1	Homo sapiens	147-152
27457217-3	2016	We showed recently that an epirubicin/docetaxel therapy is associated with an increase in the cell death marker high-mobility group box 1 protein (HMGB1) in the circulation.	Docetaxel	38-47	high mobility group box 1	Homo sapiens	112-137
27457217-3	2016	We showed recently that an epirubicin/docetaxel therapy is associated with an increase in the cell death marker high-mobility group box 1 protein (HMGB1) in the circulation.	Docetaxel	38-47	high mobility group box 1	Homo sapiens	147-152
27285673-8	2016	The expression of HMGB1 in preeclamptic placentae or in first trimester and term placentae that had been treated with uric acid was measured.	Uric Acid	118-127	high mobility group box 1	Homo sapiens	18-23
27285673-10	2016	The circulating levels of uric acid were significantly increased in preeclampsia and correlated with the expression of HMGB1.	Uric Acid	26-35	high mobility group box 1	Homo sapiens	119-124
27602152-11	2016	The results revealed that the oncogenic cluster miRs 221/222 were more highly expressed by the most undifferentiated cell line [SK-N-BE(2)] compared with the the less tumorigenic cell line (SH-SY5Y) and that exogenous HMGB1 increases this expression.	sk-n-be	128-135	high mobility group box 1	Homo sapiens	218-223
27522665-0	2016	Methotrexate affects HMGB1 expression in rheumatoid arthritis, and the downregulation of HMGB1 prevents rheumatoid arthritis progression.	Methotrexate	0-12	high mobility group box 1	Homo sapiens	21-26
27522665-2	2016	Recent studies have shown that methotrexate (MTX) may inhibit the expression of HMGB1.	Methotrexate	31-43	high mobility group box 1	Homo sapiens	80-85
27522665-2	2016	Recent studies have shown that methotrexate (MTX) may inhibit the expression of HMGB1.	Methotrexate	45-48	high mobility group box 1	Homo sapiens	80-85
27522665-3	2016	This study examined whether HMGB1 might be involved in the treatment of RA using MTX.	Methotrexate	81-84	high mobility group box 1	Homo sapiens	28-33
27522665-10	2016	At the tissue level, HMGB1 expression in synovial membrane did not differ significantly between the OA and RA-MTX groups, but was significantly lower in these groups than in the RA-noMTX group.	Methotrexate	110-113	high mobility group box 1	Homo sapiens	21-26
27522665-13	2016	These results showed that MTX reduced HMGB1 expression in RA synovial tissues, and through the downregulation of HMGB1 expression in tissues, MTX may slow disease progression of RA.	Methotrexate	26-29	high mobility group box 1	Homo sapiens	38-43
27522665-13	2016	These results showed that MTX reduced HMGB1 expression in RA synovial tissues, and through the downregulation of HMGB1 expression in tissues, MTX may slow disease progression of RA.	Methotrexate	142-145	high mobility group box 1	Homo sapiens	113-118
27602152-12	2016	In addition, HMGB1 modulates PTEN expression via miR-221/222, as demonstrated by transiently blocking miR-221/222 with anti-sense oligonucleotides.	Oligonucleotides	130-146	high mobility group box 1	Homo sapiens	13-18
27682500-0	2016	[The wle of high mobility group protein B1(HMGB-1) on inflammatony responese and pulmonary fibrosis induced by silica dusty].	Silicon Dioxide	111-117	high mobility group box 1	Homo sapiens	12-42
27378565-7	2016	Noteworthy, salicylic acid, a metabolite of aspirin, has been recently found to inhibit HMGB1.	Salicylic Acid	12-26	high mobility group box 1	Homo sapiens	88-93
27378565-7	2016	Noteworthy, salicylic acid, a metabolite of aspirin, has been recently found to inhibit HMGB1.	Aspirin	44-51	high mobility group box 1	Homo sapiens	88-93
27378565-9	2016	Notably, high levels of serum HMGB1, in particular of the hyper-acetylated and disulfide isoforms, are sensitive disease biomarkers and are associated with different disease stages.	Disulfides	79-88	high mobility group box 1	Homo sapiens	30-35
27544687-6	2016	We also found that both glycyrrhizin-mediated inhibition of HMGB1 and intracerebroventricular neutralizing antibody treatments before middle cerebral artery occlusion onset diminish infarct volume.	Glycyrrhizic Acid	24-36	high mobility group box 1	Homo sapiens	60-65
27622063-8	2016	We show that both platinum drugs triggered translocation of calreticulin and HSP70, as well as the release of ATP and HMGB1.	Platinum	18-26	high mobility group box 1	Homo sapiens	118-123
26888251-9	2016	HMGB1 was significantly increased in RECs and Muller cells grown in high-glucose culture conditions, which was subsequently reduced with Compound 49b treatment.	Glucose	73-80	high mobility group box 1	Homo sapiens	0-5
26888251-10	2016	Our findings suggest that high glucose may increase HMGB1 levels that lead to increased TLR4 signaling.	Glucose	31-38	high mobility group box 1	Homo sapiens	52-57
27553758-10	2016	Direct in vitro BBB integrity assessment further revealed a significant and concentration-dependent increase in paracellular permeability to dextrans by HMGB1 or alpha-thrombin, possibly through disruption of zona occludins-1 bands.	Dextrans	141-149	high mobility group box 1	Homo sapiens	153-158
27682500-0	2016	[The wle of high mobility group protein B1(HMGB-1) on inflammatony responese and pulmonary fibrosis induced by silica dusty].	Silicon Dioxide	111-117	high mobility group box 1	Homo sapiens	43-49
26546554-9	2016	It was observed that aluminum potentially enhanced protein levels of PERK, EIF2alpha, caspase 9, caspase 3, and inflammatory markers like NF-kappaB, NLRP3, HMGB1, and nitric oxide (NO).	Aluminum	21-29	high mobility group box 1	Homo sapiens	156-161
27434276-12	2016	Ex vivo, recombinant-HMGB1 potentiated cytokine release (e.g. TNF-alpha) when combined with lipoarabinomannan.	lipoarabinomannan	92-109	high mobility group box 1	Homo sapiens	21-26
26845344-8	2016	The functional consequence of HMGB1 depletion in HCT116 and INS1 cells was reduced insulin and TCF7L2 mRNA expression, TCF7L2 transcriptional activity and glucose stimulated insulin secretion.	Glucose	155-162	high mobility group box 1	Homo sapiens	30-35
27474498-7	2016	administration of the anti-HMGB1-neutralizing antibody or recombinant human soluble thrombomodulin (rhsTM), known to inactivate HMGB1, prevented the development of hyperalgesia and/or allodynia induced by paclitaxel or vincristine in rats.	Paclitaxel	205-215	high mobility group box 1	Homo sapiens	27-32
27474498-7	2016	administration of the anti-HMGB1-neutralizing antibody or recombinant human soluble thrombomodulin (rhsTM), known to inactivate HMGB1, prevented the development of hyperalgesia and/or allodynia induced by paclitaxel or vincristine in rats.	Paclitaxel	205-215	high mobility group box 1	Homo sapiens	128-133
27474498-7	2016	administration of the anti-HMGB1-neutralizing antibody or recombinant human soluble thrombomodulin (rhsTM), known to inactivate HMGB1, prevented the development of hyperalgesia and/or allodynia induced by paclitaxel or vincristine in rats.	Vincristine	219-230	high mobility group box 1	Homo sapiens	27-32
27174706-5	2016	In addition, we evaluated the expression of the high mobility group box-1 protein (HMGB1), a chromatin remodelling protein involved in DSBs repair and obesity.	dsbs	135-139	high mobility group box 1	Homo sapiens	48-73
26482581-2	2016	Recent findings suggest that the redox state of HMGB1 is a critical molecular feature of HMGB1 such that the reduced form (fr-HMGB1) is chemotactic, while the disulfide form (ds-HMGB1) is pro-inflammatory.	Disulfides	159-168	high mobility group box 1	Homo sapiens	48-53
26482581-2	2016	Recent findings suggest that the redox state of HMGB1 is a critical molecular feature of HMGB1 such that the reduced form (fr-HMGB1) is chemotactic, while the disulfide form (ds-HMGB1) is pro-inflammatory.	Disulfides	159-168	high mobility group box 1	Homo sapiens	89-94
26482581-2	2016	Recent findings suggest that the redox state of HMGB1 is a critical molecular feature of HMGB1 such that the reduced form (fr-HMGB1) is chemotactic, while the disulfide form (ds-HMGB1) is pro-inflammatory.	Disulfides	159-168	high mobility group box 1	Homo sapiens	89-94
26482581-2	2016	Recent findings suggest that the redox state of HMGB1 is a critical molecular feature of HMGB1 such that the reduced form (fr-HMGB1) is chemotactic, while the disulfide form (ds-HMGB1) is pro-inflammatory.	Disulfides	159-168	high mobility group box 1	Homo sapiens	89-94
26482581-16	2016	Consistent with prior reports, the present findings demonstrate that the disulfide form of HMGB1 not only potentiates the neuroinflammatory response to a subsequent immune challenge in vivo, but also potentiates the sickness response to that challenge.	Disulfides	73-82	high mobility group box 1	Homo sapiens	91-96
26482581-19	2016	Taken together, the present results suggest that the redox state of HMGB1 is a critical determinant of the priming properties of HMGB1 such that the disulfide form of HMGB1 induces a primed immunophenotype in the CNS, which may result in an exacerbated neuroinflammatory response upon exposure to a subsequent pro-inflammatory stimulus.	Disulfides	149-158	high mobility group box 1	Homo sapiens	68-73
26482581-19	2016	Taken together, the present results suggest that the redox state of HMGB1 is a critical determinant of the priming properties of HMGB1 such that the disulfide form of HMGB1 induces a primed immunophenotype in the CNS, which may result in an exacerbated neuroinflammatory response upon exposure to a subsequent pro-inflammatory stimulus.	Disulfides	149-158	high mobility group box 1	Homo sapiens	129-134
26482581-19	2016	Taken together, the present results suggest that the redox state of HMGB1 is a critical determinant of the priming properties of HMGB1 such that the disulfide form of HMGB1 induces a primed immunophenotype in the CNS, which may result in an exacerbated neuroinflammatory response upon exposure to a subsequent pro-inflammatory stimulus.	Disulfides	149-158	high mobility group box 1	Homo sapiens	129-134
26896489-4	2016	High mobility group box 1 (HMGB1) protein is considered to be involved in the removal of the lesions as it binds with high affinity to cisplatin/DNA adducts.	Cisplatin	135-144	high mobility group box 1	Homo sapiens	0-25
26896489-4	2016	High mobility group box 1 (HMGB1) protein is considered to be involved in the removal of the lesions as it binds with high affinity to cisplatin/DNA adducts.	Cisplatin	135-144	high mobility group box 1	Homo sapiens	27-32
26896489-8	2016	H1299 cells overexpressing HMGB1 were significantly sensitized to treatment with cisplatin demonstrating the close relation between the role of HMGB1 in repair of cis-platinated DNA and the efficiency of the anticancer drug, the process being modulated by the C-terminus.	Cisplatin	81-90	high mobility group box 1	Homo sapiens	27-32
26896489-8	2016	H1299 cells overexpressing HMGB1 were significantly sensitized to treatment with cisplatin demonstrating the close relation between the role of HMGB1 in repair of cis-platinated DNA and the efficiency of the anticancer drug, the process being modulated by the C-terminus.	Cisplatin	81-90	high mobility group box 1	Homo sapiens	144-149
26896489-9	2016	In A549 cells with functional p53, the repair of cisplatin/DNA adducts is determined by a complex action of HMGB1 and p53 as an increase of DNA repair capacity was registered only after silencing of both proteins.	Cisplatin	49-58	high mobility group box 1	Homo sapiens	108-113
27174706-5	2016	In addition, we evaluated the expression of the high mobility group box-1 protein (HMGB1), a chromatin remodelling protein involved in DSBs repair and obesity.	dsbs	135-139	high mobility group box 1	Homo sapiens	83-88
27174706-7	2016	Concordantly, 1) HMGB1 levels of obese individuals increased and decreased at 2h- or 4 h-post mutagen treatment, respectively, and 2) the opposite occurred for the normal weight adolescents where the protein was down-expressed at 2h and over-expressed at 4h.	Deuterium	78-80	high mobility group box 1	Homo sapiens	17-22
26952810-4	2016	MIF-induced ROS led to ERK phosphorylation, which facilitated HMGB1 release from the nucleus to the cytoplasm.	ros	12-15	high mobility group box 1	Homo sapiens	62-67
27446084-9	2016	Interestingly, exposure of the cells to HMGB1 in inflammatory conditions increased synergistically Amigo2 expression and significantly reduced Cd-mediated cellular toxicity.	Cadmium	143-145	high mobility group box 1	Homo sapiens	40-45
26733616-0	2016	HMGB1 and Its Hyperacetylated Isoform are Sensitive and Specific Serum Biomarkers to Detect Asbestos Exposure and to Identify Mesothelioma Patients.	Asbestos	92-100	high mobility group box 1	Homo sapiens	0-5
26733616-1	2016	PURPOSE: To determine whether serum levels of high mobility group box protein 1 (HMGB1) could differentiate malignant mesothelioma patients, asbestos-exposed individuals, and unexposed controls.	Asbestos	141-149	high mobility group box 1	Homo sapiens	81-86
26733616-4	2016	RESULTS: HMGB1 serum levels reliably distinguished malignant mesothelioma patients, asbestos-exposed individuals, and unexposed controls.	Asbestos	84-92	high mobility group box 1	Homo sapiens	9-14
26733616-5	2016	Total HMGB1 was significantly higher in malignant mesothelioma patients and asbestos-exposed individuals compared with healthy controls.	Asbestos	76-84	high mobility group box 1	Homo sapiens	6-11
26733616-6	2016	Hyperacetylated HMGB1 was significantly higher in malignant mesothelioma patients compared with asbestos-exposed individuals and healthy controls, and did not vary with tumor stage.	Asbestos	96-104	high mobility group box 1	Homo sapiens	16-21
26733616-7	2016	At the cut-off value of 2.00 ng/mL, the sensitivity and specificity of serum hyperacetylated HMGB1 in differentiating malignant mesothelioma patients from asbestos-exposed individuals and healthy controls was 100%, outperforming other previously proposed biomarkers.	Asbestos	155-163	high mobility group box 1	Homo sapiens	93-98
26733616-9	2016	CONCLUSIONS: Our results are significant and clinically relevant as they provide the first biomarker of asbestos exposure and indicate that hyperacetylated HMGB1 is an accurate biomarker to differentiate malignant mesothelioma patients from individuals occupationally exposed to asbestos and unexposed controls.	Asbestos	104-112	high mobility group box 1	Homo sapiens	156-161
26733616-9	2016	CONCLUSIONS: Our results are significant and clinically relevant as they provide the first biomarker of asbestos exposure and indicate that hyperacetylated HMGB1 is an accurate biomarker to differentiate malignant mesothelioma patients from individuals occupationally exposed to asbestos and unexposed controls.	Asbestos	279-287	high mobility group box 1	Homo sapiens	156-161
26921471-0	2016	In-vivo evidence that high mobility group box 1 exerts deleterious effects in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model and Parkinson"s disease which can be attenuated by glycyrrhizin.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	82-126	high mobility group box 1	Homo sapiens	22-47
26921471-0	2016	In-vivo evidence that high mobility group box 1 exerts deleterious effects in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model and Parkinson"s disease which can be attenuated by glycyrrhizin.	Glycyrrhizic Acid	184-196	high mobility group box 1	Homo sapiens	22-47
27348219-5	2016	Our results showed that HMGB1 levels are increased in patients with CCHFV, DOBV or PUUV infection.	dobv	75-79	high mobility group box 1	Homo sapiens	24-29
27348219-7	2016	Our results indicate that HMGB1 could be a useful prognostic biomarker for disease severity in PUUV and CCHFV infection, where the difference between the mild and severe patients group was highly significant.	puuv	95-99	high mobility group box 1	Homo sapiens	26-31
27348219-8	2016	Even in patients with severe DOBV infection concentrations of HMGB1 were 2.8-times higher than in the mild group, but the difference was not statistically significant.	dobv	29-33	high mobility group box 1	Homo sapiens	62-67
26873936-5	2016	Aspirin consumption significantly blocked thrombin- and collagen-induced increases in exosome cargo levels of chemokines and HMGB1, without altering total exosome secretion or GPVI cargo.	Aspirin	0-7	high mobility group box 1	Homo sapiens	125-130
26923673-0	2016	Structural aspects of the interaction of anticancer drug Actinomycin-D to the GC rich region of hmgb1 gene.	Dactinomycin	57-70	high mobility group box 1	Homo sapiens	96-101
26923673-5	2016	The molecular interaction of actinomycin (ACT) with the regulatory region of hmgb1 gene was characterized by spectroscopic, calorimetric and molecular docking studies.	Dactinomycin	29-40	high mobility group box 1	Homo sapiens	77-82
26923673-6	2016	The hypochromic and bathochromic shift in the absorption spectrum, stabilization of 25RY duplex against thermal denaturation, perturbation of CD spectrum of duplex and enhancement of fluorescence intensity of actinomycin indicate strong binding of actinomycin to the hmgb1 promoter region (25RY).The energetics was characterized to be endothermic and entropy driven.	Dactinomycin	209-220	high mobility group box 1	Homo sapiens	267-272
26923673-6	2016	The hypochromic and bathochromic shift in the absorption spectrum, stabilization of 25RY duplex against thermal denaturation, perturbation of CD spectrum of duplex and enhancement of fluorescence intensity of actinomycin indicate strong binding of actinomycin to the hmgb1 promoter region (25RY).The energetics was characterized to be endothermic and entropy driven.	Dactinomycin	248-259	high mobility group box 1	Homo sapiens	267-272
26956470-0	2016	Propofol Protects Rats and Human Alveolar Epithelial Cells Against Lipopolysaccharide-Induced Acute Lung Injury via Inhibiting HMGB1 Expression.	Propofol	0-8	high mobility group box 1	Homo sapiens	127-132
26956470-10	2016	Propofol protects rats and human alveolar epithelial cells against HMGB1 expression in a rat model of LPS-induced ALI.	Propofol	0-8	high mobility group box 1	Homo sapiens	67-72
27247778-7	2016	Plasma levels of HMGB-1 on day 1 correlated with prognostic parameters (estimated interval to return of spontaneous circulation, lactate, and NH3), tissue damage, systemic inflammation, and disease severity.	Lactic Acid	129-136	high mobility group box 1	Homo sapiens	17-23
27247709-2	2016	We show that HMGB1 alters the structure and stability of the canonical nucleosome (N) in a nonenzymatic, adenosine triphosphate-independent manner.	Adenosine Triphosphate	105-127	high mobility group box 1	Homo sapiens	13-18
27009165-7	2016	In particular, doxorubicin triggers an HMGB1 autocrine/paracrine loop with its receptor, TLR4, which is also upregulated in DX-LCLs and is responsible for NF-kappaB activation and a delayed apoptosis that allows a prolonged stimulation of EBV-specific T-cell precursors.	Doxorubicin	15-26	high mobility group box 1	Homo sapiens	39-44
26873936-7	2016	The plasma platelet-derived exosome number is lower and its chemokine and HMGB1 levels higher after age 65 yr. Aspirin consumption significantly suppressed cargo protein levels of plasma platelet-derived exosomes without altering total levels of exosomes.	Aspirin	111-118	high mobility group box 1	Homo sapiens	74-79
27035254-7	2016	HMGB1 increased FITC-dextran permeability, but suppressed epithelial resistance in a dose- and time-dependent manner.	fluorescein isothiocyanate dextran	16-28	high mobility group box 1	Homo sapiens	0-5
27035254-11	2016	Anti-RAGE antibody and the ERK1/2 inhibitor, U0126, attenuated the HMGB1-mediated changes in barrier permeability, restored the expression levels of occludin and claudin-1 and pevented the redistribution of E-cadherin and beta-catenin.	U 0126	45-50	high mobility group box 1	Homo sapiens	67-72
25787746-5	2016	RESULTS: Studies from our laboratory employing reverse transcription polymerase chain reaction (RT-PCR) to assess mRNA, immunohistochemistry and Western blot analysis to assess protein expression, and others suggest that ethanol increases brain neuroimmune gene and protein expression through two distinct mechanisms involving (1) systemic induction of innate immune molecules that are transported from blood to the brain and (2) the direct release of high-mobility group box 1 (HMGB1) from neurons in the brain.	Ethanol	221-228	high mobility group box 1	Homo sapiens	452-477
25787746-5	2016	RESULTS: Studies from our laboratory employing reverse transcription polymerase chain reaction (RT-PCR) to assess mRNA, immunohistochemistry and Western blot analysis to assess protein expression, and others suggest that ethanol increases brain neuroimmune gene and protein expression through two distinct mechanisms involving (1) systemic induction of innate immune molecules that are transported from blood to the brain and (2) the direct release of high-mobility group box 1 (HMGB1) from neurons in the brain.	Ethanol	221-228	high mobility group box 1	Homo sapiens	479-484
25787746-8	2016	Expression of HMGB1, TLRs, and other ISMs is increased several-fold in the human orbital frontal cortex, and expression of these molecules is highly correlated with each other as well as lifetime alcohol consumption and age of drinking onset.	Alcohols	196-203	high mobility group box 1	Homo sapiens	14-19
25787746-9	2016	CONCLUSIONS: The persistent and cumulative nature of alcohol on HMGB1 and TLR gene induction support their involvement in alcohol-induced long-term changes in brain function and neurodegeneration.	Alcohols	53-60	high mobility group box 1	Homo sapiens	64-69
25787746-9	2016	CONCLUSIONS: The persistent and cumulative nature of alcohol on HMGB1 and TLR gene induction support their involvement in alcohol-induced long-term changes in brain function and neurodegeneration.	Alcohols	122-129	high mobility group box 1	Homo sapiens	64-69
28773427-4	2016	In this study, Vascular Endothelial Growth Factor (VEGF) and High Mobility Group Box 1 (HMGB1) were used for incorporation into poly-epsilon-caprolactone (PCL)-coated porous titanium implants.	polycaprolactone	128-153	high mobility group box 1	Homo sapiens	61-86
28773427-4	2016	In this study, Vascular Endothelial Growth Factor (VEGF) and High Mobility Group Box 1 (HMGB1) were used for incorporation into poly-epsilon-caprolactone (PCL)-coated porous titanium implants.	polycaprolactone	128-153	high mobility group box 1	Homo sapiens	88-93
28773427-4	2016	In this study, Vascular Endothelial Growth Factor (VEGF) and High Mobility Group Box 1 (HMGB1) were used for incorporation into poly-epsilon-caprolactone (PCL)-coated porous titanium implants.	polycaprolactone	155-158	high mobility group box 1	Homo sapiens	61-86
28773427-4	2016	In this study, Vascular Endothelial Growth Factor (VEGF) and High Mobility Group Box 1 (HMGB1) were used for incorporation into poly-epsilon-caprolactone (PCL)-coated porous titanium implants.	polycaprolactone	155-158	high mobility group box 1	Homo sapiens	88-93
26592934-0	2016	Anti-septic effects of dabrafenib on HMGB1-mediated inflammatory responses.	dabrafenib	23-33	high mobility group box 1	Homo sapiens	37-42
26481429-3	2016	The extracellular function of HMGB1 is dependent upon redox modification of cysteine residues that control chemoattractant and cytokine-inducing properties.	Cysteine	76-84	high mobility group box 1	Homo sapiens	30-35
26481429-5	2016	RECENT ADVANCES: HMGB1 isoforms have been shown to be more sensitive biomarkers than ALT for predicting DILI development and the requirement for liver transplant following acetaminophen (APAP) overdose.	Acetaminophen	172-185	high mobility group box 1	Homo sapiens	17-22
26481429-5	2016	RECENT ADVANCES: HMGB1 isoforms have been shown to be more sensitive biomarkers than ALT for predicting DILI development and the requirement for liver transplant following acetaminophen (APAP) overdose.	Acetaminophen	187-191	high mobility group box 1	Homo sapiens	17-22
26715031-6	2016	The redox states of the cysteines in positions 23, 45, and 106 determine the biological activity of the extracellular HMGB1.	Cysteine	24-33	high mobility group box 1	Homo sapiens	118-123
25532033-7	2016	Monomethylation of lysine 43 (K43), a proposed neutrophil-specific PTM, was strongly associated with high HMGB1 levels, implying that neutrophils are a source of released HMGB1.	Lysine	19-25	high mobility group box 1	Homo sapiens	106-111
25532033-7	2016	Monomethylation of lysine 43 (K43), a proposed neutrophil-specific PTM, was strongly associated with high HMGB1 levels, implying that neutrophils are a source of released HMGB1.	Lysine	19-25	high mobility group box 1	Homo sapiens	171-176
26592934-4	2016	Here, we examined the effects of dabrafenib (DAB) on the modulation of HMGB1-mediated septic responses.	dabrafenib	33-43	high mobility group box 1	Homo sapiens	71-76
26592934-4	2016	Here, we examined the effects of dabrafenib (DAB) on the modulation of HMGB1-mediated septic responses.	dabrafenib	45-48	high mobility group box 1	Homo sapiens	71-76
26592934-5	2016	DAB inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses by enhancing the expressions of cell adhesion molecules (CAMs) in human endothelial cells.	dabrafenib	0-3	high mobility group box 1	Homo sapiens	29-34
26592934-5	2016	DAB inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses by enhancing the expressions of cell adhesion molecules (CAMs) in human endothelial cells.	dabrafenib	0-3	high mobility group box 1	Homo sapiens	53-58
26592934-6	2016	In addition, treatment with DAB inhibited the HMGB1 secretion by CLP and sepsis-related mortality and pulmonary injury.	dabrafenib	28-31	high mobility group box 1	Homo sapiens	46-51
26592934-7	2016	This study demonstrated that DAB could be alternative therapeutic options for sepsis or septic shock via the inhibition of the HMGB1 signaling pathway.	dabrafenib	29-32	high mobility group box 1	Homo sapiens	127-132
27026438-11	2016	CNT-L tended to induce stronger cytotoxicity and 8-nitroG formation than CNT-S. Endocytosis inhibitors, TLR9 siRNA and antibodies against HMGB1 and RAGE largely reduced MWCNT-induced 8-nitroG formation.	8-nitroguanine	183-191	high mobility group box 1	Homo sapiens	138-143
27026438-0	2016	Multi-walled carbon nanotube induces nitrative DNA damage in human lung epithelial cells via HMGB1-RAGE interaction and Toll-like receptor 9 activation.	Carbon	13-19	high mobility group box 1	Homo sapiens	93-98
27026438-8	2016	The release of HMGB1 and double-stranded DNA (dsDNA) into the culture supernatant from MWCNT-treated cells was examined by ELISA and fluorometric analysis, respectively.	mwcnt	87-92	high mobility group box 1	Homo sapiens	15-20
27026438-16	2016	The HMGB1-DNA complex binds to RAGE on neighboring cells and then CpG DNA is recognized by TLR9 in lysosomes, leading to generation of nitric oxide and 8-nitroG formation.	Nitric Oxide	135-147	high mobility group box 1	Homo sapiens	4-9
27026438-16	2016	The HMGB1-DNA complex binds to RAGE on neighboring cells and then CpG DNA is recognized by TLR9 in lysosomes, leading to generation of nitric oxide and 8-nitroG formation.	8-nitroguanine	152-160	high mobility group box 1	Homo sapiens	4-9
26962684-5	2016	When injected into established cancers, LTX-315 caused a transiently hemorrhagic focal necrosis that was accompanied by massive release of HMGB1 (from close-to-all cancer cells), as well as caspase-3 activation in a fraction of the cells.	LTX-315	40-47	high mobility group box 1	Homo sapiens	139-144
27033788-7	2016	According to the results of MTT, the growth of HEC-1A cells was obviously inhibited after transfection of HEC-1A HMGB1 shRNA (P&lt;0.05).	monooxyethylene trimethylolpropane tristearate	28-31	high mobility group box 1	Homo sapiens	113-118
26346170-11	2016	In summary, our results demonstrate that 14-3-3sigma induces cisplatin resistance in ESCC cells and that 14-3-3sigma-mediated cisplatin resistance involves DNA repair molecules HMGB1 and XPA.	Cisplatin	126-135	high mobility group box 1	Homo sapiens	177-182
26948869-3	2016	HMGB1 allosterically inhibits the tetrameric pyruvate kinase isoform M2, thus blocking glucose-driven aerobic respiration.	Glucose	87-94	high mobility group box 1	Homo sapiens	0-5
26760176-2	2016	OBJECTIVES: To verify high-mobility group box 1 protein (HMGB1) levels in CF patients according to glucose tolerance state, and analyze relationships with insulin secretion and resistance.	Glucose	99-106	high mobility group box 1	Homo sapiens	22-47
26760176-2	2016	OBJECTIVES: To verify high-mobility group box 1 protein (HMGB1) levels in CF patients according to glucose tolerance state, and analyze relationships with insulin secretion and resistance.	Glucose	99-106	high mobility group box 1	Homo sapiens	57-62
26899177-0	2016	EGCG in Green Tea Induces Aggregation of HMGB1 Protein through Large Conformational Changes with Polarized Charge Redistribution.	epigallocatechin gallate	0-4	high mobility group box 1	Homo sapiens	41-46
26899177-2	2016	Recent experimental evidences indicate that EGCG can induce the aggregation of HMGB1 protein, a late mediator of inflammation, which subsequently stimulates the autophagic degradation and thus provides protection from lethal endotoxemia and sepsis.	epigallocatechin gallate	44-48	high mobility group box 1	Homo sapiens	79-84
26899177-3	2016	In this study, we use molecular dynamics (MD) simulations to explore the underlying molecular mechanism of this aggregation of HMGB1 facilitated by EGCG.	epigallocatechin gallate	148-152	high mobility group box 1	Homo sapiens	127-132
26899177-4	2016	Our simulation results reveal that EGCG firmly binds to HMGB1 near Cys106, which supports previous preliminary experimental evidence.	epigallocatechin gallate	35-39	high mobility group box 1	Homo sapiens	56-61
26899177-5	2016	A large HMGB1 conformational change is observed, where Box A and Box B, two homogenous domains of HMGB1, are repositioned and packed together by EGCG.	epigallocatechin gallate	145-149	high mobility group box 1	Homo sapiens	8-13
26899177-5	2016	A large HMGB1 conformational change is observed, where Box A and Box B, two homogenous domains of HMGB1, are repositioned and packed together by EGCG.	epigallocatechin gallate	145-149	high mobility group box 1	Homo sapiens	98-103
26899177-7	2016	We suggest that the highly polarized charge distribution leads to the aggregation of HMGB1, which differs from the previous hypothesis that two HMGB1 monomers are linked by the dimer of EGCG.	epigallocatechin gallate	186-190	high mobility group box 1	Homo sapiens	85-90
26578599-4	2016	Here, we demonstrate that HMGB1 recognizes TFO-ICLs in human cells, and its depletion increases ICL-induced mutagenesis in human cells without altering the mutation spectra.	tfo	43-46	high mobility group box 1	Homo sapiens	26-31
26453003-0	2016	Ketamine attenuates high mobility group box-1-induced inflammatory responses in endothelial cells.	Ketamine	0-8	high mobility group box 1	Homo sapiens	20-45
26453003-3	2016	However, the effects of ketamine on HMGB1-mediated proinflammatory responses have not been fully investigated.	Ketamine	24-32	high mobility group box 1	Homo sapiens	36-41
26453003-4	2016	In the present study, we investigated the effects of ketamine on HMGB1-activated endothelial cells and explored the underlying mechanisms.	Ketamine	53-61	high mobility group box 1	Homo sapiens	65-70
26453003-6	2016	The anti-inflammatory activities of ketamine were determined by measuring solute flux, leukocyte adhesion and migration, and activation of proinflammatory proteins in HMGB1-activated endothelial cells.	Ketamine	36-44	high mobility group box 1	Homo sapiens	167-172
26872033-6	2016	In preceding immunohistochemistry experiments using paraffin-block sections from endometriosis (N = 33) and control (N = 27) group, retrospectively, HMGB-1 expression was shown in both epithelial and stromal cell.	Paraffin	52-60	high mobility group box 1	Homo sapiens	149-155
26453003-8	2016	RESULTS: We found that ketamine inhibited the HMGB1-mediated barrier disruption, neutrophil adhesion and migration, and expression of cell adhesion molecules in a dose-dependent manner.	Ketamine	23-31	high mobility group box 1	Homo sapiens	46-51
26453003-9	2016	Furthermore, ketamine downregulated the TLR-2 and -4, expression in HMGB1-activated endothelial cells.	Ketamine	13-21	high mobility group box 1	Homo sapiens	68-73
26453003-12	2016	CONCLUSIONS: Our study has demonstrated that ketamine exerts anti-inflammatory effects in HMGB1-mediated proinflammatory responses in a dose-dependent manner.	Ketamine	45-53	high mobility group box 1	Homo sapiens	90-95
26346170-9	2016	14-3-3sigma, HMGB1, and XPA were preferentially expressed in cisplatin-resistant SLMT-1 cells when compared to those more sensitive to cisplatin.	Cisplatin	61-70	high mobility group box 1	Homo sapiens	13-18
26346170-10	2016	In ESCC patients with poor response to cisplatin-based chemoradiation, their pre-treatment tumors expressed higher expression of HMGB1 than those with response to such treatment.	Cisplatin	39-48	high mobility group box 1	Homo sapiens	129-134
26739898-8	2016	Treatment with PI3K inhibitor (LY294006) and beta-catenin shRNA reversed HMGB1-induced EMT.	ly294006	31-39	high mobility group box 1	Homo sapiens	73-78
26848281-1	2016	BACKGROUND: Conditioning regimens including total body irradiation (TBI) or cyclophosphamide can mobilize high-mobility group box 1 (HMGB1) to peripheral blood.	Cyclophosphamide	76-92	high mobility group box 1	Homo sapiens	106-131
26848281-1	2016	BACKGROUND: Conditioning regimens including total body irradiation (TBI) or cyclophosphamide can mobilize high-mobility group box 1 (HMGB1) to peripheral blood.	Cyclophosphamide	76-92	high mobility group box 1	Homo sapiens	133-138
26848281-7	2016	Additionally, levels of HMGB1 at day 0 were significantly increased in TBI+ patients and cyclophosphamide/TBI patients.	Cyclophosphamide	89-105	high mobility group box 1	Homo sapiens	24-29
26382001-7	2016	In addition, the MTT assay, growth curve, and the colony forming assay confirmed the promotion by HMGB1 to the proliferation of CNE-2 cells, depending on RAGE.	monooxyethylene trimethylolpropane tristearate	17-20	high mobility group box 1	Homo sapiens	98-103
27627916-0	2016	Inhibitory Effect of Three Diketopiperazines from Marine-Derived Bacteria on HMGB1-Induced Septic Responses in Vitro and in Vivo.	Diketopiperazines	27-44	high mobility group box 1	Homo sapiens	77-82
27627916-5	2016	Here, three diketopiperazines (1-3) isolated from two strains of marine-derived bacteria were investigated for their potential activities against HMGB1-mediated septic responses.	Diketopiperazines	12-29	high mobility group box 1	Homo sapiens	146-151
27826978-6	2016	RESULTS: Our data showed a clear band of ~ 684 bp and ~ 981 bp related to HMGB1 and E7-HMGB1 genes in agarose gel, respectively.	Sepharose	102-109	high mobility group box 1	Homo sapiens	74-79
27826978-6	2016	RESULTS: Our data showed a clear band of ~ 684 bp and ~ 981 bp related to HMGB1 and E7-HMGB1 genes in agarose gel, respectively.	Sepharose	102-109	high mobility group box 1	Homo sapiens	87-92
27910767-4	2016	Emerging evidence indicates that melphalan can foster an immunogenic microenvironment by inducing immunogenic cell death (ICD) as characterized by membrane translocation of endoplasmic reticulum protein calreticulin (CRT) and by release of chromatin-binding protein high-mobility group box 1 (HMGB1).	Melphalan	33-42	high mobility group box 1	Homo sapiens	266-291
27184952-9	2016	High-mobility group box 1 (HMGB1) was rapidly released and associated with TLR4 after TNF-alpha stimulation with a peak at 5 min, which was prevented by N-acetylcysteine, an antioxidant.	Acetylcysteine	153-169	high mobility group box 1	Homo sapiens	0-25
27184952-9	2016	High-mobility group box 1 (HMGB1) was rapidly released and associated with TLR4 after TNF-alpha stimulation with a peak at 5 min, which was prevented by N-acetylcysteine, an antioxidant.	Acetylcysteine	153-169	high mobility group box 1	Homo sapiens	27-32
27184952-10	2016	Glycyrrhizin (HMGB1 inhibitor), HMGB1-neutralizing antibody and siRNA depletion of HMGB1 all suppressed TNF-alpha-induced Syk activation and ET-1 production.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	14-19
27184952-11	2016	CONCLUSION: Upon TNF-alpha stimulation, TLR4 is activated by HMGB1 that is immediately released after the generation of reactive oxygen species, and plays a crucial role in the signal transduction.	Reactive Oxygen Species	120-143	high mobility group box 1	Homo sapiens	61-66
27910767-4	2016	Emerging evidence indicates that melphalan can foster an immunogenic microenvironment by inducing immunogenic cell death (ICD) as characterized by membrane translocation of endoplasmic reticulum protein calreticulin (CRT) and by release of chromatin-binding protein high-mobility group box 1 (HMGB1).	Melphalan	33-42	high mobility group box 1	Homo sapiens	293-298
26567221-0	2016	N-linked glycosylation plays a crucial role in the secretion of HMGB1.	Nitrogen	0-1	high mobility group box 1	Homo sapiens	64-69
25139532-7	2016	Furthermore, the response to NACRT was found to be significantly associated with the preoperative serum HMGB-1 levels.	nacrt	29-34	high mobility group box 1	Homo sapiens	104-110
25139532-8	2016	The use of NACRT contributes to preoperative serum HMGB-1 elevation, and these were risk factors for the occurrence of severe postoperative pulmonary complications in patients with esophageal cancer after thoracic esophagectomy.	nacrt	11-16	high mobility group box 1	Homo sapiens	51-57
26567221-3	2016	Here, we identified the role of N-glycosylation of HMGB1 in extracellular secretion.	Nitrogen	32-33	high mobility group box 1	Homo sapiens	51-56
26567221-4	2016	We found two consensus (N37 and N134) and one non-consensus (N135) residues that were N-glycosylated in HMGB1 by performing liquid chromatography tandem mass spectrometry (LC-MS/MS) and analyzing for N-glycan composition and structure.	Nitrogen	24-25	high mobility group box 1	Homo sapiens	104-109
26567221-4	2016	We found two consensus (N37 and N134) and one non-consensus (N135) residues that were N-glycosylated in HMGB1 by performing liquid chromatography tandem mass spectrometry (LC-MS/MS) and analyzing for N-glycan composition and structure.	n-glycan	200-208	high mobility group box 1	Homo sapiens	104-109
26567221-5	2016	Inhibition of N-glycosylation with tunicamycin resulted in a molecular shift of HMGB1 as assessed by gel electrophoresis.	Nitrogen	14-15	high mobility group box 1	Homo sapiens	80-85
26567221-5	2016	Inhibition of N-glycosylation with tunicamycin resulted in a molecular shift of HMGB1 as assessed by gel electrophoresis.	Tunicamycin	35-46	high mobility group box 1	Homo sapiens	80-85
26567221-8	2016	Taken together, we propose that HMGB1 is N-glycosylated, and that this is important for its DNA interaction and is a prerequisite for its nucleocytoplasmic transport and extracellular secretion.	Nitrogen	41-42	high mobility group box 1	Homo sapiens	32-37
26334381-0	2015	Simvastatin protects the heart against ischemia reperfusion injury via inhibiting HMGB1 expression through PI3K/Akt signal pathways.	Simvastatin	0-11	high mobility group box 1	Homo sapiens	82-87
26966912-6	2016	Glycyrrhetic acid inhibits the chemotactic and mitogenic function of HMGB1, binding to the hydrophobic residues that delimit the pockets in box A and B.	Glycyrrhetinic Acid	0-17	high mobility group box 1	Homo sapiens	69-74
26702616-10	2015	MTX upregulated autophagy through its ability to enhance the expression of HMGB1 and Beclin-1 rather than through the Akt/mTOR pathway.	Methotrexate	0-3	high mobility group box 1	Homo sapiens	75-80
26515875-11	2016	In addition, blockade of JNK MAPK and NF-kappaB phosphorylation prohibited HMGB1-induced production of pro-osteogenic factors, and mineralization of VICs.	vics	149-153	high mobility group box 1	Homo sapiens	75-80
25307746-8	2015	Moreover, PGZ inhibited proliferative activity and invasive potential, and induced apoptosis and cell cycle arrest in HCC cells resulting in increased expression of PPARgamma and decreased expression of RAGE, NF-kappaB, HMGB1, p38MAPK, Ki-67, MMP-2, and CyclinD1.	Pioglitazone	10-13	high mobility group box 1	Homo sapiens	220-225
27337797-5	2015	After treating the schizophrenics with the neuroleptic risperidone for 6 months, the serum levels of HMGB1, IL-1beta, TNF-alpha and IL-6 were decreased.	Risperidone	55-66	high mobility group box 1	Homo sapiens	101-106
27337797-8	2015	HMGB1 may play a proinflammatory role in schizophrenia and the decrease of HMGB1 after neuroleptic risperidone treatment may be a marker of mental symptoms remission.	Risperidone	99-110	high mobility group box 1	Homo sapiens	75-80
26293782-4	2015	In vitro, EGCG divergently affected HMGB1-mediated production of several chemokines: reducing CXCL15 and RANTES/CCL5, but elevating G-CSF and MIP-1alpha/CCL3 production by peritoneal macrophages.	epigallocatechin gallate	10-14	high mobility group box 1	Homo sapiens	36-41
26769828-7	2015	Short-term (5 days) riboflavin deprivation resulted in the pathological macrophages activation, manifested especially in a reduction of cell viability and excess release of tumor necrosis factor-alpha (TNF-alpha) and high-mobility group box 1 (HMGB1) protein.	Riboflavin	20-30	high mobility group box 1	Homo sapiens	217-242
26769828-7	2015	Short-term (5 days) riboflavin deprivation resulted in the pathological macrophages activation, manifested especially in a reduction of cell viability and excess release of tumor necrosis factor-alpha (TNF-alpha) and high-mobility group box 1 (HMGB1) protein.	Riboflavin	20-30	high mobility group box 1	Homo sapiens	244-249
26884867-5	2015	HMGB1 siRNAs were designed and chemically synthesized, and then transfected into the breast cancer cell line MCF-7 with lipofectamine 2000.	Lipofectamine	120-138	high mobility group box 1	Homo sapiens	0-5
26349060-0	2015	The HIV Protease Inhibitor Saquinavir Inhibits HMGB1-Driven Inflammation by Targeting the Interaction of Cathepsin V with TLR4/MyD88.	Saquinavir	27-37	high mobility group box 1	Homo sapiens	47-52
26397184-5	2015	Anticancer agents including doxorubicin, cisplatin and etoposide each induced HMGB1 upregulation, promoted cytosolic HMGB1 translocation and the elevation of autophagic activity in human NB cells.	Doxorubicin	28-39	high mobility group box 1	Homo sapiens	78-83
26349060-1	2015	Extracellular high-mobility group box 1 (HMGB1) (disulfide form), via activation of toll-like receptor 4 (TLR4)-dependent signaling, is a strong driver of pathologic inflammation in both acute and chronic conditions.	Disulfides	49-58	high mobility group box 1	Homo sapiens	14-39
26349060-1	2015	Extracellular high-mobility group box 1 (HMGB1) (disulfide form), via activation of toll-like receptor 4 (TLR4)-dependent signaling, is a strong driver of pathologic inflammation in both acute and chronic conditions.	Disulfides	49-58	high mobility group box 1	Homo sapiens	41-46
26349060-4	2015	Here we report that the first-generation HIV-PI saquinavir (SQV), as well as a newly identified mammalian protease inhibitor STO33438 (334), potently block disulfide HMGB1-induced TLR4 activation, as assayed by the production of TNF-alpha by human monocyte-derived macrophages (THP-1).	sto33438	125-133	high mobility group box 1	Homo sapiens	166-171
26349060-4	2015	Here we report that the first-generation HIV-PI saquinavir (SQV), as well as a newly identified mammalian protease inhibitor STO33438 (334), potently block disulfide HMGB1-induced TLR4 activation, as assayed by the production of TNF-alpha by human monocyte-derived macrophages (THP-1).	Disulfides	156-165	high mobility group box 1	Homo sapiens	166-171
26349060-10	2015	Disulfide HMGB1 drives pathologic inflammation in many models by activating signaling through TLR4.	Disulfides	0-9	high mobility group box 1	Homo sapiens	10-15
26349060-11	2015	Cell-based screening identified the mammalian protease cathepsin V as a novel therapeutic target to inhibit TLR4-mediated inflammation induced by extracellular HMGB1 (disulfide form).	Disulfides	167-176	high mobility group box 1	Homo sapiens	160-165
26349060-12	2015	We identified two protease inhibitors (PIs) that block cathepsin V and thereby inhibit disulfide HMGB1-induced TLR4 activation: saquinavir (SQV), a first-generation PI targeting viral HIV protease and STO33438 (334), targeting mammalian proteases.	Disulfides	87-96	high mobility group box 1	Homo sapiens	97-102
26349060-12	2015	We identified two protease inhibitors (PIs) that block cathepsin V and thereby inhibit disulfide HMGB1-induced TLR4 activation: saquinavir (SQV), a first-generation PI targeting viral HIV protease and STO33438 (334), targeting mammalian proteases.	Saquinavir	128-138	high mobility group box 1	Homo sapiens	97-102
26397184-5	2015	Anticancer agents including doxorubicin, cisplatin and etoposide each induced HMGB1 upregulation, promoted cytosolic HMGB1 translocation and the elevation of autophagic activity in human NB cells.	Doxorubicin	28-39	high mobility group box 1	Homo sapiens	117-122
26397184-5	2015	Anticancer agents including doxorubicin, cisplatin and etoposide each induced HMGB1 upregulation, promoted cytosolic HMGB1 translocation and the elevation of autophagic activity in human NB cells.	Cisplatin	41-50	high mobility group box 1	Homo sapiens	78-83
26397184-5	2015	Anticancer agents including doxorubicin, cisplatin and etoposide each induced HMGB1 upregulation, promoted cytosolic HMGB1 translocation and the elevation of autophagic activity in human NB cells.	Cisplatin	41-50	high mobility group box 1	Homo sapiens	117-122
26397184-5	2015	Anticancer agents including doxorubicin, cisplatin and etoposide each induced HMGB1 upregulation, promoted cytosolic HMGB1 translocation and the elevation of autophagic activity in human NB cells.	Etoposide	55-64	high mobility group box 1	Homo sapiens	78-83
26397184-5	2015	Anticancer agents including doxorubicin, cisplatin and etoposide each induced HMGB1 upregulation, promoted cytosolic HMGB1 translocation and the elevation of autophagic activity in human NB cells.	Etoposide	55-64	high mobility group box 1	Homo sapiens	117-122
26397184-9	2015	In addition, we found that HMGB1 facilitated autophagic progression and reduced oxidative stress induced by doxorubicin.	Doxorubicin	108-119	high mobility group box 1	Homo sapiens	27-32
26596890-6	2015	Anti-HMGB1 antibody levels were analysed in patient and control (n = 112) sera by an in-house ELISA using recombinant histidine-tagged HMGB1.	Histidine	118-127	high mobility group box 1	Homo sapiens	135-140
26597985-4	2016	In this study, we showed that SBP1, -2, and -3 individually bind different basic amino acids with exquisite specificity.	Amino Acids, Basic	75-92	high mobility group box 1	Homo sapiens	30-34
26548953-6	2015	Induced asymmetry involving tilting of the nonamer-binding domain dimer of RAG1 upon binding of HMGB1-bent 12-RSS or 23-RSS underlies the molecular mechanism for the 12/23 rule.	12-rss	107-113	high mobility group box 1	Homo sapiens	96-101
26548953-6	2015	Induced asymmetry involving tilting of the nonamer-binding domain dimer of RAG1 upon binding of HMGB1-bent 12-RSS or 23-RSS underlies the molecular mechanism for the 12/23 rule.	23-rss	117-123	high mobility group box 1	Homo sapiens	96-101
26557438-0	2015	Suberoylanilide hydroxamic acid suppresses hepatic stellate cells activation by HMGB1 dependent reduction of NF-kappaB1.	Vorinostat	0-31	high mobility group box 1	Homo sapiens	80-85
26525891-6	2015	In HepG2 cells, palmitic acid (PA)-induced pro-inflammatory cytokines release were blocked by HMGB1 small interfering RNA (siRNA) transfection.	Palmitic Acid	16-29	high mobility group box 1	Homo sapiens	94-99
26525891-6	2015	In HepG2 cells, palmitic acid (PA)-induced pro-inflammatory cytokines release were blocked by HMGB1 small interfering RNA (siRNA) transfection.	Palmitic Acid	31-33	high mobility group box 1	Homo sapiens	94-99
26557438-7	2015	Bioinformatic analyses of these altered genes highlighted the high mobility group box 1 (HMGB1) pathway was one of the most relevant pathways that contributed to SAHA induced suppression of HSCs activation.	Vorinostat	162-166	high mobility group box 1	Homo sapiens	62-87
26557438-7	2015	Bioinformatic analyses of these altered genes highlighted the high mobility group box 1 (HMGB1) pathway was one of the most relevant pathways that contributed to SAHA induced suppression of HSCs activation.	Vorinostat	162-166	high mobility group box 1	Homo sapiens	89-94
26557438-8	2015	Further studies demonstrated the increased acetylation of intracellular HMGB1 in SAHA treated HSCs, and this increasing is most likely to be responsible for SAHA induced down-regulation of nuclear factor kappa B1 (NF-kappaB1) and is one of the main underlying mechanisms for the therapeutic effect of SAHA for liver fibrosis.	Vorinostat	81-85	high mobility group box 1	Homo sapiens	72-77
26557438-8	2015	Further studies demonstrated the increased acetylation of intracellular HMGB1 in SAHA treated HSCs, and this increasing is most likely to be responsible for SAHA induced down-regulation of nuclear factor kappa B1 (NF-kappaB1) and is one of the main underlying mechanisms for the therapeutic effect of SAHA for liver fibrosis.	Vorinostat	157-161	high mobility group box 1	Homo sapiens	72-77
26557438-8	2015	Further studies demonstrated the increased acetylation of intracellular HMGB1 in SAHA treated HSCs, and this increasing is most likely to be responsible for SAHA induced down-regulation of nuclear factor kappa B1 (NF-kappaB1) and is one of the main underlying mechanisms for the therapeutic effect of SAHA for liver fibrosis.	Vorinostat	157-161	high mobility group box 1	Homo sapiens	72-77
26040768-10	2015	The results demonstrated that the expression level of HMGB1 in A549/DDP cells was much higher than that of A549 cells; moreover, transfection with HMGB1 shRNA in A549/DDP cells decreased the IC50 value of cisplatin in A549/DDP cells.	Cisplatin	205-214	high mobility group box 1	Homo sapiens	54-59
26040768-10	2015	The results demonstrated that the expression level of HMGB1 in A549/DDP cells was much higher than that of A549 cells; moreover, transfection with HMGB1 shRNA in A549/DDP cells decreased the IC50 value of cisplatin in A549/DDP cells.	Cisplatin	205-214	high mobility group box 1	Homo sapiens	147-152
26040768-5	2015	Firstly, we detected the expression levels of HMGB1 by by real-time PCR and western blotting analysis, and the results demonstrated that HMGB1 was much higher expressed in non-small cell lung cancer cell lines, including A549, SPC-1-1, NCI-2170, SK-MES-1, and NCI-H1299, compared with that of WI-38.	sk-mes	246-252	high mobility group box 1	Homo sapiens	137-142
26875270-11	2015	The expression of HMGB1 protein in Pgenesil-1/HMGB1 siRNA group (0.134 +- 0.048) was significantly lower than that of Pgenesil-1 group (0.581+- 0.032) and untransfected group (0.514 +- 0.069) (P &lt; 0.05).	pgenesil-1	35-45	high mobility group box 1	Homo sapiens	18-23
26875270-11	2015	The expression of HMGB1 protein in Pgenesil-1/HMGB1 siRNA group (0.134 +- 0.048) was significantly lower than that of Pgenesil-1 group (0.581+- 0.032) and untransfected group (0.514 +- 0.069) (P &lt; 0.05).	pgenesil-1	35-45	high mobility group box 1	Homo sapiens	46-51
26875270-12	2015	ELISA results showed that IL-1beta and TNF-alpha in supernatants of Pgenesil-1/HMGB1 siRNA group were significantly lower than those of Pgenesil-1 group and untransfected group (P &lt; 0.05).	pgenesil-1	68-78	high mobility group box 1	Homo sapiens	79-84
26875270-12	2015	ELISA results showed that IL-1beta and TNF-alpha in supernatants of Pgenesil-1/HMGB1 siRNA group were significantly lower than those of Pgenesil-1 group and untransfected group (P &lt; 0.05).	pgenesil	68-76	high mobility group box 1	Homo sapiens	79-84
26454330-3	2015	This study explored HMGB-1 as a therapeutic target for DR treatment through observing its role in retinal ganglion cells (GRCs) in a high glucose environment.	Glucose	138-145	high mobility group box 1	Homo sapiens	20-26
26770371-0	2015	Effect of high mobility group box 1 on the human retinal pigment epithelial cell in high-glucose condition.	Glucose	89-96	high mobility group box 1	Homo sapiens	10-35
26770371-6	2015	In the advanced in-vitro study, we detect the protective effect of HMGB1 on the RPE cells in high glucose condition.	Glucose	98-105	high mobility group box 1	Homo sapiens	67-72
26770371-10	2015	Besides, HMGB1 treatment would up-regulate the expression of VEGFA in the RPE cells in high glucose condition.	Glucose	92-99	high mobility group box 1	Homo sapiens	9-14
26537405-3	2015	We found that hairpin polyamide 1 triggers the release of the damage-associated molecular patterns calreticulin, ATP and HMGB1 in a slow necrotic-type cell death.	Nylons	22-31	high mobility group box 1	Homo sapiens	121-126
26469759-5	2015	Supernatants from DTX-treated DU145 tumor cells, which were shown to contain HMGB1, effectively induced sCLU from newly-plated DU145 tumor cells and protected them from DTX toxicity.	Docetaxel	18-21	high mobility group box 1	Homo sapiens	77-82
26469759-5	2015	Supernatants from DTX-treated DU145 tumor cells, which were shown to contain HMGB1, effectively induced sCLU from newly-plated DU145 tumor cells and protected them from DTX toxicity.	Docetaxel	169-172	high mobility group box 1	Homo sapiens	77-82
26454330-9	2015	RESULTS: HMGB-1 mRNA was up-regulated (P=0.015) and protein secretion increased (P=0.022) in the high glucose environment.	Glucose	102-109	high mobility group box 1	Homo sapiens	9-15
26248639-3	2015	It is revealed that HMGB1 (high-mobility group protein B1) was the most commonly found protein that recognizes all Pt(II)-DNA probes and prefers cisplatin-DNA probes more than the others.	Cisplatin	145-154	high mobility group box 1	Homo sapiens	20-25
26248639-3	2015	It is revealed that HMGB1 (high-mobility group protein B1) was the most commonly found protein that recognizes all Pt(II)-DNA probes and prefers cisplatin-DNA probes more than the others.	Cisplatin	145-154	high mobility group box 1	Homo sapiens	27-57
26813430-11	2015	MTT assay showed that the cell proliferation in the HMGB1-siRNA group was significantly inhibited when compared with that in the HMGB1-siRNA-Neg group and control group (P&lt;0.05).	monooxyethylene trimethylolpropane tristearate	0-3	high mobility group box 1	Homo sapiens	52-57
25943534-9	2015	The antitumor activity of anti-PD-L1 was enhanced by combination with oxaliplatin, which resulted in increased release of HMGB1 within CT26 tumors.	Oxaliplatin	70-81	high mobility group box 1	Homo sapiens	122-127
26273067-12	2015	CONCLUSIONS: We conclude that altered OPN expression in CAVS affects cellular HMGB1 function inducing cytoplasmic translocation and secretion of HMGB1 in endothelial cells and VICs, thus indicating a regulatory role for OPN in the progression of CAVS through alteration of HMGB1 function.	vics	176-180	high mobility group box 1	Homo sapiens	78-83
26206236-0	2015	Inhibitory effects of polyozellin from Polyozellus multiplex on HMGB1-mediated septic responses.	polyozellin	22-33	high mobility group box 1	Homo sapiens	64-69
26206236-4	2015	METHODS: The anti-inflammatory activities of polyozellin were determined by measuring permeability, human neutrophil adhesion and migration, and activation of proinflammatory proteins in HMGB1-activated HUVECs and mice.	polyozellin	45-56	high mobility group box 1	Homo sapiens	187-192
26206236-5	2015	RESULTS: According to the results, polyozellin effectively inhibited lipopolysaccharide (LPS)-induced release of HMGB1, and suppressed HMGB1-mediated septic responses, such as hyperpermeability, adhesion and migration of leukocytes, and expression of cell adhesion molecules.	polyozellin	35-46	high mobility group box 1	Homo sapiens	113-118
26206236-5	2015	RESULTS: According to the results, polyozellin effectively inhibited lipopolysaccharide (LPS)-induced release of HMGB1, and suppressed HMGB1-mediated septic responses, such as hyperpermeability, adhesion and migration of leukocytes, and expression of cell adhesion molecules.	polyozellin	35-46	high mobility group box 1	Homo sapiens	135-140
26206236-6	2015	In addition, polyozellin suppressed the production of tumor necrosis factor-alpha and interleukin (IL)-6, and the activation of nuclear factor-kappaB and extracellular signal-regulated kinases 1/2 by HMGB1.	polyozellin	13-24	high mobility group box 1	Homo sapiens	200-205
26206236-7	2015	CONCLUSION: Collectively, these results indicate that P. multiplex containing polyozellin could be commercialized as functional food for preventing and treatment of various severe vascular inflammatory diseases via inhibition of the HMGB1 signaling pathway.	polyozellin	78-89	high mobility group box 1	Homo sapiens	233-238
25956731-6	2015	The equipotent P2Y2R agonists ATP and UTP enhanced proliferation, RAGE expression and HMGB1 secretion in IL-1beta-pretreated VSMCs.	Adenosine Triphosphate	30-33	high mobility group box 1	Homo sapiens	86-91
25956731-6	2015	The equipotent P2Y2R agonists ATP and UTP enhanced proliferation, RAGE expression and HMGB1 secretion in IL-1beta-pretreated VSMCs.	Uridine Triphosphate	38-41	high mobility group box 1	Homo sapiens	86-91
25956731-6	2015	The equipotent P2Y2R agonists ATP and UTP enhanced proliferation, RAGE expression and HMGB1 secretion in IL-1beta-pretreated VSMCs.	vsmcs	125-130	high mobility group box 1	Homo sapiens	86-91
25956731-9	2015	The ERK, AKT, PKC, Rac-1 and ROCK2 pathways were involved in UTP-induced cell proliferation and migration, MMP-2 and HMGB1 secretion and RAGE expression in the IL-1beta-pretreated VSMCs.	Uridine Triphosphate	61-64	high mobility group box 1	Homo sapiens	117-122
26406975-4	2015	Many of the intra- and extracellular functions of HMGB1 depend on redox-sensitive cysteine residues of the protein.	Cysteine	82-90	high mobility group box 1	Homo sapiens	50-55
26337661-0	2015	Role of high-mobility group box 1 in methamphetamine-induced activation and migration of astrocytes.	Methamphetamine	37-52	high mobility group box 1	Homo sapiens	8-33
26337661-8	2015	RESULTS: Exposure of C6 cells to methamphetamine increased the expression of HMGB1 via the activation of sigma-1R, Src, ERK mitogen-activated protein kinase, and downstream NF-kappaB p65 pathways.	Methamphetamine	33-48	high mobility group box 1	Homo sapiens	77-82
26337661-10	2015	Knockdown of HMGB1 in astrocytes transfected with HMGB1 siRNA attenuated the increased cell activation and migration induced by methamphetamine, thereby implicating the role of HMGB1 in the activation and migration of C6 cells and primary human astrocytes.	Methamphetamine	128-143	high mobility group box 1	Homo sapiens	13-18
26337661-10	2015	Knockdown of HMGB1 in astrocytes transfected with HMGB1 siRNA attenuated the increased cell activation and migration induced by methamphetamine, thereby implicating the role of HMGB1 in the activation and migration of C6 cells and primary human astrocytes.	Methamphetamine	128-143	high mobility group box 1	Homo sapiens	50-55
26337661-10	2015	Knockdown of HMGB1 in astrocytes transfected with HMGB1 siRNA attenuated the increased cell activation and migration induced by methamphetamine, thereby implicating the role of HMGB1 in the activation and migration of C6 cells and primary human astrocytes.	Methamphetamine	128-143	high mobility group box 1	Homo sapiens	50-55
26337661-11	2015	CONCLUSIONS: This study demonstrated that methamphetamine-mediated activation and migration of astrocytes involved HMGB1 up-regulation through an autocrine mechanism.	Methamphetamine	42-57	high mobility group box 1	Homo sapiens	115-120
26337661-12	2015	Targeting HMGB1 could provide insights into the development of a potential therapeutic approach for alleviation of cell activation and migration of astrocytes induced by methamphetamine.	Methamphetamine	170-185	high mobility group box 1	Homo sapiens	10-15
26408615-1	2015	OBJECTIVE: To determine the effect of p38 MAPK inhibitor (SB203580) on TNF-alpha -induced high mobility group protein B1 (HMGB1) expression in microglial cells.	SB 203580	58-66	high mobility group box 1	Homo sapiens	90-120
26408615-1	2015	OBJECTIVE: To determine the effect of p38 MAPK inhibitor (SB203580) on TNF-alpha -induced high mobility group protein B1 (HMGB1) expression in microglial cells.	SB 203580	58-66	high mobility group box 1	Homo sapiens	122-127
26408615-5	2015	The TNF-alpha-induced HMGB1 protein and mRNA expression was suppressed by SB203580.	SB 203580	74-82	high mobility group box 1	Homo sapiens	22-27
26813430-11	2015	MTT assay showed that the cell proliferation in the HMGB1-siRNA group was significantly inhibited when compared with that in the HMGB1-siRNA-Neg group and control group (P&lt;0.05).	monooxyethylene trimethylolpropane tristearate	0-3	high mobility group box 1	Homo sapiens	129-134
27057465-2	2016	This effect is in part due to the capacity of anthracyclines to induce immunogenic cell death (ICD), a cell death modality that is preceded by autophagy and followed by HMGB1 release.	Anthracyclines	46-60	high mobility group box 1	Homo sapiens	169-174
26079697-0	2015	Ethanol directly induced HMGB1 release through NOX2/NLRP1 inflammasome in neuronal cells.	Ethanol	0-7	high mobility group box 1	Homo sapiens	25-30
26079697-3	2015	The present study was designed to test whether ethanol directly induced HMGB1 release and to explore the cellular and molecular mechanism mediating its action.	Ethanol	47-54	high mobility group box 1	Homo sapiens	72-77
26245198-0	2015	HMGB1: a novel protein that induced platelets active and aggregation via Toll-like receptor-4, NF-kappaB and cGMP dependent mechanisms.	Cyclic GMP	109-113	high mobility group box 1	Homo sapiens	0-5
26245198-11	2015	iv) We proposed that extracellular HMGB1 seems to promote the phosphorylation of GPIIb/IIIa and subsequent platelet aggregation via TLR4/NF-kappaB and cGMP pathway.	Cyclic GMP	151-155	high mobility group box 1	Homo sapiens	35-40
25816800-2	2015	HMGB1 has been implicated in the pathophysiology of several neuroinflammatory conditions including ischemia, traumatic brain injury, seizure and chronic ethanol use.	Ethanol	153-160	high mobility group box 1	Homo sapiens	0-5
26079697-4	2015	It was found that ethanol increased significant HMGB1 release from SH-SY5Y cells and from cultured primary cortical neurons as detected by ELISA assay.	Ethanol	18-25	high mobility group box 1	Homo sapiens	48-53
26079697-8	2015	In addition, z-YVAD-fmk, an inhibitor of caspase-1, decreased the ethanol-induced HMGB1 release.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	13-23	high mobility group box 1	Homo sapiens	82-87
26079697-8	2015	In addition, z-YVAD-fmk, an inhibitor of caspase-1, decreased the ethanol-induced HMGB1 release.	Ethanol	66-73	high mobility group box 1	Homo sapiens	82-87
26079697-9	2015	It is concluded that ethanol-induced HMGB1 release is associated with NOX2/NLRP1 inflammasome signaling, which represents a novel mechanism of ethanol-associated neuron injury.	Ethanol	21-28	high mobility group box 1	Homo sapiens	37-42
26079697-9	2015	It is concluded that ethanol-induced HMGB1 release is associated with NOX2/NLRP1 inflammasome signaling, which represents a novel mechanism of ethanol-associated neuron injury.	Ethanol	143-150	high mobility group box 1	Homo sapiens	37-42
25743565-3	2015	We accessed this question by monitoring the effects of posttreatment carbazole derivatives on LPS- and CLP-mediated release of HMGB1 and HMGB1-mediated regulation of proinflammatory responses in human umbilical vein endothelial cells (HUVECs) and septic mice.	carbazole	69-78	high mobility group box 1	Homo sapiens	127-132
26140987-2	2015	In order to down-regulate HMGB1 expression in airway epithelial cells, siRNA directed against HMGB1 was delivered through nanocomplexes based on a cationic copolymer of poly(N-2-hydroxyethyl)-d,l-aspartamide (PHEA) by using H441 cells.	copolymer	156-165	high mobility group box 1	Homo sapiens	94-99
26140987-2	2015	In order to down-regulate HMGB1 expression in airway epithelial cells, siRNA directed against HMGB1 was delivered through nanocomplexes based on a cationic copolymer of poly(N-2-hydroxyethyl)-d,l-aspartamide (PHEA) by using H441 cells.	poly(n-2-hydroxyethyl)-d,l-aspartamide	169-207	high mobility group box 1	Homo sapiens	94-99
26140987-2	2015	In order to down-regulate HMGB1 expression in airway epithelial cells, siRNA directed against HMGB1 was delivered through nanocomplexes based on a cationic copolymer of poly(N-2-hydroxyethyl)-d,l-aspartamide (PHEA) by using H441 cells.	Phenethylamines	209-213	high mobility group box 1	Homo sapiens	94-99
26140987-10	2015	PEGylated PHEA-Spm/siRNA nanocomplexes were able to down-regulate HMGB1 mRNA levels up to 61% of control cells.	Phenethylamines	10-14	high mobility group box 1	Homo sapiens	66-71
26140987-12	2015	In conclusion, we have found optimal conditions for down-regulation of HMGB1 by siRNA delivery mediated by polyaminoacidic polymers in airway epithelial cells in the absence of cytotoxicity.	polyaminoacidic polymers	107-131	high mobility group box 1	Homo sapiens	71-76
25743565-3	2015	We accessed this question by monitoring the effects of posttreatment carbazole derivatives on LPS- and CLP-mediated release of HMGB1 and HMGB1-mediated regulation of proinflammatory responses in human umbilical vein endothelial cells (HUVECs) and septic mice.	carbazole	69-78	high mobility group box 1	Homo sapiens	137-142
25743565-4	2015	The new 3"-N-substituted carbazole derivatives 1-5 inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses in human endothelial cells.	3"-n-substituted carbazole	8-34	high mobility group box 1	Homo sapiens	76-81
25743565-4	2015	The new 3"-N-substituted carbazole derivatives 1-5 inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses in human endothelial cells.	3"-n-substituted carbazole	8-34	high mobility group box 1	Homo sapiens	100-105
26124331-0	2015	High-mobility Group Box 1 and Mitogen-activated Protein Kinase activated Protein Kinase-2 Are Up-regulated in Gemcitabine-resistant Pancreatic Cancer Cells.	gemcitabine	110-121	high mobility group box 1	Homo sapiens	0-25
26143914-5	2015	Two box A domains of HMGB1 collaborate in an unusual configuration in which the Phe37 residues of both domains stack together and intercalate the same CG base pair, generating highly kinked DNA.	cysteinylglycine	151-153	high mobility group box 1	Homo sapiens	21-26
26124331-9	2015	CONCLUSION: The increase of both HMGB1 and MAPKAPK2 in KLM1-R cells compared to KLM1 suggest the possibility of the activation of the pathway of HSP27 by HMGB1 and MAPKAPK2 in gemcitabine-resistant KLM1-R cells.	gemcitabine	176-187	high mobility group box 1	Homo sapiens	33-38
26124331-9	2015	CONCLUSION: The increase of both HMGB1 and MAPKAPK2 in KLM1-R cells compared to KLM1 suggest the possibility of the activation of the pathway of HSP27 by HMGB1 and MAPKAPK2 in gemcitabine-resistant KLM1-R cells.	gemcitabine	176-187	high mobility group box 1	Homo sapiens	154-159
26101955-7	2015	SA suppresses both the chemoattractant activity of fully reduced HMGB1 and the increased expression of proinflammatory cytokine genes and cyclooxygenase 2 (COX-2) induced by disulfide HMGB1.	Disulfides	174-183	high mobility group box 1	Homo sapiens	184-189
25861801-18	2015	In contrast to TLR4- and TLR2-binding lipopolysaccharide used as a positive control, disulfide-HMGB1 did not stimulate proinflammatory cytokines.	Disulfides	85-94	high mobility group box 1	Homo sapiens	95-100
26109393-13	2015	CG + GG genotype was associated with high HMGB1 levels compared with the genotype CC at 4 h (p = 0.023), and 24 h (p = 0.015) after CPB.	cysteinylglycine	0-2	high mobility group box 1	Homo sapiens	42-47
26101955-0	2015	Aspirin"s Active Metabolite Salicylic Acid Targets High Mobility Group Box 1 to Modulate Inflammatory Responses.	Aspirin	0-7	high mobility group box 1	Homo sapiens	51-76
26101955-8	2015	Natural and synthetic SA derivatives with greater potency for inhibition of HMGB1 were identified, providing proof-of-concept that new molecules with high efficacy against sterile inflammation are attainable.	Salicylic Acid	22-24	high mobility group box 1	Homo sapiens	76-81
26101955-0	2015	Aspirin"s Active Metabolite Salicylic Acid Targets High Mobility Group Box 1 to Modulate Inflammatory Responses.	Salicylic Acid	28-42	high mobility group box 1	Homo sapiens	51-76
26101955-5	2015	SA-binding sites on HMGB1 were identified in the HMG-box domains by nuclear magnetic resonance (NMR) spectroscopic studies and confirmed by mutational analysis.	Salicylic Acid	0-2	high mobility group box 1	Homo sapiens	20-25
26101955-9	2015	An HMGB1 protein mutated in one of the SA-binding sites identified by NMR chemical shift perturbation studies retained chemoattractant activity, but lost binding of and inhibition by SA and its derivatives, thereby firmly establishing that SA binding to HMGB1 directly suppresses its proinflammatory activities.	Salicylic Acid	39-41	high mobility group box 1	Homo sapiens	3-8
26101955-7	2015	SA suppresses both the chemoattractant activity of fully reduced HMGB1 and the increased expression of proinflammatory cytokine genes and cyclooxygenase 2 (COX-2) induced by disulfide HMGB1.	Salicylic Acid	0-2	high mobility group box 1	Homo sapiens	65-70
26101955-9	2015	An HMGB1 protein mutated in one of the SA-binding sites identified by NMR chemical shift perturbation studies retained chemoattractant activity, but lost binding of and inhibition by SA and its derivatives, thereby firmly establishing that SA binding to HMGB1 directly suppresses its proinflammatory activities.	Salicylic Acid	39-41	high mobility group box 1	Homo sapiens	254-259
26101955-7	2015	SA suppresses both the chemoattractant activity of fully reduced HMGB1 and the increased expression of proinflammatory cytokine genes and cyclooxygenase 2 (COX-2) induced by disulfide HMGB1.	Salicylic Acid	0-2	high mobility group box 1	Homo sapiens	184-189
26101955-9	2015	An HMGB1 protein mutated in one of the SA-binding sites identified by NMR chemical shift perturbation studies retained chemoattractant activity, but lost binding of and inhibition by SA and its derivatives, thereby firmly establishing that SA binding to HMGB1 directly suppresses its proinflammatory activities.	Salicylic Acid	183-185	high mobility group box 1	Homo sapiens	3-8
26101955-9	2015	An HMGB1 protein mutated in one of the SA-binding sites identified by NMR chemical shift perturbation studies retained chemoattractant activity, but lost binding of and inhibition by SA and its derivatives, thereby firmly establishing that SA binding to HMGB1 directly suppresses its proinflammatory activities.	Salicylic Acid	183-185	high mobility group box 1	Homo sapiens	3-8
26101955-10	2015	Identification of HMGB1 as a pharmacological target of SA/aspirin provides new insights into the mechanisms of action of one of the world"s longest and most used natural and synthetic drugs.	Salicylic Acid	55-57	high mobility group box 1	Homo sapiens	18-23
26101955-10	2015	Identification of HMGB1 as a pharmacological target of SA/aspirin provides new insights into the mechanisms of action of one of the world"s longest and most used natural and synthetic drugs.	Aspirin	58-65	high mobility group box 1	Homo sapiens	18-23
26068794-0	2015	Aspirin delays mesothelioma growth by inhibiting HMGB1-mediated tumor progression.	Aspirin	0-7	high mobility group box 1	Homo sapiens	49-54
26068794-3	2015	We hypothesized that ASA may exert anticancer properties in MM by abrogating the carcinogenic effects of HMGB1.	Aspirin	21-24	high mobility group box 1	Homo sapiens	105-110
26068794-4	2015	Using HMGB1-secreting and -non-secreting human MM cell lines, we determined whether aspirin inhibited the hallmarks of HMGB1-induced MM cell growth in vitro and in vivo.	Aspirin	84-91	high mobility group box 1	Homo sapiens	119-124
26068794-5	2015	Our data demonstrated that ASA and its metabolite, salicylic acid (SA), inhibit motility, migration, invasion and anchorage-independent colony formation of MM cells via a novel HMGB1-mediated mechanism.	Aspirin	27-30	high mobility group box 1	Homo sapiens	177-182
26068794-5	2015	Our data demonstrated that ASA and its metabolite, salicylic acid (SA), inhibit motility, migration, invasion and anchorage-independent colony formation of MM cells via a novel HMGB1-mediated mechanism.	Salicylic Acid	51-65	high mobility group box 1	Homo sapiens	177-182
26068794-5	2015	Our data demonstrated that ASA and its metabolite, salicylic acid (SA), inhibit motility, migration, invasion and anchorage-independent colony formation of MM cells via a novel HMGB1-mediated mechanism.	Salicylic Acid	28-30	high mobility group box 1	Homo sapiens	177-182
26068794-6	2015	ASA/SA, at serum concentrations comparable to those achieved in humans taking therapeutic doses of aspirin, and BoxA, a specific inhibitor of HMGB1, markedly reduced MM growth in xenograft mice and significantly improved survival of treated animals.	Salicylic Acid	1-3	high mobility group box 1	Homo sapiens	142-147
26068794-7	2015	The effects of ASA and BoxA were cyclooxygenase-2 independent and were not additive, consistent with both acting via inhibition of HMGB1 activity.	Aspirin	15-18	high mobility group box 1	Homo sapiens	131-136
26068794-8	2015	Our findings provide a rationale for the well documented, yet poorly understood antitumorigenic activity of aspirin, which we show proceeds via HMGB1 inhibition.	Aspirin	108-115	high mobility group box 1	Homo sapiens	144-149
26261543-0	2015	MiR-218 inhibits HMGB1-mediated autophagy in endometrial carcinoma cells during chemotherapy.	mir-218	0-7	high mobility group box 1	Homo sapiens	17-22
25856291-8	2015	Xenon treatment enhanced HIF-1alpha, which attenuated HMGB-1 translocation and NF-kappaB activation in A549 cells with oxidative and inflammatory stress.	Xenon	0-5	high mobility group box 1	Homo sapiens	54-60
25856291-11	2015	CONCLUSION: Xenon treatment confers protection against distant lung injury triggered by renal graft IRI, which is likely through the activation of mTOR-HIF-1alpha pathway and suppression of the HMGB-1 translocation from nuclei to cytoplasm.	Xenon	12-17	high mobility group box 1	Homo sapiens	194-200
26045910-0	2015	Increase in the Level of Proinflammatory Cytokine HMGB1 in Nasal Fluids of Patients With Rhinitis and its Sequestration by Glycyrrhizin Induces Eosinophil Cell Death.	Glycyrrhizic Acid	123-135	high mobility group box 1	Homo sapiens	50-55
26045910-6	2015	We also found that a formulation containing the HMGB1-binding compound glycyrrhizin (GLT) reduced the HMGB1 content in nasal fluids of rhinitis patients to an extent similar to that with nasal budesonide treatment.	Glycyrrhizic Acid	71-83	high mobility group box 1	Homo sapiens	48-53
26045910-6	2015	We also found that a formulation containing the HMGB1-binding compound glycyrrhizin (GLT) reduced the HMGB1 content in nasal fluids of rhinitis patients to an extent similar to that with nasal budesonide treatment.	Glycyrrhizic Acid	71-83	high mobility group box 1	Homo sapiens	102-107
26157321-15	2015	miR-218 can negatively regulate the HMGB1 protein expression and inhibit the proliferation and invasion of pancreatic cancer cells.	mir-218	0-7	high mobility group box 1	Homo sapiens	36-41
26157323-0	2015	microRNA-218 promotes gemcitabine sensitivity in human pancreatic cancer cells by regulating HMGB1 expression.	gemcitabine	22-33	high mobility group box 1	Homo sapiens	93-98
26157323-11	2015	miR-218 promoted the sensitivity of PANC-1 cells to GEM, which was achieved mainly through regulating the expression of HMGB1 in PANC-1 cells.	mir-218	0-7	high mobility group box 1	Homo sapiens	120-125
26261543-6	2015	HMGB1 was upregulated in paclitaxel resistant EC cells, it mediated autophagy and contributed to chemotherapy resistance in endometrial carcinoma in vitro.	Paclitaxel	25-35	high mobility group box 1	Homo sapiens	0-5
26261550-0	2015	HMGB1 is activated in type 2 diabetes mellitus patients and in mesangial cells in response to high glucose.	Glucose	99-106	high mobility group box 1	Homo sapiens	0-5
26261550-4	2015	In the present study, we examined the promotion by high glucose to High-mobility group box-1 (HMGB1) in patients with type 2 diabetes mellitus or in renal mesangial SV40 MES 13 cells.	Glucose	56-63	high mobility group box 1	Homo sapiens	67-92
26261550-4	2015	In the present study, we examined the promotion by high glucose to High-mobility group box-1 (HMGB1) in patients with type 2 diabetes mellitus or in renal mesangial SV40 MES 13 cells.	Glucose	56-63	high mobility group box 1	Homo sapiens	94-99
26261550-4	2015	In the present study, we examined the promotion by high glucose to High-mobility group box-1 (HMGB1) in patients with type 2 diabetes mellitus or in renal mesangial SV40 MES 13 cells.	2-(N-morpholino)ethanesulfonic acid	170-173	high mobility group box 1	Homo sapiens	94-99
26261550-7	2015	The in vitro results indicated that HMGB1 mediated the D-glucose-induced pro-inflammatory cytokines in mesangial cells.	Glucose	55-64	high mobility group box 1	Homo sapiens	36-41
26261550-9	2015	In summary, the present study indicated that HMGB1 was significantly promoted by the glucose in vivo or in vitro, in an association with an upregulation of pro-inflammatory cytokines, via activating NF-kappaB signaling pathway.	Glucose	85-92	high mobility group box 1	Homo sapiens	45-50
26261550-10	2015	And the strategy of HMGB1 inhibition reduced the upregulation of pro-inflammatory cytokines in response to high glucose, via inhibiting the NF-kappaB signaling pathway.	Glucose	112-119	high mobility group box 1	Homo sapiens	20-25
25192219-3	2015	Therefore, we hypothesized that CS promotes neutrophil necrosis with subsequent release of damage-associated molecular patterns (DAMPs), including high mobility group box 1 (HMGB1), alarming the innate immune system.	Cesium	32-34	high mobility group box 1	Homo sapiens	147-172
25940319-0	2015	Retraction Note to: Nafamostat mesilate inhibits the expression of HMGB1 in lipopolysaccharide-induced acute lung injury.	nafamostat	20-39	high mobility group box 1	Homo sapiens	67-72
25873535-5	2015	A Pt(II) N-heterocyclic carbene complex was found to display the characteristic hallmarks of a type II ICD inducer, namely focused oxidative endoplasmic reticulum (ER) stress, calreticulin exposure, and both HMGB1 and ATP release, and thus identified as the first small-molecule immuno-chemotherapeutic agent.	carbene	24-31	high mobility group box 1	Homo sapiens	208-213
25966225-9	2015	Furthermore, HMGB1 expression level was positively correlated with 8-hydroxyguanosine, vascular cell adhesion molecule 1, nuclear factor-kB, CD3, and CD68 expression.	8-hydroxyguanosine	67-85	high mobility group box 1	Homo sapiens	13-18
25651569-10	2015	Direct activation of proximal tubular cells by uric acid resulted in (C-X-C motif) ligand 12 and high mobility group box-1 release and accelerated macrophage recruitment and the M1 phenotype.	Uric Acid	47-56	high mobility group box 1	Homo sapiens	97-122
25192219-3	2015	Therefore, we hypothesized that CS promotes neutrophil necrosis with subsequent release of damage-associated molecular patterns (DAMPs), including high mobility group box 1 (HMGB1), alarming the innate immune system.	Cesium	32-34	high mobility group box 1	Homo sapiens	174-179
25561283-0	2015	HMGB1 Silencing Potentiates the Anti-inflammatory Effects of Sodium Ferulate in ox-LDL-Stimulated Vascular Smooth Muscle Cells.	ferulic acid	61-76	high mobility group box 1	Homo sapiens	0-5
25561283-3	2015	In addition, we also sought to determine whether HMGB1 knockdown could potentiate the anti-inflammatory effects of sodium ferulate.	ferulic acid	115-130	high mobility group box 1	Homo sapiens	49-54
25817178-0	2015	Irbesartan attenuates production of high-mobility group box 1 in response to lipopolysaccharide via downregulation of interferon-beta production.	Irbesartan	0-10	high mobility group box 1	Homo sapiens	36-61
25983116-0	2015	Quercetin protects necrotic insult and promotes apoptosis by attenuating the expression of RAGE and its ligand HMGB1 in human breast adenocarcinoma cells.	Quercetin	0-9	high mobility group box 1	Homo sapiens	111-116
25983116-6	2015	This study was aimed to examine the biological potential of quercetin on the regulation of RAGE- and HMGB1-mediated activation of NF-kappaB and induction of apoptotic cell death in MCF-7 cells.	Quercetin	60-69	high mobility group box 1	Homo sapiens	101-106
25983116-7	2015	Our findings demonstrate that quercetin inhibits the expression of RAGE and HMGB1 in MCF-7 cells.	Quercetin	30-39	high mobility group box 1	Homo sapiens	76-81
25983116-9	2015	Taken together, these results suggest that quercetin plays an important role in modulating RAGE and HMGB1 signaling and induces apoptotic cell death in MCF-7 cells.	Quercetin	43-52	high mobility group box 1	Homo sapiens	100-105
25726846-10	2015	Silencing of c-Jun ablated the HMGB1-induced proliferation in PASMC.	pasmc	62-67	high mobility group box 1	Homo sapiens	31-36
25755254-0	2015	Carbon-ion beams induce production of an immune mediator protein, high mobility group box 1, at levels comparable with X-ray irradiation.	Carbon	0-6	high mobility group box 1	Homo sapiens	66-91
25578401-5	2015	In the present study, we explored the mechanisms whereby HMGB1 regulates tumor cell autophagy during nutrient depletion (the cells were cultured in Hank"s balanced salt solution, HBSS).	hank"s balanced salt solution	148-177	high mobility group box 1	Homo sapiens	57-62
25578401-5	2015	In the present study, we explored the mechanisms whereby HMGB1 regulates tumor cell autophagy during nutrient depletion (the cells were cultured in Hank"s balanced salt solution, HBSS).	hbss	179-183	high mobility group box 1	Homo sapiens	57-62
25755254-2	2015	Here, we examined whether carbon-ion beams, as well as X-rays, can induce HMGB1 release from human cancer cell lines.	Carbon	26-32	high mobility group box 1	Homo sapiens	74-79
25755254-8	2015	X-rays and carbon-ion beams significantly increased HMGB1 levels in the culture supernatants of A549, NCI-H460 and WiDr cells at 72 h post-irradiation with a D10 dose.	Carbon	11-17	high mobility group box 1	Homo sapiens	52-57
25755254-9	2015	Furthermore, irradiation with X-rays or carbon-ion beams significantly increased HMGB1 levels in the culture supernatants of all five cell lines at 96 h post-irradiation.	Carbon	40-46	high mobility group box 1	Homo sapiens	81-86
26131056-2	2015	This study was to investigate the relationship between average blood glucose level and HMGB1 level in CAD with T2DM patients.	Glucose	69-76	high mobility group box 1	Homo sapiens	87-92
25769801-7	2015	In addition, synergistic NO accumulation along with direct HMGB1-LPS binding was also observed when primary microglial cultures were treated with LPS (5 ng/ml) and HMGB1 accumulated in NMDA-conditioned medium (NCM).	N-Methylaspartate	185-189	high mobility group box 1	Homo sapiens	59-64
25769801-7	2015	In addition, synergistic NO accumulation along with direct HMGB1-LPS binding was also observed when primary microglial cultures were treated with LPS (5 ng/ml) and HMGB1 accumulated in NMDA-conditioned medium (NCM).	N-Methylaspartate	185-189	high mobility group box 1	Homo sapiens	164-169
25769801-10	2015	Together these results show HBHP has anti-inflammatory effects, and that it inhibits synergism caused by the binding of HMGB1 and LPS.	hbhp	28-32	high mobility group box 1	Homo sapiens	120-125
26131056-10	2015	Increased blood glucose levels may contribute to the increased HMGB1 levels.	Glucose	16-23	high mobility group box 1	Homo sapiens	63-68
25612780-7	2015	CONCLUSIONS: Collectively, this study suggested that the HMGB1-mediated Mcl-1 transcription upregulation is a key mechanism by which autophagy protects oral cancer cells against vincristine-induced apoptosis.	Vincristine	178-189	high mobility group box 1	Homo sapiens	57-62
25831509-3	2015	We have developed single-molecule assays to examine RSS binding by RAG1/2 and their cofactor high-mobility group-box protein 1 (HMGB1) as they proceed through the steps of this reaction.	RSS	52-55	high mobility group box 1	Homo sapiens	128-133
25807407-0	2015	Ketamine reduces LPS-induced HMGB1 via activation of the Nrf2/HO-1 pathway and NF-kappaB suppression.	Ketamine	0-8	high mobility group box 1	Homo sapiens	29-34
25612780-3	2015	RESEARCH DESIGN AND METHODS: In this study, we determined that HMGB1 released by oral cancer cells protected the cells against apoptosis caused by vincristine by upregulating the transcription of Mcl-1.	Vincristine	147-158	high mobility group box 1	Homo sapiens	63-68
25612780-6	2015	HMGB1 expression inhibited blocked the Mcl-1 transcription increase and reduced Mcl-1 expression, demonstrate that HMGB1 is required for the upregulation of Mcl-1 transcriptional, and thereby maintaining Mcl-1 protein expression levels is required for the survival of oral cancer cells by vincristine.	Vincristine	289-300	high mobility group box 1	Homo sapiens	0-5
25612780-6	2015	HMGB1 expression inhibited blocked the Mcl-1 transcription increase and reduced Mcl-1 expression, demonstrate that HMGB1 is required for the upregulation of Mcl-1 transcriptional, and thereby maintaining Mcl-1 protein expression levels is required for the survival of oral cancer cells by vincristine.	Vincristine	289-300	high mobility group box 1	Homo sapiens	115-120
25807407-7	2015	RESULTS: Ketamine treatment dose-dependently attenuated the increased levels of proinflammatory mediators (HMGB1, nitric oxide, tumor necrosis factor alpha, and interleukin 1beta) and increased the HO-1 protein expression in LPS-activated macrophages.	Ketamine	9-17	high mobility group box 1	Homo sapiens	107-112
25807407-2	2015	In the present study, we investigated whether ketamine inhibits release of high mobility group box 1 (HMGB1), a late-phase cytokine of sepsis, in lipopolysaccharide (LPS)-stimulated macrophages through heme oxygenase-1 (HO-1) induction.	Ketamine	46-54	high mobility group box 1	Homo sapiens	75-100
25807407-11	2015	CONCLUSION: Ketamine inhibits the release of HMGB1 in LPS-stimulated macrophages, and this effect is at least partly mediated by the activation of the Nrf2/HO-1 pathway and NF-kappaB suppression.	Ketamine	12-20	high mobility group box 1	Homo sapiens	45-50
25807407-2	2015	In the present study, we investigated whether ketamine inhibits release of high mobility group box 1 (HMGB1), a late-phase cytokine of sepsis, in lipopolysaccharide (LPS)-stimulated macrophages through heme oxygenase-1 (HO-1) induction.	Ketamine	46-54	high mobility group box 1	Homo sapiens	102-107
25715249-10	2015	By contrast, the secretion of the nuclear-associated danger signal HMGB1 is independent of cysteine oxidation, as shown by experiments with a cysteine-free HMGB1 mutant.	Cysteine	91-99	high mobility group box 1	Homo sapiens	67-72
25652880-5	2015	Western blot analysis and ELISA were used to assess the effects of gefitinib, an epidermal growth factor receptor inhibitor, on autophagy and HMGB1 release in BGC-823 cells.	Gefitinib	67-76	high mobility group box 1	Homo sapiens	142-147
25652880-10	2015	Gefitinib increased autophagy and cytoplasmic HMGB1 release from the BGC-823 cells.	Gefitinib	0-9	high mobility group box 1	Homo sapiens	46-51
25652880-11	2015	Extracellular HMGB1 in autophagic cell supernatant promoted proliferation that was abolished by glycyrrhizic acid, an HMGB1 inhibitor.	Glycyrrhizic Acid	96-113	high mobility group box 1	Homo sapiens	14-19
25652880-11	2015	Extracellular HMGB1 in autophagic cell supernatant promoted proliferation that was abolished by glycyrrhizic acid, an HMGB1 inhibitor.	Glycyrrhizic Acid	96-113	high mobility group box 1	Homo sapiens	118-123
25385285-3	2015	The cell proliferation, invasion, apoptosis and the gene and protein expression of HMGB1 and NF-kappaB were detected using a tetrazolium assay, Transwell cell invasion assays, a caspase-3 activity assay, western blot analysis and reverse transcription quantitative polymerase chain reaction, respectively.	Tetrazolium Salts	125-136	high mobility group box 1	Homo sapiens	83-88
25582705-9	2015	Collectively, our results demonstrate that PA prevents experimental pulmonary fibrosis by modulating HMGB1/RAGE pathway.	protocatechualdehyde	43-45	high mobility group box 1	Homo sapiens	101-106
25879749-8	2015	The newly generated mCRP induced platelets activation on ANCA-induced netting neutrophils, enhanced D-dimer formation, and enhanced high mobility group box 1 secretion by platelets.	mcrp	20-24	high mobility group box 1	Homo sapiens	132-157
29449921-0	2015	HMGB1 bound to cisplatin-DNA adducts undergoes extensive acetylation and phosphorylation in vivo.	Cisplatin	15-24	high mobility group box 1	Homo sapiens	0-5
29449921-2	2015	For many years, HMGB1 has been known to be a recognition protein for cisplatin-DNA lesions.	Cisplatin	69-78	high mobility group box 1	Homo sapiens	16-21
29449921-5	2015	Interestingly, at least 4 subforms of HMGB1 bind to cisplatin-DNA adducts.	Cisplatin	52-61	high mobility group box 1	Homo sapiens	38-43
25582705-0	2015	Protocatechuic aldehyde ameliorates experimental pulmonary fibrosis by modulating HMGB1/RAGE pathway.	Aldehydes	15-23	high mobility group box 1	Homo sapiens	82-87
25715249-10	2015	By contrast, the secretion of the nuclear-associated danger signal HMGB1 is independent of cysteine oxidation, as shown by experiments with a cysteine-free HMGB1 mutant.	Cysteine	142-150	high mobility group box 1	Homo sapiens	67-72
25452436-2	2015	SUMMARY ANSWER: HMGB1 appears to be involved in regulating inflammatory reactions in testes, as HMGB1 is translocated from testicular cells during the course of EAO and blocking its action by ethyl pyruvate (EP) reduces disease progression and spermatogenic damage.	ethyl pyruvate	192-206	high mobility group box 1	Homo sapiens	16-21
25543984-0	2015	Adsorption properties of an activated carbon for 18 cytokines and HMGB1 from inflammatory model plasma.	Carbon	38-44	high mobility group box 1	Homo sapiens	66-71
25543984-1	2015	The ability of an activated carbon (AC) to adsorb 18 different cytokines with molecular weights ranging from 8 kDa to 70 kDa and high mobility group box-1 (HMGB1) from inflammatory model plasma at 310 K and the mechanisms of adsorption were examined.	Carbon	28-34	high mobility group box 1	Homo sapiens	129-154
25543984-1	2015	The ability of an activated carbon (AC) to adsorb 18 different cytokines with molecular weights ranging from 8 kDa to 70 kDa and high mobility group box-1 (HMGB1) from inflammatory model plasma at 310 K and the mechanisms of adsorption were examined.	Carbon	28-34	high mobility group box 1	Homo sapiens	156-161
25452436-2	2015	SUMMARY ANSWER: HMGB1 appears to be involved in regulating inflammatory reactions in testes, as HMGB1 is translocated from testicular cells during the course of EAO and blocking its action by ethyl pyruvate (EP) reduces disease progression and spermatogenic damage.	ethyl pyruvate	192-206	high mobility group box 1	Homo sapiens	96-101
25452436-19	2015	In support, HMGB1 triggered extracellular signal regulated kinase (ERK)1/2 and cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) activation in SC and PTC, while TM responded to HMGB1 stimulation with p38 mitogen-activated protein kinase (MAPK) and p65 nuclear factor Kappa B (NF-kB) phosphorylation followed by increased tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) mRNA levels.	Cyclic AMP	79-109	high mobility group box 1	Homo sapiens	12-17
25452436-19	2015	In support, HMGB1 triggered extracellular signal regulated kinase (ERK)1/2 and cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) activation in SC and PTC, while TM responded to HMGB1 stimulation with p38 mitogen-activated protein kinase (MAPK) and p65 nuclear factor Kappa B (NF-kB) phosphorylation followed by increased tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) mRNA levels.	Cyclic AMP	111-115	high mobility group box 1	Homo sapiens	12-17
25973018-12	2015	BCG induced HMGB1, IL-6, IL-10 and TNF-alpha production effectively in PMA-treated THP-1 cells.	Tetradecanoylphorbol Acetate	71-74	high mobility group box 1	Homo sapiens	12-17
25434832-7	2015	Moreover, treatment of CRC cells with TRAIL or ABT-737 induces a release of endogenous HMGB1 into the extracellular space, and preincubation with glycyrrhizin, an HMGB1 inhibitor, significantly inhibits induction of cell death by TRAIL and ABT-737, suggesting that HMGB1 functionally contributes to the execution of cell death triggered by pro-apoptotic agents.	ABT-737	47-54	high mobility group box 1	Homo sapiens	163-168
25434832-7	2015	Moreover, treatment of CRC cells with TRAIL or ABT-737 induces a release of endogenous HMGB1 into the extracellular space, and preincubation with glycyrrhizin, an HMGB1 inhibitor, significantly inhibits induction of cell death by TRAIL and ABT-737, suggesting that HMGB1 functionally contributes to the execution of cell death triggered by pro-apoptotic agents.	Glycyrrhizic Acid	146-158	high mobility group box 1	Homo sapiens	87-92
25434832-7	2015	Moreover, treatment of CRC cells with TRAIL or ABT-737 induces a release of endogenous HMGB1 into the extracellular space, and preincubation with glycyrrhizin, an HMGB1 inhibitor, significantly inhibits induction of cell death by TRAIL and ABT-737, suggesting that HMGB1 functionally contributes to the execution of cell death triggered by pro-apoptotic agents.	Glycyrrhizic Acid	146-158	high mobility group box 1	Homo sapiens	163-168
25434832-7	2015	Moreover, treatment of CRC cells with TRAIL or ABT-737 induces a release of endogenous HMGB1 into the extracellular space, and preincubation with glycyrrhizin, an HMGB1 inhibitor, significantly inhibits induction of cell death by TRAIL and ABT-737, suggesting that HMGB1 functionally contributes to the execution of cell death triggered by pro-apoptotic agents.	Glycyrrhizic Acid	146-158	high mobility group box 1	Homo sapiens	163-168
25434832-5	2015	HMGB1-triggered cell death is associated with intracellular ROS release, and overexpression of Bcl-2 blocks both the increase of ROS as well as HMGB1-dependent cell death.	ros	60-63	high mobility group box 1	Homo sapiens	0-5
25434832-5	2015	HMGB1-triggered cell death is associated with intracellular ROS release, and overexpression of Bcl-2 blocks both the increase of ROS as well as HMGB1-dependent cell death.	ros	129-132	high mobility group box 1	Homo sapiens	0-5
25434832-6	2015	Importantly, treatment with recombinant HMGB1 or overexpression of endogenous HMGB1 strongly sensitizes CRC cells to the cytotoxic activity of the pro-apoptotic death ligand TRAIL as well as the small molecule Bcl-2 family inhibitor ABT-737.	ABT-737	233-240	high mobility group box 1	Homo sapiens	40-45
25247290-9	2015	Disease control coincided with supplementary etoposide therapy initiated to boost apoptotic cell death, when systemic HMGB1 levels drastically declined and the molecule emerged mainly in its oxidized, noninflammatory isoform.	Etoposide	45-54	high mobility group box 1	Homo sapiens	118-123
25434832-6	2015	Importantly, treatment with recombinant HMGB1 or overexpression of endogenous HMGB1 strongly sensitizes CRC cells to the cytotoxic activity of the pro-apoptotic death ligand TRAIL as well as the small molecule Bcl-2 family inhibitor ABT-737.	ABT-737	233-240	high mobility group box 1	Homo sapiens	78-83
25434832-7	2015	Moreover, treatment of CRC cells with TRAIL or ABT-737 induces a release of endogenous HMGB1 into the extracellular space, and preincubation with glycyrrhizin, an HMGB1 inhibitor, significantly inhibits induction of cell death by TRAIL and ABT-737, suggesting that HMGB1 functionally contributes to the execution of cell death triggered by pro-apoptotic agents.	ABT-737	47-54	high mobility group box 1	Homo sapiens	87-92
25434832-7	2015	Moreover, treatment of CRC cells with TRAIL or ABT-737 induces a release of endogenous HMGB1 into the extracellular space, and preincubation with glycyrrhizin, an HMGB1 inhibitor, significantly inhibits induction of cell death by TRAIL and ABT-737, suggesting that HMGB1 functionally contributes to the execution of cell death triggered by pro-apoptotic agents.	ABT-737	47-54	high mobility group box 1	Homo sapiens	163-168
25377911-6	2015	Moreover, a glycyrrhizic acid derivative, a blocker of HMGB1 release, reduced UUO-mediated kidney injury and ameliorated UUO-induced renal fibrosis.	Glycyrrhizic Acid	12-29	high mobility group box 1	Homo sapiens	55-60
25973309-0	2015	Reactive oxygen species regulate the differentiation of acute promyelocytic leukemia cells through HMGB1-mediated autophagy.	Reactive Oxygen Species	0-23	high mobility group box 1	Homo sapiens	99-104
25973309-5	2015	HMGB1 was vital for the differentiation of ROS-mediated NB4 cells and its up-regulation promoted ATRA-induced autophagy and the degradation of PML-RARalpha.	Reactive Oxygen Species	43-46	high mobility group box 1	Homo sapiens	0-5
25973309-6	2015	Furthermore, ATRA treatment elevated the levels of ROS, enhanced autophagic flux and thereby promoted cytosolic translocation of HMGB1.	Tretinoin	13-17	high mobility group box 1	Homo sapiens	129-134
25973309-7	2015	HMGB1 regulated the interactions between ubiquitin-binding adaptor protein p62/SQSTM and PML-RARalpha so as to affect the degradation of PML-RARalpha during ATRA-induced autophagy.	Tretinoin	157-161	high mobility group box 1	Homo sapiens	0-5
25973309-9	2015	The overall results suggested that HMGB1 is an essential regulator of ROS-induced cell differentiation.	Reactive Oxygen Species	70-73	high mobility group box 1	Homo sapiens	35-40
26695754-2	2015	Ethanol exposure activates signaling pathways featuring high-mobility group box 1 and Toll-like receptor 4 (TLR4), resulting in induction of the transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells, which regulates expression of several cytokine genes involved in innate immunity, and its target genes.	Ethanol	0-7	high mobility group box 1	Homo sapiens	56-81
25607248-0	2015	Poly-ADP-ribosylation of HMGB1 regulates TNFSF10/TRAIL resistance through autophagy.	poly-adp	0-8	high mobility group box 1	Homo sapiens	25-30
25778491-0	2015	HMGB1-mediated autophagy modulates sensitivity of colorectal cancer cells to oxaliplatin via MEK/ERK signaling pathway.	Oxaliplatin	77-88	high mobility group box 1	Homo sapiens	0-5
25778491-3	2015	Administration of oxaliplatin to human CRC cells significantly enhanced the expression of HMGB1, which regulated the autophagy response and negatively regulate the cell apoptosis.	Oxaliplatin	18-29	high mobility group box 1	Homo sapiens	90-95
25778491-4	2015	Moreover, a decreased oxaliplatin -induced autophagy response and an increased apoptosis level were detected in stable CRC cells harboring HMGB1 shRNA.	Oxaliplatin	22-33	high mobility group box 1	Homo sapiens	139-144
25778491-6	2015	Taken together, these data suggest that HMGB1-mediated autophagy modulates sensitivity of colorectal cancer cells to oxaliplatin via MEK/ERK signaling pathway.	Oxaliplatin	117-128	high mobility group box 1	Homo sapiens	40-45
25896065-10	2015	An HMGB-1 inhibitor glycyrrhizin suppressed high glucose-induced Syk activation.	Glycyrrhizic Acid	20-32	high mobility group box 1	Homo sapiens	3-9
25896065-10	2015	An HMGB-1 inhibitor glycyrrhizin suppressed high glucose-induced Syk activation.	Glucose	49-56	high mobility group box 1	Homo sapiens	3-9
25896065-9	2015	High-mobility group box-1 (HMGB-1), an endogenous activator of TLR4, rapidly increased in TLR4 immunoprecipitates upon high glucose stimulation, and this association was reduced by N-acetylcysteine, an antioxidant.	Glucose	124-131	high mobility group box 1	Homo sapiens	0-25
25896065-12	2015	High glucose induces an immediate, reactive oxygen species-dependent, extracellular release of HMGB-1 which binds to TLR4 and activates it, leading to Syk activation.	Glucose	5-12	high mobility group box 1	Homo sapiens	95-101
25896065-9	2015	High-mobility group box-1 (HMGB-1), an endogenous activator of TLR4, rapidly increased in TLR4 immunoprecipitates upon high glucose stimulation, and this association was reduced by N-acetylcysteine, an antioxidant.	Glucose	124-131	high mobility group box 1	Homo sapiens	27-33
25896065-12	2015	High glucose induces an immediate, reactive oxygen species-dependent, extracellular release of HMGB-1 which binds to TLR4 and activates it, leading to Syk activation.	Reactive Oxygen Species	35-58	high mobility group box 1	Homo sapiens	95-101
25896065-9	2015	High-mobility group box-1 (HMGB-1), an endogenous activator of TLR4, rapidly increased in TLR4 immunoprecipitates upon high glucose stimulation, and this association was reduced by N-acetylcysteine, an antioxidant.	Acetylcysteine	181-197	high mobility group box 1	Homo sapiens	0-25
26299081-13	2015	In OA patients, HMGB-1 in the KL2/3 group was higher than in the KL4 group.	adenosine-2',3'-vanadate	30-33	high mobility group box 1	Homo sapiens	16-22
25896065-9	2015	High-mobility group box-1 (HMGB-1), an endogenous activator of TLR4, rapidly increased in TLR4 immunoprecipitates upon high glucose stimulation, and this association was reduced by N-acetylcysteine, an antioxidant.	Acetylcysteine	181-197	high mobility group box 1	Homo sapiens	27-33
26299081-13	2015	In OA patients, HMGB-1 in the KL2/3 group was higher than in the KL4 group.	sinapultide	65-68	high mobility group box 1	Homo sapiens	16-22
26260962-7	2015	Moreover, recent studies have described models of epilepsy induced by the administration of bicuculline and kainic acid that highlight the nature of HMGB1-TLR4 interactions, their intracellular signaling pathway as well as their role in ictiogenesis and epileptic recurrence.The aim of our review is to focus on different branches of innate immunity and their role in epilepsy, emphasizing the role of immune related molecules in epileptogenesis and highlighting the research implications for novel therapeutic strategies.	Bicuculline	92-103	high mobility group box 1	Homo sapiens	149-154
26260962-7	2015	Moreover, recent studies have described models of epilepsy induced by the administration of bicuculline and kainic acid that highlight the nature of HMGB1-TLR4 interactions, their intracellular signaling pathway as well as their role in ictiogenesis and epileptic recurrence.The aim of our review is to focus on different branches of innate immunity and their role in epilepsy, emphasizing the role of immune related molecules in epileptogenesis and highlighting the research implications for novel therapeutic strategies.	Kainic Acid	108-119	high mobility group box 1	Homo sapiens	149-154
27163120-5	2014	Combining CMT-3 with TSN-SS led to enhanced accumulation of endogenous LC3-II, but reduced HMGB1 cytoplasmic translocation.	tanshinone II A sodium sulfonate	21-27	high mobility group box 1	Homo sapiens	91-96
25311659-0	2015	Interaction of adriamycin with a regulatory element of hmgb1: spectroscopic and calorimetric approach.	Doxorubicin	15-25	high mobility group box 1	Homo sapiens	55-60
25311659-3	2015	Because of the clear association between HMGB1 and cancer, we studied the binding of adriamycin (ADM), a well-known anticancer drug with the promoter region (-165 to -183) of hmgb1 by using a variety of spectroscopic, calorimetric techniques, and in-silico molecular modeling.	Doxorubicin	85-95	high mobility group box 1	Homo sapiens	175-180
25311659-3	2015	Because of the clear association between HMGB1 and cancer, we studied the binding of adriamycin (ADM), a well-known anticancer drug with the promoter region (-165 to -183) of hmgb1 by using a variety of spectroscopic, calorimetric techniques, and in-silico molecular modeling.	Doxorubicin	97-100	high mobility group box 1	Homo sapiens	175-180
24940804-4	2015	Proteomic analysis showed that SIRT1 deacetylates HMGB1 at four lysine residues (55, 88, 90, and 177) within the proinflammatory and nuclear localization signal domains of HMGB1.	Lysine	64-70	high mobility group box 1	Homo sapiens	50-55
24940804-4	2015	Proteomic analysis showed that SIRT1 deacetylates HMGB1 at four lysine residues (55, 88, 90, and 177) within the proinflammatory and nuclear localization signal domains of HMGB1.	Lysine	64-70	high mobility group box 1	Homo sapiens	172-177
24940804-7	2015	Conversely, resveratrol pretreatment led to decreased HMGB1 acetylation, its nuclear retention, decreased systemic release, and reduced tubular damage.	Resveratrol	12-23	high mobility group box 1	Homo sapiens	54-59
25512109-8	2014	The effect of an HMGB1 neutralizing antibody on Dox resistance induced by extracellular HMGB1 from non-viable Dox-treated cancer cells or recombinant HMGB1 was also investigated.	Doxorubicin	48-51	high mobility group box 1	Homo sapiens	17-22
25512109-8	2014	The effect of an HMGB1 neutralizing antibody on Dox resistance induced by extracellular HMGB1 from non-viable Dox-treated cancer cells or recombinant HMGB1 was also investigated.	Doxorubicin	48-51	high mobility group box 1	Homo sapiens	88-93
25512109-8	2014	The effect of an HMGB1 neutralizing antibody on Dox resistance induced by extracellular HMGB1 from non-viable Dox-treated cancer cells or recombinant HMGB1 was also investigated.	Doxorubicin	48-51	high mobility group box 1	Homo sapiens	88-93
25512109-11	2014	Intracellular HMGB1 expression was induced in BCF-CM-treated breast cancer cells and also in Dox-treated cells.	Doxorubicin	93-96	high mobility group box 1	Homo sapiens	14-19
25512109-12	2014	Extracellular HMGB1 was strongly expressed in the CM after Dox-induced MDA-MB-231 cell death and was higher in cells pre-treated with BCF-CM than NTF-CM.	Doxorubicin	59-62	high mobility group box 1	Homo sapiens	14-19
25512109-14	2014	Recombinant HMGB1 was shown to increase Dox resistance and this was associated with evidence of autophagy.	Doxorubicin	40-43	high mobility group box 1	Homo sapiens	12-17
25512109-15	2014	Anti-HMGB1 neutralizing antibody significantly reduced the effect of extracellular HMGB1 released from dying cancer cells or of recombinant HMGB1 on Dox resistance.	Doxorubicin	149-152	high mobility group box 1	Homo sapiens	5-10
25512109-15	2014	Anti-HMGB1 neutralizing antibody significantly reduced the effect of extracellular HMGB1 released from dying cancer cells or of recombinant HMGB1 on Dox resistance.	Doxorubicin	149-152	high mobility group box 1	Homo sapiens	83-88
25512109-15	2014	Anti-HMGB1 neutralizing antibody significantly reduced the effect of extracellular HMGB1 released from dying cancer cells or of recombinant HMGB1 on Dox resistance.	Doxorubicin	149-152	high mobility group box 1	Homo sapiens	83-88
25499383-8	2014	In the overall comparison, reduction of both SBP and DBP with eplerenone was greater than other antihypertensive agents (WMD for SBP -1.50 mm Hg, p &lt; 0.0001; WMD for DBP -0.54 mm Hg, p &lt; 0.00001); this was essentially driven by a greater anti-hypertensive action vs enalapril and losartan for SBP and vs losartan for DBP.	Eplerenone	62-72	high mobility group box 1	Homo sapiens	129-135
25864748-4	2015	This study was undertaken to analyze whether disrupting the microtubule cytoskeleton by colchicine modulates transcriptional levels of MEFV, NF-kappaB p65, NLRP3, HMGB1, and caspase-3 in neutrophils from patients with familial Mediterranean fever (FMF) and healthy subjects.	Colchicine	88-98	high mobility group box 1	Homo sapiens	163-168
26226834-5	2015	BQ123 and FAK inhibitor or shRNA, but not BQ788, completely abolished the promoting effect of ET-1 on the expression of HMGB1.	cyclo(Trp-Asp-Pro-Val-Leu)	0-5	high mobility group box 1	Homo sapiens	120-125
26226834-7	2015	In the presence of the transcription inhibitor actinomycin D, the HMGB1 mRNA level markedly decreased over time, and ET-1 dose-dependently rescued the HMGB1 mRNA level.	Dactinomycin	47-60	high mobility group box 1	Homo sapiens	66-71
26226834-7	2015	In the presence of the transcription inhibitor actinomycin D, the HMGB1 mRNA level markedly decreased over time, and ET-1 dose-dependently rescued the HMGB1 mRNA level.	Dactinomycin	47-60	high mobility group box 1	Homo sapiens	151-156
25549101-7	2014	In starvation-stressed TBP/Q36 and TBP/Q79 cells, increased reactive oxygen species generation accelerated the cytoplasmic translocation of HMGB1, which accompanied autophagy activation.	Oxygen	69-75	high mobility group box 1	Homo sapiens	140-145
25926862-9	2014	The HMGB1 levels were higher in patients with infection during the clinical course, the HMGB1 levels in non-survivors were higher than those in survivors, and positively correlated with DAO activity, L/M ratio, the concentration of endotoxin (R = 0.484, P &lt;0.01).	lauric acid	186-189	high mobility group box 1	Homo sapiens	88-93
27163120-7	2014	As an ovel candidate for cancer therapy, CMT-3 may be used in combination with TSN-SS, which possibly facilitates the execution of a death signal (e.g. autophagy) and prevents the survival of an inducer (e.g. HMGB1 cytoplasmic translocation), thus improving its therapeutic effect.	tanshinone II A sodium sulfonate	79-85	high mobility group box 1	Homo sapiens	209-214
24780928-9	2014	We found that different intracellular sources of ROS are triggered by contact allergens, and an important role for HMGB1 in chemical allergen-induced IL-18 production was demonstrated.	Reactive Oxygen Species	49-52	high mobility group box 1	Homo sapiens	115-120
25014009-3	2014	The degree to which HMGB1 activates a receptor is thought to be dependent upon the oxidative state of the ligand, resulting in the functional isoforms of all-thiol HMGB1 (at-HMGB1) acting through RAGE, and disufide HMGB1 (ds-HMGB1) interacting with TLR4.	Sulfhydryl Compounds	158-163	high mobility group box 1	Homo sapiens	20-25
25014009-3	2014	The degree to which HMGB1 activates a receptor is thought to be dependent upon the oxidative state of the ligand, resulting in the functional isoforms of all-thiol HMGB1 (at-HMGB1) acting through RAGE, and disufide HMGB1 (ds-HMGB1) interacting with TLR4.	Sulfhydryl Compounds	158-163	high mobility group box 1	Homo sapiens	164-169
25014009-3	2014	The degree to which HMGB1 activates a receptor is thought to be dependent upon the oxidative state of the ligand, resulting in the functional isoforms of all-thiol HMGB1 (at-HMGB1) acting through RAGE, and disufide HMGB1 (ds-HMGB1) interacting with TLR4.	Sulfhydryl Compounds	158-163	high mobility group box 1	Homo sapiens	164-169
25014009-3	2014	The degree to which HMGB1 activates a receptor is thought to be dependent upon the oxidative state of the ligand, resulting in the functional isoforms of all-thiol HMGB1 (at-HMGB1) acting through RAGE, and disufide HMGB1 (ds-HMGB1) interacting with TLR4.	Sulfhydryl Compounds	158-163	high mobility group box 1	Homo sapiens	164-169
25014009-3	2014	The degree to which HMGB1 activates a receptor is thought to be dependent upon the oxidative state of the ligand, resulting in the functional isoforms of all-thiol HMGB1 (at-HMGB1) acting through RAGE, and disufide HMGB1 (ds-HMGB1) interacting with TLR4.	Sulfhydryl Compounds	158-163	high mobility group box 1	Homo sapiens	164-169
25014009-3	2014	The degree to which HMGB1 activates a receptor is thought to be dependent upon the oxidative state of the ligand, resulting in the functional isoforms of all-thiol HMGB1 (at-HMGB1) acting through RAGE, and disufide HMGB1 (ds-HMGB1) interacting with TLR4.	disufide	206-214	high mobility group box 1	Homo sapiens	20-25
25014009-3	2014	The degree to which HMGB1 activates a receptor is thought to be dependent upon the oxidative state of the ligand, resulting in the functional isoforms of all-thiol HMGB1 (at-HMGB1) acting through RAGE, and disufide HMGB1 (ds-HMGB1) interacting with TLR4.	disufide	206-214	high mobility group box 1	Homo sapiens	164-169
25014009-3	2014	The degree to which HMGB1 activates a receptor is thought to be dependent upon the oxidative state of the ligand, resulting in the functional isoforms of all-thiol HMGB1 (at-HMGB1) acting through RAGE, and disufide HMGB1 (ds-HMGB1) interacting with TLR4.	disufide	206-214	high mobility group box 1	Homo sapiens	164-169
25014009-3	2014	The degree to which HMGB1 activates a receptor is thought to be dependent upon the oxidative state of the ligand, resulting in the functional isoforms of all-thiol HMGB1 (at-HMGB1) acting through RAGE, and disufide HMGB1 (ds-HMGB1) interacting with TLR4.	disufide	206-214	high mobility group box 1	Homo sapiens	164-169
25014009-3	2014	The degree to which HMGB1 activates a receptor is thought to be dependent upon the oxidative state of the ligand, resulting in the functional isoforms of all-thiol HMGB1 (at-HMGB1) acting through RAGE, and disufide HMGB1 (ds-HMGB1) interacting with TLR4.	disufide	206-214	high mobility group box 1	Homo sapiens	164-169
25052363-11	2014	A positive correlation was found between urinary HMGB1/creatinine ratio and CD4(+) T cells/creatinine ratio (P = 0 028) and effector memory T cells/creatinine ratio (P = 0 039) in urine.	Creatinine	55-65	high mobility group box 1	Homo sapiens	49-54
25052363-11	2014	A positive correlation was found between urinary HMGB1/creatinine ratio and CD4(+) T cells/creatinine ratio (P = 0 028) and effector memory T cells/creatinine ratio (P = 0 039) in urine.	Creatinine	91-101	high mobility group box 1	Homo sapiens	49-54
25052363-11	2014	A positive correlation was found between urinary HMGB1/creatinine ratio and CD4(+) T cells/creatinine ratio (P = 0 028) and effector memory T cells/creatinine ratio (P = 0 039) in urine.	Creatinine	91-101	high mobility group box 1	Homo sapiens	49-54
25419374-0	2014	Intraoperative systemic lidocaine inhibits the expression of HMGB1 in patients undergoing radical hysterectomy.	Lidocaine	24-33	high mobility group box 1	Homo sapiens	61-66
25004063-0	2014	Novel role of resveratrol: suppression of high-mobility group protein box 1 nucleocytoplasmic translocation by the upregulation of sirtuin 1 in sepsis-induced liver injury.	Resveratrol	14-25	high mobility group box 1	Homo sapiens	42-75
25004063-2	2014	We hypothesized that resveratrol (RESV) administration would inhibit nuclear-cytoplasmic HMGB1 translocation in hepatocytes, which is associated with sirtuin 1 (SIRT1) upregulation.	Resveratrol	21-32	high mobility group box 1	Homo sapiens	89-94
25004063-2	2014	We hypothesized that resveratrol (RESV) administration would inhibit nuclear-cytoplasmic HMGB1 translocation in hepatocytes, which is associated with sirtuin 1 (SIRT1) upregulation.	Resveratrol	34-38	high mobility group box 1	Homo sapiens	89-94
25004063-9	2014	Resveratrol inhibited HMGB1 cytoplasmic translocation.	Resveratrol	0-11	high mobility group box 1	Homo sapiens	22-27
25004063-10	2014	Nicotinamide, an SIRT1 inhibitor, reduced the SIRT1-mediated suppression of HMGB1 translocation and aggravated cecal ligation and puncture-induced liver damage.	Niacinamide	0-12	high mobility group box 1	Homo sapiens	76-81
25004063-13	2014	CONCLUSIONS: Resveratrol protects against sepsis-induced liver injury through the SIRT1-mediated HMGB1 nucleocytoplasmic translocation pathway, a new potential therapeutic target in sepsis-induced liver injury.	Resveratrol	13-24	high mobility group box 1	Homo sapiens	97-102
25419374-4	2014	The present study sought to determine whether intraoperative systemic lidocaine could attenuate the level of HMGB1 by inhibiting it expression in PBMC from patients underwent radical hysterectomy.	Lidocaine	70-79	high mobility group box 1	Homo sapiens	109-114
25419374-10	2014	The result showed that lidocaine not only attenuated the level of HMGB1 protein in serum and supernatant, but inhibited the transcription of HMGB1 mRAN in PBMC.	Lidocaine	23-32	high mobility group box 1	Homo sapiens	66-71
25419374-10	2014	The result showed that lidocaine not only attenuated the level of HMGB1 protein in serum and supernatant, but inhibited the transcription of HMGB1 mRAN in PBMC.	Lidocaine	23-32	high mobility group box 1	Homo sapiens	141-146
25419374-11	2014	The present study of us demonstrated that intraoperative systemic lidocaine can attenuate the level of HMGB1 and inhibit its expression in PBMC from patients underwent radical hysterectomy.	Lidocaine	66-75	high mobility group box 1	Homo sapiens	103-108
25419374-12	2014	Therefore, lidocaine may play an important role in many other clinical diseases by inhibiting HMGB1.	Lidocaine	11-20	high mobility group box 1	Homo sapiens	94-99
25126737-2	2014	Increasing evidence demonstrates that HMGB1-dependent autophagy promotes chemotherapy resistance, sustains tumor metabolism requirements and T cell survival, prevents polyglutamine aggregates and excitotoxicity, and protects against endotoxemia, bacterial infection, and ischemia-reperfusion injury in vitro or in vivo.	polyglutamine	167-180	high mobility group box 1	Homo sapiens	38-43
25303153-6	2014	HMGB1 was increased in the supernatants of cells exposed to 30 mM and 11.2 mM glucose compared to control.	Glucose	78-85	high mobility group box 1	Homo sapiens	0-5
25572734-6	2014	Our results indicated that the positive expression of HMGB1 was significantly increased in the nucleus of gastric cancer tissues compared with the adjacent non-cancerous tissues (ANCT) (64.0&amp;#x0025; vs 44.0&amp;#x0025;, P=0.025), but was not linked to the clinicopathologic features, including the TNM stage (P=0.533) and metastatic lymph node (P=0.771), in patients with gastric cancer.	Adenosine Monophosphate	191-194	high mobility group box 1	Homo sapiens	54-59
25014664-7	2014	We also show that HMGB1 is a direct target of miR-let-7f-1 and forced expression of HMGB1 cDNA enhanced cisplatin sensitivity in SPARC expressed cells.	Cisplatin	104-113	high mobility group box 1	Homo sapiens	18-23
25014664-7	2014	We also show that HMGB1 is a direct target of miR-let-7f-1 and forced expression of HMGB1 cDNA enhanced cisplatin sensitivity in SPARC expressed cells.	Cisplatin	104-113	high mobility group box 1	Homo sapiens	84-89
25014664-8	2014	In summary, our results suggest that SPARC modulates cisplatin resistance by modulating the Let-7f-1 miRNA/HMGB1 axis in medulloblastoma cells.	Cisplatin	53-62	high mobility group box 1	Homo sapiens	107-112
24706001-5	2014	First, we monitored the effects of post-treatment fisetin on lipopolysaccharide (LPS) and cecal ligation and puncture (CLP)-mediated release of HMGB1 and HMGB1-mediated regulation of pro-inflammatory responses in human umbilical vein endothelial cells (HUVECs) and septic mice.	fisetin	50-57	high mobility group box 1	Homo sapiens	144-149
24706001-5	2014	First, we monitored the effects of post-treatment fisetin on lipopolysaccharide (LPS) and cecal ligation and puncture (CLP)-mediated release of HMGB1 and HMGB1-mediated regulation of pro-inflammatory responses in human umbilical vein endothelial cells (HUVECs) and septic mice.	fisetin	50-57	high mobility group box 1	Homo sapiens	154-159
25572734-6	2014	Our results indicated that the positive expression of HMGB1 was significantly increased in the nucleus of gastric cancer tissues compared with the adjacent non-cancerous tissues (ANCT) (64.0&amp;#x0025; vs 44.0&amp;#x0025;, P=0.025), but was not linked to the clinicopathologic features, including the TNM stage (P=0.533) and metastatic lymph node (P=0.771), in patients with gastric cancer.	Adenosine Monophosphate	211-214	high mobility group box 1	Homo sapiens	54-59
24970310-6	2014	To explore the possible mechanisms, the HMGB1 receptor for advanced glycation endproducts (RAGE) in the NS/PCs was blocked with anti-RAGE antibody, and c-Jun N-terminal protein kinase (JNK) in the NS/PCs was inhibited using the potent JNK inhibitor, SP600125.	pyrazolanthrone	250-258	high mobility group box 1	Homo sapiens	40-45
25062563-0	2014	Heparin attenuates HMGB1 expression in arterial tissue subjected to limb ischemia/reperfusion.	Heparin	0-7	high mobility group box 1	Homo sapiens	19-24
25188497-11	2014	We found significantly increased serum concentrations of sRAGE, esRAGE and HMGB1 in CTEPH.	cteph	84-89	high mobility group box 1	Homo sapiens	75-80
24942766-7	2014	During Period III, uptitrated patients showed further BP reductions, which were largest in those on olmesartan/amlodipine 40/10 mg. SI values increased in uptitrated patients and were highest with olmesartan/amlodipine 40/10 mg (SBP 1.62/DBP 1.41).	olmesartan	197-207	high mobility group box 1	Homo sapiens	229-234
25060178-10	2014	Therefore, the combination of a HMGB1+ and HMGB2- expression potentially predicts a poor prognosis in patients with PDAC, and these new biomarkers may be useful parameters for clinical management in the early postoperative phase.	pdac	116-120	high mobility group box 1	Homo sapiens	32-37
25126750-4	2014	Tube formations by human microvascular endothelial cells (HMVECs) were significantly increased by direct exposure to HMGB1 or to conditioned medium derived from HMGB1-stimulated RA fibroblasts, and these increases were attenuated by cilostazol, the latter of which was blocked by sirtinol.	Cilostazol	233-243	high mobility group box 1	Homo sapiens	117-122
24477600-8	2014	Moreover, adenosine inhibited thrombin-induced elevated expression of proinflammatory cytokines, IL-6 and HMGB-1; and chemokines, MCP-1, CXCL-1, and CXCL-3.	Adenosine	10-19	high mobility group box 1	Homo sapiens	106-112
25140900-4	2014	The goal of the present work was to investigate if Rose Bengal Acetate (RBAc), a powerful PS able to trigger apoptosis and autophagy, enables photosensitized HeLa cells to expose and/or release pivotal DAMPs, i.e. ATP, HSP70, HSP90, HMGB1, and calreticulin (CRT), that characterize ICD.	Rose Bengal acetate	51-70	high mobility group box 1	Homo sapiens	233-238
25140900-4	2014	The goal of the present work was to investigate if Rose Bengal Acetate (RBAc), a powerful PS able to trigger apoptosis and autophagy, enables photosensitized HeLa cells to expose and/or release pivotal DAMPs, i.e. ATP, HSP70, HSP90, HMGB1, and calreticulin (CRT), that characterize ICD.	Rose Bengal acetate	72-76	high mobility group box 1	Homo sapiens	233-238
25140900-4	2014	The goal of the present work was to investigate if Rose Bengal Acetate (RBAc), a powerful PS able to trigger apoptosis and autophagy, enables photosensitized HeLa cells to expose and/or release pivotal DAMPs, i.e. ATP, HSP70, HSP90, HMGB1, and calreticulin (CRT), that characterize ICD.	Adenosine Triphosphate	214-217	high mobility group box 1	Homo sapiens	233-238
24928512-12	2014	In serum from ethanol-fed mice and from patients with ALD, there was disulfide-bonded hyperacetylated HMGB1, disulfide-bonded non-acetylated HMGB1, and HMGB1 phosphorylated in serine 35.	Ethanol	14-21	high mobility group box 1	Homo sapiens	102-107
24928512-12	2014	In serum from ethanol-fed mice and from patients with ALD, there was disulfide-bonded hyperacetylated HMGB1, disulfide-bonded non-acetylated HMGB1, and HMGB1 phosphorylated in serine 35.	Ethanol	14-21	high mobility group box 1	Homo sapiens	141-146
24928512-12	2014	In serum from ethanol-fed mice and from patients with ALD, there was disulfide-bonded hyperacetylated HMGB1, disulfide-bonded non-acetylated HMGB1, and HMGB1 phosphorylated in serine 35.	Ethanol	14-21	high mobility group box 1	Homo sapiens	141-146
24928512-12	2014	In serum from ethanol-fed mice and from patients with ALD, there was disulfide-bonded hyperacetylated HMGB1, disulfide-bonded non-acetylated HMGB1, and HMGB1 phosphorylated in serine 35.	Disulfides	69-78	high mobility group box 1	Homo sapiens	102-107
25126750-4	2014	Tube formations by human microvascular endothelial cells (HMVECs) were significantly increased by direct exposure to HMGB1 or to conditioned medium derived from HMGB1-stimulated RA fibroblasts, and these increases were attenuated by cilostazol, the latter of which was blocked by sirtinol.	Cilostazol	233-243	high mobility group box 1	Homo sapiens	161-166
25126750-4	2014	Tube formations by human microvascular endothelial cells (HMVECs) were significantly increased by direct exposure to HMGB1 or to conditioned medium derived from HMGB1-stimulated RA fibroblasts, and these increases were attenuated by cilostazol, the latter of which was blocked by sirtinol.	sirtinol	280-288	high mobility group box 1	Homo sapiens	161-166
24996221-0	2014	HMGB1-mediated autophagy promotes docetaxel resistance in human lung adenocarcinoma.	Docetaxel	34-43	high mobility group box 1	Homo sapiens	0-5
24905701-0	2014	Genomic analysis and differential expression of HMG and S100A family in human arthritis: upregulated expression of chemokines, IL-8 and nitric oxide by HMGB1.	Nitric Oxide	136-148	high mobility group box 1	Homo sapiens	152-157
24905701-11	2014	The recombinant HMGB1 utilized in this study shows properties that are similar to disulfide-HMGB1.	Disulfides	82-91	high mobility group box 1	Homo sapiens	16-21
24905701-11	2014	The recombinant HMGB1 utilized in this study shows properties that are similar to disulfide-HMGB1.	Disulfides	82-91	high mobility group box 1	Homo sapiens	92-97
24863048-0	2014	Evaluation of in vitro properties of predicted kinases that phosphorylate serine residues within nuclear localization signal 1 of high mobility group box 1.	Serine	74-80	high mobility group box 1	Homo sapiens	130-155
24863048-5	2014	Among the predicted kinases, protein kinase C phosphorylated Ser(46) of HMGB1-derived peptides, and a mutagenesis experiment confirmed that phosphorylation at this site could induce the translocation of the N-terminal region of NLS1-containing HMGB1 into the cytosol.	Serine	61-64	high mobility group box 1	Homo sapiens	72-77
24863048-5	2014	Among the predicted kinases, protein kinase C phosphorylated Ser(46) of HMGB1-derived peptides, and a mutagenesis experiment confirmed that phosphorylation at this site could induce the translocation of the N-terminal region of NLS1-containing HMGB1 into the cytosol.	Serine	61-64	high mobility group box 1	Homo sapiens	244-249
24983978-7	2014	RESULTS: Fecal HMGB1 increased by 5-, 11-, 18-, and 24-folds with dextran sodium sulphate doses of 0.25%, 0.50%, 1%, and 4%, respectively, showing that the protein detected a high-grade and a subclinical inflammation.	dextran sodium sulphate	66-89	high mobility group box 1	Homo sapiens	15-20
24838617-7	2014	Using the potent PI3K/Akt inhibitor, LY294002, we explored the likely mechanism of HMGB1-induced NS/PC proliferation.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	37-45	high mobility group box 1	Homo sapiens	83-88
24838617-10	2014	LY294002 effectively reduced phospho-Akt levels and reduced NS/PC proliferation induced by HMGB1 in vitro.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	high mobility group box 1	Homo sapiens	91-96
24996221-8	2014	RESULTS: HMGB1 translocated from the nucleus to the cytoplasm in LAD cells exposed to docetaxel and acted as a positive regulator of autophagy, which inhibited apoptosis and increased drug resistance.	Docetaxel	86-95	high mobility group box 1	Homo sapiens	9-14
24996221-9	2014	Suppression of HMGB1 restored the sensitivity of LAD cells to docetaxel both in vivo and in vitro.	Docetaxel	62-71	high mobility group box 1	Homo sapiens	15-20
24996221-11	2014	CONCLUSIONS: Our results demonstrated that HMGB1-regulated autophagy is a significant contributor to docetaxel resistance in LAD cells.	Docetaxel	101-110	high mobility group box 1	Homo sapiens	43-48
24996221-12	2014	Suppression of HMGB1 or limiting HMGB1 cytosolic translocation diminished autophagic protection in response to docetaxel in LAD cells.	Docetaxel	111-120	high mobility group box 1	Homo sapiens	15-20
24996221-12	2014	Suppression of HMGB1 or limiting HMGB1 cytosolic translocation diminished autophagic protection in response to docetaxel in LAD cells.	Docetaxel	111-120	high mobility group box 1	Homo sapiens	33-38
25182828-0	2014	[Serum levels and clinical significance of high mobility group protein B1 in patients with delayed encephalopathy after acute carbon monoxide poisoning].	Carbon Monoxide	126-141	high mobility group box 1	Homo sapiens	43-73
24773263-4	2014	The mean (SD) levels of the nuclear protein plasma high-mobility group box 1 increased significantly from 5.1 (2.2) ng ml(-1) during (16.6 (7.3) ng ml(-1) ) and after (14.3 (8.2) ng ml(-1) ) cardiopulmonary bypass in the saline group.	Sodium Chloride	221-227	high mobility group box 1	Homo sapiens	51-76
24359220-3	2014	RECENT ADVANCES: Low levels of ROS modify Atg4 and high mobility group box 1 (HMGB1) proteins, activate AMP-activated protein kinase (AMPK) and apoptosis signal-regulating kinase/c-Jun N-terminal kinase (JNK) pathways, or transactivate various proteins that could upregulate autophagy, leading to reductions in apoptosis.	Reactive Oxygen Species	31-34	high mobility group box 1	Homo sapiens	51-76
24359220-3	2014	RECENT ADVANCES: Low levels of ROS modify Atg4 and high mobility group box 1 (HMGB1) proteins, activate AMP-activated protein kinase (AMPK) and apoptosis signal-regulating kinase/c-Jun N-terminal kinase (JNK) pathways, or transactivate various proteins that could upregulate autophagy, leading to reductions in apoptosis.	Reactive Oxygen Species	31-34	high mobility group box 1	Homo sapiens	78-83
25080914-8	2014	The MTT assay demonstrated that HMGB1 knockdown significantly reduced the cell proliferation.	monooxyethylene trimethylolpropane tristearate	4-7	high mobility group box 1	Homo sapiens	32-37
25182828-1	2014	OBJECTIVE: To investigate the changes in serum level of high mobility group protein B1 (HMGB1) in patients with delayed encephalopathy after acute carbon monoxide poisoning and the clinical significance of these changes.	Carbon Monoxide	147-162	high mobility group box 1	Homo sapiens	56-86
25182828-1	2014	OBJECTIVE: To investigate the changes in serum level of high mobility group protein B1 (HMGB1) in patients with delayed encephalopathy after acute carbon monoxide poisoning and the clinical significance of these changes.	Carbon Monoxide	147-162	high mobility group box 1	Homo sapiens	88-93
25182828-5	2014	RESULTS: In the acute stage of carbon monoxide poisoning, the serum HMGB1 level of delayed encephalopathy group was significantly higher than those of the carbon monoxide poisoning group and the control group (P &lt; 0.01).	Carbon Monoxide	31-46	high mobility group box 1	Homo sapiens	68-73
25182828-5	2014	RESULTS: In the acute stage of carbon monoxide poisoning, the serum HMGB1 level of delayed encephalopathy group was significantly higher than those of the carbon monoxide poisoning group and the control group (P &lt; 0.01).	Carbon Monoxide	155-170	high mobility group box 1	Homo sapiens	68-73
25182828-8	2014	CONCLUSION: HMGB1, as an important late mediator of inflammation, is involved in the inflammatory reaction in delayed encephalopathy, and is positively correlated with HDS and ADL scores, indicating that it can be used as one of the major indicators in monitoring carbon monoxide poisoning.	Carbon Monoxide	264-279	high mobility group box 1	Homo sapiens	12-17
24684392-1	2014	The aim of the present study was to investigate the association of genetic polymorphisms in high mobility group box 1 and 2 (HMGB1 and HMGB2, respectively) with platinum-based chemotherapy responses in Chinese lung cancer patients.	Platinum	161-169	high mobility group box 1	Homo sapiens	92-123
24684392-1	2014	The aim of the present study was to investigate the association of genetic polymorphisms in high mobility group box 1 and 2 (HMGB1 and HMGB2, respectively) with platinum-based chemotherapy responses in Chinese lung cancer patients.	Platinum	161-169	high mobility group box 1	Homo sapiens	125-130
24684392-5	2014	We found that rs1412125 and rs2249825 of HMGB1 were significantly associated with the platinum-based chemotherapy response in both recessive and genotypic models.	Platinum	86-94	high mobility group box 1	Homo sapiens	41-46
24684392-8	2014	The HMGB1 SNPs (rs1412125 and rs2249825) were associated with platinum-based chemotherapy responses in Chinese lung cancer patients.	Platinum	62-70	high mobility group box 1	Homo sapiens	4-9
24684392-9	2014	In conclusion, HMGB1 SNPs may serve as potential biomarkers for predicting the efficacy of platinum-based chemotherapy.	Platinum	91-99	high mobility group box 1	Homo sapiens	15-20
24581270-0	2014	Andrographolide inhibits HMGB1-induced inflammatory responses in human umbilical vein endothelial cells and in murine polymicrobial sepsis.	andrographolide	0-15	high mobility group box 1	Homo sapiens	25-30
24467264-9	2014	In cultured endothelial cells, human kallistatin via its heparin-binding site inhibited HMGB1-induced nuclear factor-kappaB activation and inflammatory gene expression.	Heparin	57-64	high mobility group box 1	Homo sapiens	88-93
24965297-1	2014	Intraperitoneal glucose degradation products (GDP) load influences systemic advanced glycation end products (AGEs) but the effects on soluble receptor for AGEs (s-RAGE) and its proinflammatory ligands: extracellular newly identified receptor for advanced glycation end-products binding protein(EN-RAGE) and high mobility group box-1 protein (HMGB-1) are unknown.	Glucose	16-23	high mobility group box 1	Homo sapiens	307-332
24965297-1	2014	Intraperitoneal glucose degradation products (GDP) load influences systemic advanced glycation end products (AGEs) but the effects on soluble receptor for AGEs (s-RAGE) and its proinflammatory ligands: extracellular newly identified receptor for advanced glycation end-products binding protein(EN-RAGE) and high mobility group box-1 protein (HMGB-1) are unknown.	Glucose	16-23	high mobility group box 1	Homo sapiens	342-348
24965297-9	2014	A lower intraperitoneal GDP load is associated with decreased plasma levels of EN-RAGE and HMGB-1.	Guanosine Diphosphate	24-27	high mobility group box 1	Homo sapiens	91-97
24574398-7	2014	That and the pattern of viral determinants maintained in gemcitabine-treated cells suggested the activation of an inflammasome/caspase 1 (CASP1) platform alongside DNA detachment and/or nuclear exclusion of HMGB1 during early stages of the viral life cycle.	gemcitabine	57-68	high mobility group box 1	Homo sapiens	207-212
24468889-4	2014	METHODS: We investigated the effects of PL on HMGB1-mediated inflammatory response by monitoring the effects of PL on lipopolysaccharide or cecal ligation and puncture (CLP)-mediated release of HMGB1, as well as on the modulation of HMGB1-mediated inflammatory responses.	piperlonguminine	40-42	high mobility group box 1	Homo sapiens	46-51
24468889-7	2014	In addition, treatment with PL reduced the CLP-induced release of HMGB1 and sepsis-related mortality.	piperlonguminine	28-30	high mobility group box 1	Homo sapiens	66-71
24468889-8	2014	CONCLUSION: These results indicate that PL could be a candidate therapeutic agent for various severe vascular inflammatory diseases via inhibition of the HMGB1 signaling pathway.	piperlonguminine	40-42	high mobility group box 1	Homo sapiens	154-159
24776932-3	2014	In vitro the effect of atorvastatin on the production of HMGB1 by lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVEC) was assessed.	Atorvastatin	23-35	high mobility group box 1	Homo sapiens	57-62
24776932-6	2014	HMGB1 levels were reduced in GPA patients on statins and prednisolone.	Prednisolone	57-69	high mobility group box 1	Homo sapiens	0-5
24776932-7	2014	In vitro, atorvastatin reduced HMGB1 levels in supernatants of activated HUVEC.	Atorvastatin	10-22	high mobility group box 1	Homo sapiens	31-36
24776932-9	2014	Statins and prednisolone are associated with reduced serum HMGB1 levels and atorvastatin decreases HMGB1 release by activated HUVEC in vitro, indicating an additional anti-inflammatory effect of statins.	Prednisolone	12-24	high mobility group box 1	Homo sapiens	59-64
24776932-9	2014	Statins and prednisolone are associated with reduced serum HMGB1 levels and atorvastatin decreases HMGB1 release by activated HUVEC in vitro, indicating an additional anti-inflammatory effect of statins.	Atorvastatin	76-88	high mobility group box 1	Homo sapiens	99-104
24412753-3	2014	BTB, as a negative regulator of cell cycle progression, was identified as a HMGB1 interacting partner.	btb	0-3	high mobility group box 1	Homo sapiens	76-81
24412753-4	2014	The ectopic expression of HMGB1 activates cell growth by suppressing BTB-induced cell death, decreasing Bax and p53 expression, while enhancing Bcl-xL, Bcl-2, cyclin D1, and NF-kappaB expression.	btb	69-72	high mobility group box 1	Homo sapiens	26-31
24412753-5	2014	HMGB1 activates the FAK/PI3K/mTOR signaling cascade, and BTB prominently inhibits HMGB1-induced oncogenesis.	btb	57-60	high mobility group box 1	Homo sapiens	82-87
24549588-6	2014	MTT and apoptosis assays were also performed and it was demonstrated that extracellular HMGB1 subsequently enhanced resistance to the P-gp-related drugs, adriamycin and vincristine.	monooxyethylene trimethylolpropane tristearate	0-3	high mobility group box 1	Homo sapiens	88-93
24077682-0	2014	Anti-septic effects of pellitorine in HMGB1-induced inflammatory responses in vitro and in vivo.	pellitorine	23-34	high mobility group box 1	Homo sapiens	38-43
24077682-3	2014	In this study, we investigated the anti-septic effects of PT against pro-inflammatory responses in human umbilical vein endothelial cells (HUVECs) induced by HMGB1 and the associated signaling pathways.	pellitorine	58-60	high mobility group box 1	Homo sapiens	158-163
24549588-7	2014	In brief, this study demonstrated that extracellular HMGB1 may promote drug resistance to adriamycin and vincristine by upregulating P-gp in human gastric adenocarcinoma cells.	Doxorubicin	90-100	high mobility group box 1	Homo sapiens	53-58
24549588-7	2014	In brief, this study demonstrated that extracellular HMGB1 may promote drug resistance to adriamycin and vincristine by upregulating P-gp in human gastric adenocarcinoma cells.	Vincristine	105-116	high mobility group box 1	Homo sapiens	53-58
24549588-6	2014	MTT and apoptosis assays were also performed and it was demonstrated that extracellular HMGB1 subsequently enhanced resistance to the P-gp-related drugs, adriamycin and vincristine.	Doxorubicin	154-164	high mobility group box 1	Homo sapiens	88-93
24549588-6	2014	MTT and apoptosis assays were also performed and it was demonstrated that extracellular HMGB1 subsequently enhanced resistance to the P-gp-related drugs, adriamycin and vincristine.	Vincristine	169-180	high mobility group box 1	Homo sapiens	88-93
24531895-2	2014	Recently, it was shown that different redox states of the three cysteines of HMGB1 endow it with mutually exclusive activities, such as inducing chemotaxis or the transcription of cytokines and chemokines, via the interaction with different receptors.	Cysteine	64-73	high mobility group box 1	Homo sapiens	77-82
24262631-2	2014	Given that no evidence for roles of HMGB1 in visceral pain signaling is available, we asked if HMGB1 participates in bladder pain accompanying cystitis caused by cyclophosphamide in mice, using the anti-HMGB1 neutralizing antibody and recombinant human soluble thrombomodulin (rhsTM) that sequesters HMGB1 and promotes its degradation by thrombin.	Cyclophosphamide	162-178	high mobility group box 1	Homo sapiens	95-100
24070090-7	2014	Leukocyte activation abated in the presence of inhibitors of HMGB1 or of catalase, which catalyzes the dismutation of hydrogen peroxide into water and molecular oxygen.	Hydrogen Peroxide	118-135	high mobility group box 1	Homo sapiens	61-66
24070090-7	2014	Leukocyte activation abated in the presence of inhibitors of HMGB1 or of catalase, which catalyzes the dismutation of hydrogen peroxide into water and molecular oxygen.	Water	141-146	high mobility group box 1	Homo sapiens	61-66
23373897-5	2014	By damaging cells, superoxide and peroxynitrite promote leakage of HMGB1.	Superoxides	19-29	high mobility group box 1	Homo sapiens	67-72
24070090-7	2014	Leukocyte activation abated in the presence of inhibitors of HMGB1 or of catalase, which catalyzes the dismutation of hydrogen peroxide into water and molecular oxygen.	Oxygen	161-167	high mobility group box 1	Homo sapiens	61-66
23373897-5	2014	By damaging cells, superoxide and peroxynitrite promote leakage of HMGB1.	Peroxynitrous Acid	34-47	high mobility group box 1	Homo sapiens	67-72
24070090-10	2014	INNOVATION AND CONCLUSION: ROS dramatically increase the ability of extracellular HMGB1 to activate blood leukocytes.	Reactive Oxygen Species	27-30	high mobility group box 1	Homo sapiens	82-87
23373897-6	2014	RECENT ADVANCES: The activity of HMGB1 strongly depends on its redox state: Inflammatory-active HMGB1 requires an intramolecular disulfide bond (Cys23 and Cys45) and a reduced Cys106.	Disulfides	129-138	high mobility group box 1	Homo sapiens	33-38
24420848-0	2014	Metformin protects against hyperglycemia-induced cardiomyocytes injury by inhibiting the expressions of receptor for advanced glycation end products and high mobility group box 1 protein.	Metformin	0-9	high mobility group box 1	Homo sapiens	153-178
23373897-6	2014	RECENT ADVANCES: The activity of HMGB1 strongly depends on its redox state: Inflammatory-active HMGB1 requires an intramolecular disulfide bond (Cys23 and Cys45) and a reduced Cys106.	Disulfides	129-138	high mobility group box 1	Homo sapiens	96-101
24431405-5	2014	Using in vitro models with mouse and human malignant mesothelioma cells, curcumin is shown to induce pyroptosis through activation of caspase-1 and increased release of high-mobility group box 1 (HMGB1) without processing of IL-1beta and IL-18.	Curcumin	73-81	high mobility group box 1	Homo sapiens	169-194
24431405-5	2014	Using in vitro models with mouse and human malignant mesothelioma cells, curcumin is shown to induce pyroptosis through activation of caspase-1 and increased release of high-mobility group box 1 (HMGB1) without processing of IL-1beta and IL-18.	Curcumin	73-81	high mobility group box 1	Homo sapiens	196-201
24362470-4	2014	Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70).	Fluorouracil	104-108	high mobility group box 1	Homo sapiens	134-159
24362470-4	2014	Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70).	Fluorouracil	104-108	high mobility group box 1	Homo sapiens	161-166
24362470-5	2014	After OXA/5-Fu therapy, the sera of CRC patients also exhibited increased levels of HMGB1 and HSP70, both of which are well-known DAMPs.	Oxaliplatin	6-9	high mobility group box 1	Homo sapiens	84-89
24362470-5	2014	After OXA/5-Fu therapy, the sera of CRC patients also exhibited increased levels of HMGB1 and HSP70, both of which are well-known DAMPs.	Fluorouracil	10-14	high mobility group box 1	Homo sapiens	84-89
24370952-5	2014	We determined that high amplitude cyclic stretch (18% CS) increased HMGB1 expression (2-4-fold) via a signaling pathway with critical involvement of the transcription factor, STAT3.	Cesium	54-56	high mobility group box 1	Homo sapiens	68-73
24370952-6	2014	Concomitant exposure to 18% CS and oxidative stress (H2O2) augmented HMGB1 expression (~13 fold increase) whereas lipopolysaccharide (LPS) challenge increased HMGB1 expression in static EC, but not in 18% CS-challenged EC.	Cesium	28-30	high mobility group box 1	Homo sapiens	69-74
24370952-6	2014	Concomitant exposure to 18% CS and oxidative stress (H2O2) augmented HMGB1 expression (~13 fold increase) whereas lipopolysaccharide (LPS) challenge increased HMGB1 expression in static EC, but not in 18% CS-challenged EC.	Hydrogen Peroxide	53-57	high mobility group box 1	Homo sapiens	69-74
24370952-7	2014	In contrast, physiologic, low amplitude cyclic stretch (5% CS) attenuated both oxidative H2O2- and LPS-induced increases in HMGB1 expression, suggesting that physiologic mechanical stress is protective.	Cesium	59-61	high mobility group box 1	Homo sapiens	124-129
24370952-7	2014	In contrast, physiologic, low amplitude cyclic stretch (5% CS) attenuated both oxidative H2O2- and LPS-induced increases in HMGB1 expression, suggesting that physiologic mechanical stress is protective.	Hydrogen Peroxide	89-93	high mobility group box 1	Homo sapiens	124-129
24362470-4	2014	Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70).	Oxaliplatin	63-74	high mobility group box 1	Homo sapiens	134-159
24362470-4	2014	Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70).	Oxaliplatin	63-74	high mobility group box 1	Homo sapiens	161-166
24362470-4	2014	Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70).	Oxaliplatin	76-79	high mobility group box 1	Homo sapiens	134-159
24362470-4	2014	Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70).	Oxaliplatin	76-79	high mobility group box 1	Homo sapiens	161-166
24362470-4	2014	Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70).	Fluorouracil	88-102	high mobility group box 1	Homo sapiens	134-159
24362470-4	2014	Here, we found that colorectal cancer (CRC) cells treated with oxaliplatin (OXA) and/or 5-fluorouracil (5-Fu) released high levels of high-mobility group box 1 (HMGB1) and heat shock protein 70 (HSP70).	Fluorouracil	88-102	high mobility group box 1	Homo sapiens	161-166
24551219-2	2014	Recent reports from several laboratories provided evidence that a number of both the intracellular and extracellular functions of HMGB1 may depend on redox-sensitive cysteine residues of the protein.	Cysteine	166-174	high mobility group box 1	Homo sapiens	130-135
24524683-1	2014	An MS-based proteomic strategy combined with chemically functionalized gold nanoparticles as affinity probes was developed and validated by successful identification and quantification of HMGB1, which is well characterized to interact selectively with 1,2-cross-linked DNA by cisplatin, from whole cell lysates.	Cisplatin	276-285	high mobility group box 1	Homo sapiens	188-193
24551070-4	2014	We previously found increased HMGB1 in post-mortem alcoholic human brain as well as in ethanol treated mice and rat brain slice cultures.	Ethanol	87-94	high mobility group box 1	Homo sapiens	30-35
25004875-0	2014	Baicalein inhibits HMGB1 release and MMP-2/-9 expression in lipopolysaccharide-induced cardiac hypertrophy.	baicalein	0-9	high mobility group box 1	Homo sapiens	19-24
23318458-5	2014	RAGE and HMGB1 coordinately enhanced tumor cell mitochondrial complex I activity, ATP production, tumor cell proliferation and migration.	Adenosine Triphosphate	82-85	high mobility group box 1	Homo sapiens	9-14
23318458-6	2014	Lack of RAGE or inhibition of HMGB1 release diminished ATP production and slowed tumor growth in vitro and in vivo.	Adenosine Triphosphate	55-58	high mobility group box 1	Homo sapiens	30-35
24361892-0	2014	Ethyl pyruvate inhibits proliferation and induces apoptosis of hepatocellular carcinoma via regulation of the HMGB1-RAGE and AKT pathways.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	110-115
24361892-7	2014	Real-time PCR, Western blotting and immunofluorescence demonstrated ethyl pyruvate reduced the HMGB1-RAGE and AKT pathways.	ethyl pyruvate	68-82	high mobility group box 1	Homo sapiens	95-100
25826983-4	2014	The article presents the proposed role of dipeptide vilon (Lys-Glu) and tetrapeptide epitalon (Ala-Glu-Asp-Gly) in CCL11 and HMGB1 genes regulation as activators of their expression.	Dipeptides	42-51	high mobility group box 1	Homo sapiens	125-130
25826983-4	2014	The article presents the proposed role of dipeptide vilon (Lys-Glu) and tetrapeptide epitalon (Ala-Glu-Asp-Gly) in CCL11 and HMGB1 genes regulation as activators of their expression.	lysylglutamic acid	59-66	high mobility group box 1	Homo sapiens	125-130
25826983-4	2014	The article presents the proposed role of dipeptide vilon (Lys-Glu) and tetrapeptide epitalon (Ala-Glu-Asp-Gly) in CCL11 and HMGB1 genes regulation as activators of their expression.	alanyl-glutamyl-aspartyl-glycine	95-110	high mobility group box 1	Homo sapiens	125-130
25004875-4	2014	In addition, pretreatment with baicalein inhibited LPS-induced early (e.g., tumor necrosis factor-alpha (TNF-alpha) and interleukin-6) and late (e.g., high mobility group box 1 (HMGB1) pro-inflammatory cytokine release, inducible nitric oxide synthase (iNOS) expression and NO production.	baicalein	31-40	high mobility group box 1	Homo sapiens	151-176
25004875-4	2014	In addition, pretreatment with baicalein inhibited LPS-induced early (e.g., tumor necrosis factor-alpha (TNF-alpha) and interleukin-6) and late (e.g., high mobility group box 1 (HMGB1) pro-inflammatory cytokine release, inducible nitric oxide synthase (iNOS) expression and NO production.	baicalein	31-40	high mobility group box 1	Homo sapiens	178-183
26629935-8	2014	We then investigated the effect of HMGB1 knockdown/out on the sensitivity of BUC cells treated with the anticancer drug cisplatin.	Cisplatin	120-129	high mobility group box 1	Homo sapiens	35-40
23811849-4	2014	The absence of HMGB1 expression by dying tumor cells exposed to anthracyclines or oxaliplatin compromises DC-dependent T-cell priming by tumor-associated antigens.	Anthracyclines	64-78	high mobility group box 1	Homo sapiens	15-20
23811849-5	2014	Here, we show that transplantable tumors exhibiting weak expression of nuclear HMGB1 respond to chemotherapy more effectively if the treatment is combined with the local or systemic administration of a highly purified and physiochemically defined and standardized lipopolysaccharide solution, which acts as a high-potency and exclusive TLR4 agonist, called Dendrophilin (DEN).	dendrophilin	357-369	high mobility group box 1	Homo sapiens	79-84
23811849-5	2014	Here, we show that transplantable tumors exhibiting weak expression of nuclear HMGB1 respond to chemotherapy more effectively if the treatment is combined with the local or systemic administration of a highly purified and physiochemically defined and standardized lipopolysaccharide solution, which acts as a high-potency and exclusive TLR4 agonist, called Dendrophilin (DEN).	Diethylnitrosamine	371-374	high mobility group box 1	Homo sapiens	79-84
23811849-8	2014	Moreover, DEN could restore the immunogenicity of dying tumor cells from which HMGB1 had been depleted by RNA interference.	Diethylnitrosamine	10-13	high mobility group box 1	Homo sapiens	79-84
23832118-6	2014	In this review, we provide a brief outline of the well-characterized DAMPs such as calreticulin (CRT) exposure, high-mobility group protein B1 (HMGB1), and adenosine triphosphate (ATP) release, which are induced by the morphologically distinct types of cell death.	Adenosine Triphosphate	156-178	high mobility group box 1	Homo sapiens	144-149
24184598-0	2014	Anti-septic effects of glyceollins in HMGB1-induced inflammatory responses in vitro and in vivo.	glyceollin	23-34	high mobility group box 1	Homo sapiens	38-43
24178442-0	2014	HMGB1 is involved in autophagy inhibition caused by SNCA/alpha-synuclein overexpression: a process modulated by the natural autophagy inducer corynoxine B.	corynoxine B	142-154	high mobility group box 1	Homo sapiens	0-5
24178442-8	2014	Corynoxine B, a natural autophagy inducer, restores the deficient cytosolic translocation of HMGB1 and autophagy in cells overexpressing SNCA, which may be attributed to its ability to block SNCA-HMGB1 interaction.	corynoxine B	0-12	high mobility group box 1	Homo sapiens	93-98
24178442-8	2014	Corynoxine B, a natural autophagy inducer, restores the deficient cytosolic translocation of HMGB1 and autophagy in cells overexpressing SNCA, which may be attributed to its ability to block SNCA-HMGB1 interaction.	corynoxine B	0-12	high mobility group box 1	Homo sapiens	196-201
25243124-0	2014	Adsorption of the inflammatory mediator high-mobility group box 1 by polymers with different charge and porosity.	Polymers	69-77	high mobility group box 1	Homo sapiens	40-65
25243124-4	2014	Here, we studied the adsorption of HMGB1 to anionic methacrylate-based polymers as well as to neutral polystyrene-divinylbenzene copolymers.	methacrylate-based polymers	52-79	high mobility group box 1	Homo sapiens	35-40
23852373-3	2014	The release of ATP from dying cells constitutes one of the three major hallmarks of ICD and occurs independently of the two others, namely, the pre-apoptotic exposure of calreticulin on the cell surface and the postmortem release of high-mobility group box 1 (HMBG1) into the extracellular space.	Adenosine Triphosphate	15-18	high mobility group box 1	Homo sapiens	233-258
23852373-3	2014	The release of ATP from dying cells constitutes one of the three major hallmarks of ICD and occurs independently of the two others, namely, the pre-apoptotic exposure of calreticulin on the cell surface and the postmortem release of high-mobility group box 1 (HMBG1) into the extracellular space.	Adenosine Triphosphate	15-18	high mobility group box 1	Homo sapiens	260-265
25175868-4	2014	In addition, HMGB1-TLR4 and innate immune NF-kappaB target genes are increased leading to persistent and sensitized neuroimmune responses to ethanol and other agents that release HMGB1 or directly stimulate TLR receptors and/or NMDA receptors.	Ethanol	141-148	high mobility group box 1	Homo sapiens	13-18
25175868-4	2014	In addition, HMGB1-TLR4 and innate immune NF-kappaB target genes are increased leading to persistent and sensitized neuroimmune responses to ethanol and other agents that release HMGB1 or directly stimulate TLR receptors and/or NMDA receptors.	Ethanol	141-148	high mobility group box 1	Homo sapiens	179-184
26629935-9	2014	Knockdown or knockout of HMGB1 rendered BUC cells more sensitive to cisplatin.	Cisplatin	68-77	high mobility group box 1	Homo sapiens	25-30
23895427-0	2013	The cytokine mRNA increase induced by withdrawal from chronic ethanol in the sterile environment of brain is mediated by CRF and HMGB1 release.	Ethanol	62-69	high mobility group box 1	Homo sapiens	129-134
24011512-2	2014	RAGE transduces the signals of advanced glycation end-products (AGEs), proinflammatory S100/calgranulins, and high mobility group box 1 (HMGB1), and is a one of a family of receptors for lysophosphatidic acid (LPA).	lysophosphatidic acid	187-208	high mobility group box 1	Homo sapiens	110-135
24011512-2	2014	RAGE transduces the signals of advanced glycation end-products (AGEs), proinflammatory S100/calgranulins, and high mobility group box 1 (HMGB1), and is a one of a family of receptors for lysophosphatidic acid (LPA).	lysophosphatidic acid	187-208	high mobility group box 1	Homo sapiens	137-142
24011512-2	2014	RAGE transduces the signals of advanced glycation end-products (AGEs), proinflammatory S100/calgranulins, and high mobility group box 1 (HMGB1), and is a one of a family of receptors for lysophosphatidic acid (LPA).	lysophosphatidic acid	210-213	high mobility group box 1	Homo sapiens	137-142
23895427-15	2013	The CRF1RA and the HMGB1 antagonist, ethyl pyruvate, also reduced the HMGB1 mRNA increase that followed CE withdrawal.	ethyl pyruvate	37-51	high mobility group box 1	Homo sapiens	19-24
23895427-15	2013	The CRF1RA and the HMGB1 antagonist, ethyl pyruvate, also reduced the HMGB1 mRNA increase that followed CE withdrawal.	ethyl pyruvate	37-51	high mobility group box 1	Homo sapiens	70-75
24094823-1	2013	In this study, pH-sensitive biomaterials coated polymer/DNA nanocomplexes containing a high mobility group box 1 (HMGB1) were developed as an efficient non-viral gene delivery system.	Polymers	48-55	high mobility group box 1	Homo sapiens	87-112
24091596-0	2013	HMGB1 recruits hepatic stellate cells and liver endothelial cells to sites of ethanol-induced parenchymal cell injury.	Ethanol	78-85	high mobility group box 1	Homo sapiens	0-5
24091596-3	2013	We hypothesized that HMGB1 may be released from ethanol-stimulated liver parenchymal cells and contribute to HSC and LEC recruitment.	Ethanol	48-55	high mobility group box 1	Homo sapiens	21-26
24091596-4	2013	Ethanol stimulation of rat hepatocytes and HepG2 cells resulted in translocation of HMGB1 from the nucleus as assessed by Western blot.	Ethanol	0-7	high mobility group box 1	Homo sapiens	84-89
24091596-5	2013	HMGB1 protein levels were increased in the supernatant of ethanol-treated hepatocytes compared with vehicle-treated cells.	Ethanol	58-65	high mobility group box 1	Homo sapiens	0-5
24091596-7	2013	However, the effect of CMEtOH on migration was almost entirely reversed by treatment with HMGB1-neutralizing antibody or when HepG2 cells were pretransfected with HMGB1-siRNA compared with control siRNA-transfected HepG2 cells (P &lt; 0.05).	cmetoh	23-29	high mobility group box 1	Homo sapiens	90-95
24091596-7	2013	However, the effect of CMEtOH on migration was almost entirely reversed by treatment with HMGB1-neutralizing antibody or when HepG2 cells were pretransfected with HMGB1-siRNA compared with control siRNA-transfected HepG2 cells (P &lt; 0.05).	cmetoh	23-29	high mobility group box 1	Homo sapiens	163-168
24091596-9	2013	HMGB1 stimulation of HSC increased the phosphorylation of Src and Erk and HMGB1-induced HSC migration was blocked by the Src inhibitor PP2 and the Erk inhibitor U0126.	U 0126	161-166	high mobility group box 1	Homo sapiens	0-5
24091596-9	2013	HMGB1 stimulation of HSC increased the phosphorylation of Src and Erk and HMGB1-induced HSC migration was blocked by the Src inhibitor PP2 and the Erk inhibitor U0126.	U 0126	161-166	high mobility group box 1	Homo sapiens	74-79
24091596-10	2013	Hepatocytes release HMGB1 in response to ethanol with subsequent recruitment of HSC and LEC.	Ethanol	41-48	high mobility group box 1	Homo sapiens	20-25
24094823-1	2013	In this study, pH-sensitive biomaterials coated polymer/DNA nanocomplexes containing a high mobility group box 1 (HMGB1) were developed as an efficient non-viral gene delivery system.	Polymers	48-55	high mobility group box 1	Homo sapiens	114-119
24160326-0	2013	Continuous exposure to chrysotile asbestos can cause transformation of human mesothelial cells via HMGB1 and TNF-alpha signaling.	Asbestos	34-42	high mobility group box 1	Homo sapiens	99-104
23928875-0	2013	High mobility group box 1 (HMGB1) mediates high-glucose-induced calcification in vascular smooth muscle cells of saphenous veins.	Glucose	48-55	high mobility group box 1	Homo sapiens	0-25
23928875-0	2013	High mobility group box 1 (HMGB1) mediates high-glucose-induced calcification in vascular smooth muscle cells of saphenous veins.	Glucose	48-55	high mobility group box 1	Homo sapiens	27-32
23928875-4	2013	Therefore, the role of their common ligand, high mobility group box 1 (HMGB1), in high-glucose-induced calcification in VSMC of saphenous vein was investigated.	Glucose	87-94	high mobility group box 1	Homo sapiens	44-69
23928875-4	2013	Therefore, the role of their common ligand, high mobility group box 1 (HMGB1), in high-glucose-induced calcification in VSMC of saphenous vein was investigated.	Glucose	87-94	high mobility group box 1	Homo sapiens	71-76
23928875-6	2013	We first demonstrated high-glucose-induced HMGB1 translocation from nucleus to cytosol, and this translocation was induced through a NADPH oxidase and PKC-dependent pathway.	Glucose	27-34	high mobility group box 1	Homo sapiens	43-48
23928875-8	2013	Then, we revealed downregulating HMGB1 expression abolished high-glucose-induced calcification accompanied by NFkappaB inactivation and low expression of bone morphogenetic protein-2 (BMP-2).	Glucose	65-72	high mobility group box 1	Homo sapiens	33-38
23928875-11	2013	Our findings thus suggest HMGB1 plays an important role in mediating the calcification process induced by high glucose through NFkappaB activation and BMP-2 expression in VSMC of saphenous vein.	Glucose	111-118	high mobility group box 1	Homo sapiens	26-31
24255708-2	2013	The human HMGB1 is composed of two binding motifs, known as Boxes A and B, are L-shaped alpha-helix structures, followed by a random-coil acidic tail that consists of 30 Asp and Glu residues.	Aspartic Acid	170-173	high mobility group box 1	Homo sapiens	10-15
24255708-2	2013	The human HMGB1 is composed of two binding motifs, known as Boxes A and B, are L-shaped alpha-helix structures, followed by a random-coil acidic tail that consists of 30 Asp and Glu residues.	Glutamic Acid	178-181	high mobility group box 1	Homo sapiens	10-15
24133029-8	2013	RESULTS: HMGB1 signalling pathway components including receptors for HMGB1 as well as NF-kappaB and TNFalpha/VEGF were significantly upregulated in type 2 diabetic retinas and in high glucose treated ARPE-19 cells, compared to their respective counterparts.	Glucose	184-191	high mobility group box 1	Homo sapiens	9-14
24133029-9	2013	HMGB1 blockage significantly alleviated NF-kappaB activity and VEGF secretion in ARPE-19 cells cultured with high glucose.	Glucose	114-121	high mobility group box 1	Homo sapiens	0-5
24465145-2	2013	In the postischemic brain, HMGB1 is massively released during NMDA-induced acute damage and triggers inflammatory processes.	N-Methylaspartate	62-66	high mobility group box 1	Homo sapiens	27-32
24465145-8	2013	A pull-down assay using biotin-labeled HBHP showed that HBHP binds directly to HMGB1 (more specifically to HMGB1 A box) in LCM.	Biotin	24-30	high mobility group box 1	Homo sapiens	79-84
24465145-8	2013	A pull-down assay using biotin-labeled HBHP showed that HBHP binds directly to HMGB1 (more specifically to HMGB1 A box) in LCM.	Biotin	24-30	high mobility group box 1	Homo sapiens	107-112
24427810-0	2013	Redox-sensitive structural change in the A-domain of HMGB1 and its implication for the binding to cisplatin modified DNA.	Cisplatin	98-107	high mobility group box 1	Homo sapiens	53-58
24427810-3	2013	Two cysteines, Cys23 and Cys45, in the A-domain of HMGB1 form a disulfide bond under oxidative conditions.	Cysteine	4-13	high mobility group box 1	Homo sapiens	51-56
24427810-3	2013	Two cysteines, Cys23 and Cys45, in the A-domain of HMGB1 form a disulfide bond under oxidative conditions.	Disulfides	64-73	high mobility group box 1	Homo sapiens	51-56
24427810-8	2013	The reorientation of the Phe38 ring by the disulfide bond in the A-domain may explain the reduced HMGB1 binding affinity towards cisplatinated DNA.	Disulfides	43-52	high mobility group box 1	Homo sapiens	98-103
24160326-10	2013	Similarly, HMGB1 release in vivo progressively increased for 10 or more weeks after crocidolite exposure, but returned to background levels within 8 weeks after chrysotile exposure.	Asbestos, Crocidolite	84-95	high mobility group box 1	Homo sapiens	11-16
24591411-8	2013	Correlation analysis showed that plasma levels of HMGB-1 correlated with initial serum creatinine (r = 0.275, P = 0.018), estimated glomerular filtration rate (r = -0.277, P = 0.017), the Birmingham Vasculitis Activity Score (r = 0.308, P = 0.008), and C-reactive protein level (r = 0.309, P = 0.008).	Creatinine	87-97	high mobility group box 1	Homo sapiens	50-56
24204700-7	2013	One hour after injection, ELISA showed that circulating extracellular HMGB1 levels were elevated after BMC transplantation compared to the PBS injection.	bmc	103-106	high mobility group box 1	Homo sapiens	70-75
23867237-11	2013	Adolescent intermittent ethanol exposure also increased TLR4 and HMGB1 expression at P56 that persisted into young adulthood (P80).	Ethanol	24-31	high mobility group box 1	Homo sapiens	65-70
24204700-5	2013	We thus studied the role of extracellular HMGB1 in the effect of BMC transplantation for heart failure.	bmc	65-68	high mobility group box 1	Homo sapiens	42-47
23398207-6	2013	Furthermore, (-)- gossypol treatment increased the translocation of high mobility group box 1 (HMGB1) from nuclei to cytoplasm, which can be suppressed by NAC pretreatment.	Gossypol	13-26	high mobility group box 1	Homo sapiens	68-93
24012904-0	2013	Histamine inhibits high mobility group box 1-induced adhesion molecule expression on human monocytes.	Histamine	0-9	high mobility group box 1	Homo sapiens	19-44
24012904-5	2013	This study was designed to study the inhibitory effect of histamine on HMGB1 activity.	Histamine	58-67	high mobility group box 1	Homo sapiens	71-76
24012904-6	2013	We examined the effect of histamine on HMGB1-induced expression of ICAM-1, B7.1, B7.2 and CD40 on monocytes, production of IFN-gamma and TNF-alpha and lymphocyte proliferation in PBMCs.	Histamine	26-35	high mobility group box 1	Homo sapiens	39-44
24012904-7	2013	Histamine inhibited HMGB1 activity in a concentration-dependent manner.	Histamine	0-9	high mobility group box 1	Homo sapiens	20-25
24012904-11	2013	These results together indicated that histamine inhibited HMGB1 activity.	Histamine	38-47	high mobility group box 1	Homo sapiens	58-63
23398207-0	2013	Natural Bcl-2 inhibitor (-)- gossypol induces protective autophagy via reactive oxygen species-high mobility group box 1 pathway in Burkitt lymphoma.	Gossypol	24-37	high mobility group box 1	Homo sapiens	95-120
23398207-0	2013	Natural Bcl-2 inhibitor (-)- gossypol induces protective autophagy via reactive oxygen species-high mobility group box 1 pathway in Burkitt lymphoma.	Reactive Oxygen Species	71-94	high mobility group box 1	Homo sapiens	95-120
24204700-9	2013	Echocardiography and catheterization showed enhanced cardiac function after BMC transplantation compared to PBS injection at day 28, while this effect was abolished by antibody-neutralization of HMGB1.	bmc	76-79	high mobility group box 1	Homo sapiens	195-200
24204700-10	2013	BMC transplantation reduced post-infarction fibrosis, improved neovascularization, and increased proliferation, while all these effects in repairing the failing myocardium were eliminated by HMGB1-inhibition.	bmc	0-3	high mobility group box 1	Homo sapiens	191-196
24204700-11	2013	Furthermore, BMC transplantation drove the macrophage polarization towards alternatively-activated, anti-inflammatory M2 macrophages in the heart at day 3, while this was abolished by HMGB1-inhibition.	bmc	13-16	high mobility group box 1	Homo sapiens	184-189
24204700-14	2013	These data suggest that extracellular HMGB1 contributes to the effect of BMC transplantation to recover the damaged myocardium by favorably modulating innate immunity in heart failure.	bmc	73-76	high mobility group box 1	Homo sapiens	38-43
24255785-6	2013	In pulmonary system, binding of HMGB1 to its receptor for advanced glycation end-products (RAGE) triggers the production of pro-inflammatory cytokines, chemokines, adhesion molecules and reactive oxygen species, promoting the development of ALI/ARDS.	Reactive Oxygen Species	187-210	high mobility group box 1	Homo sapiens	32-37
23398207-6	2013	Furthermore, (-)- gossypol treatment increased the translocation of high mobility group box 1 (HMGB1) from nuclei to cytoplasm, which can be suppressed by NAC pretreatment.	Gossypol	13-26	high mobility group box 1	Homo sapiens	95-100
23398207-6	2013	Furthermore, (-)- gossypol treatment increased the translocation of high mobility group box 1 (HMGB1) from nuclei to cytoplasm, which can be suppressed by NAC pretreatment.	Acetylcysteine	155-158	high mobility group box 1	Homo sapiens	68-93
23398207-6	2013	Furthermore, (-)- gossypol treatment increased the translocation of high mobility group box 1 (HMGB1) from nuclei to cytoplasm, which can be suppressed by NAC pretreatment.	Acetylcysteine	155-158	high mobility group box 1	Homo sapiens	95-100
23398207-8	2013	These results indicate that (-)- gossypol induces a protective autophagy in Burkitt lymphoma cells, partly due to ROS induction and cytosolic translocation of HMGB1.	Gossypol	28-41	high mobility group box 1	Homo sapiens	159-164
23932051-0	2013	Glycyrrhizic acid confers neuroprotection after subarachnoid hemorrhage via inhibition of high mobility group box-1 protein: a hypothesis for novel therapy of subarachnoid hemorrhage.	Glycyrrhizic Acid	0-17	high mobility group box 1	Homo sapiens	90-115
24065095-0	2013	Potential of the angiotensin receptor blockers (ARBs) telmisartan, irbesartan, and candesartan for inhibiting the HMGB1/RAGE axis in prevention and acute treatment of stroke.	Telmisartan	54-65	high mobility group box 1	Homo sapiens	114-119
23932051-11	2013	Glycyrrhizic acid (GA) which was extracted from liquorice and confirmed as a nature inhibitor of HMGB1 with little side-effects could inhibit extracellular HMGB1 cytokine activities and reduce the level of inflammatory response, thus alleviating early brain injury and cerebrovasospasm.	Glycyrrhizic Acid	0-17	high mobility group box 1	Homo sapiens	97-102
23932051-11	2013	Glycyrrhizic acid (GA) which was extracted from liquorice and confirmed as a nature inhibitor of HMGB1 with little side-effects could inhibit extracellular HMGB1 cytokine activities and reduce the level of inflammatory response, thus alleviating early brain injury and cerebrovasospasm.	Glycyrrhizic Acid	0-17	high mobility group box 1	Homo sapiens	156-161
23932051-11	2013	Glycyrrhizic acid (GA) which was extracted from liquorice and confirmed as a nature inhibitor of HMGB1 with little side-effects could inhibit extracellular HMGB1 cytokine activities and reduce the level of inflammatory response, thus alleviating early brain injury and cerebrovasospasm.	Glycyrrhizic Acid	19-21	high mobility group box 1	Homo sapiens	97-102
23932051-11	2013	Glycyrrhizic acid (GA) which was extracted from liquorice and confirmed as a nature inhibitor of HMGB1 with little side-effects could inhibit extracellular HMGB1 cytokine activities and reduce the level of inflammatory response, thus alleviating early brain injury and cerebrovasospasm.	Glycyrrhizic Acid	19-21	high mobility group box 1	Homo sapiens	156-161
24417167-8	2013	The level of HMGB1 mRNA expression in Hep-2 cells increased after the cells were induced by hypoxia for 6h PD98059 and SP600125 with 20 micromol/ L and PDTC with 50 mg/L partly inhibited extracellular release of HMGB1 in hypoxia-cultured Hcp-2 cells.	pyrazolanthrone	119-127	high mobility group box 1	Homo sapiens	13-18
24417167-8	2013	The level of HMGB1 mRNA expression in Hep-2 cells increased after the cells were induced by hypoxia for 6h PD98059 and SP600125 with 20 micromol/ L and PDTC with 50 mg/L partly inhibited extracellular release of HMGB1 in hypoxia-cultured Hcp-2 cells.	pyrazolanthrone	119-127	high mobility group box 1	Homo sapiens	212-217
24065095-0	2013	Potential of the angiotensin receptor blockers (ARBs) telmisartan, irbesartan, and candesartan for inhibiting the HMGB1/RAGE axis in prevention and acute treatment of stroke.	Irbesartan	67-77	high mobility group box 1	Homo sapiens	114-119
24065095-0	2013	Potential of the angiotensin receptor blockers (ARBs) telmisartan, irbesartan, and candesartan for inhibiting the HMGB1/RAGE axis in prevention and acute treatment of stroke.	candesartan	83-94	high mobility group box 1	Homo sapiens	114-119
23244202-4	2013	To investigate these processes, the extracellular release of HMGB1 during necrosis was characterized in vitro using Jurkat T cell leukemia cells treated to induce necrosis by freeze-thaw, heat, hydrogen peroxide or ethanol.	Hydrogen Peroxide	194-211	high mobility group box 1	Homo sapiens	61-66
23911608-8	2013	HMGB1-induced increases in ICAM-1 and P-selectin expression were also inhibited by a specific eIF2alpha inhibitor (salubrinal) and a specific JNK inhibitor (SP600125).	salubrinal	115-125	high mobility group box 1	Homo sapiens	0-5
23911608-8	2013	HMGB1-induced increases in ICAM-1 and P-selectin expression were also inhibited by a specific eIF2alpha inhibitor (salubrinal) and a specific JNK inhibitor (SP600125).	pyrazolanthrone	157-165	high mobility group box 1	Homo sapiens	0-5
23834721-0	2013	Supporting cells regulate the remodelling of aminoglycoside-injured organ of Corti, through the release of high mobility group box 1.	Aminoglycosides	45-59	high mobility group box 1	Homo sapiens	107-132
23685846-7	2013	RESULT: We demonstrated that the patients with DMPM had significantly higher serum levels of HMGB1 compared with the population who had been exposed to asbestos but did not develop DMPM.	dmpm	47-51	high mobility group box 1	Homo sapiens	93-98
23685846-8	2013	CONCLUSION: Our data suggest that serum HMGB1 concentration is a useful serum marker for DMPM.	dmpm	89-93	high mobility group box 1	Homo sapiens	40-45
23148306-9	2013	In order to bind and signal via TLR4, HMGB1 must have a reduced cysteine 106 and a disulphide linkage between cysteine 23 and 45.	Cysteine	64-72	high mobility group box 1	Homo sapiens	38-43
23148306-9	2013	In order to bind and signal via TLR4, HMGB1 must have a reduced cysteine 106 and a disulphide linkage between cysteine 23 and 45.	disulphide	83-93	high mobility group box 1	Homo sapiens	38-43
23148306-9	2013	In order to bind and signal via TLR4, HMGB1 must have a reduced cysteine 106 and a disulphide linkage between cysteine 23 and 45.	Cysteine	110-118	high mobility group box 1	Homo sapiens	38-43
23769884-8	2013	However, the pretreatment with CM1 could significantly decrease AGE or high-mobility group box-1 (HMGB1, a ligand of RAGE)-induced cytotoxicity, apoptosis and reactive oxygen species (ROS) in human umbilical vein endothelial cells (HUVECs).	Reactive Oxygen Species	159-182	high mobility group box 1	Homo sapiens	71-96
23769884-8	2013	However, the pretreatment with CM1 could significantly decrease AGE or high-mobility group box-1 (HMGB1, a ligand of RAGE)-induced cytotoxicity, apoptosis and reactive oxygen species (ROS) in human umbilical vein endothelial cells (HUVECs).	Reactive Oxygen Species	184-187	high mobility group box 1	Homo sapiens	71-96
23697559-4	2013	The phosphorylation of both extracellular signal-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) was markedly upregulated by treating with high amount of HMGB1, while pretreatment with ERK1/2 and p38 MAPK-specific inhibitors (U0126 and SB203580) could attenuate suppression of T cell immune function and nuclear factor of activated T cell (NFAT) activation induced by HMGB1, respectively.	U 0126	252-257	high mobility group box 1	Homo sapiens	180-185
23697559-4	2013	The phosphorylation of both extracellular signal-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) was markedly upregulated by treating with high amount of HMGB1, while pretreatment with ERK1/2 and p38 MAPK-specific inhibitors (U0126 and SB203580) could attenuate suppression of T cell immune function and nuclear factor of activated T cell (NFAT) activation induced by HMGB1, respectively.	U 0126	252-257	high mobility group box 1	Homo sapiens	394-399
23697559-4	2013	The phosphorylation of both extracellular signal-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) was markedly upregulated by treating with high amount of HMGB1, while pretreatment with ERK1/2 and p38 MAPK-specific inhibitors (U0126 and SB203580) could attenuate suppression of T cell immune function and nuclear factor of activated T cell (NFAT) activation induced by HMGB1, respectively.	SB 203580	262-270	high mobility group box 1	Homo sapiens	180-185
23697559-4	2013	The phosphorylation of both extracellular signal-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) was markedly upregulated by treating with high amount of HMGB1, while pretreatment with ERK1/2 and p38 MAPK-specific inhibitors (U0126 and SB203580) could attenuate suppression of T cell immune function and nuclear factor of activated T cell (NFAT) activation induced by HMGB1, respectively.	SB 203580	262-270	high mobility group box 1	Homo sapiens	394-399
23697559-5	2013	HMGB1-induced activity of ERK1/2 and p38 was not fully inhibited in the presence of U0126 or SB203580.	U 0126	84-89	high mobility group box 1	Homo sapiens	0-5
23697559-5	2013	HMGB1-induced activity of ERK1/2 and p38 was not fully inhibited in the presence of U0126 or SB203580.	SB 203580	93-101	high mobility group box 1	Homo sapiens	0-5
23244202-4	2013	To investigate these processes, the extracellular release of HMGB1 during necrosis was characterized in vitro using Jurkat T cell leukemia cells treated to induce necrosis by freeze-thaw, heat, hydrogen peroxide or ethanol.	Ethanol	215-222	high mobility group box 1	Homo sapiens	61-66
23207101-5	2013	Notably, only one of the redox forms of HMGB1, the one where all cysteines are reduced (all-thiol), can bind CXCL12.	Cysteine	65-74	high mobility group box 1	Homo sapiens	40-45
23647088-6	2013	After exposure to H2O2, a marked decrease in cell viability (&lt;50%) was demonstrated, and this was significantly ameliorated upon culture at 32 C. Significantly intracellular damage was found to affect the 24-hour H2O2-exposed cells in 37 C (P &lt; .05), including an increase in apoptosis and necrosis, intracellular ROS, caspase-3 activity, HMGB1 protein expression, and some alterations to the cell cycle.	Hydrogen Peroxide	18-22	high mobility group box 1	Homo sapiens	345-350
23647088-6	2013	After exposure to H2O2, a marked decrease in cell viability (&lt;50%) was demonstrated, and this was significantly ameliorated upon culture at 32 C. Significantly intracellular damage was found to affect the 24-hour H2O2-exposed cells in 37 C (P &lt; .05), including an increase in apoptosis and necrosis, intracellular ROS, caspase-3 activity, HMGB1 protein expression, and some alterations to the cell cycle.	Hydrogen Peroxide	216-220	high mobility group box 1	Homo sapiens	345-350
23390034-8	2013	CONCLUSION: Elevations in plasma miR-122, HMGB1, and necrosis K18 identified subsequent ALI development in patients on admission to the hospital, soon after acetaminophen overdose, and in patients with ALTs in the normal range.	ali	88-91	high mobility group box 1	Homo sapiens	42-47
23712703-4	2013	However, the receptor for advanced glycation end products (RAGE) blocker RAGE-Ab (5 mug/ml) or 10 muM c-Jun N-terminal kinases (JNK) inhibitor SP600125 could inhibit HMGB1-induced the release of inflammation cytokines including TNF-alpha, IL-8, IL-10, and MCP-1 in a dose-dependent manner.	pyrazolanthrone	143-151	high mobility group box 1	Homo sapiens	166-171
23712703-5	2013	Furthermore, HMGB1-induced RAGE protein expression, JNK and NF-kappaB activation were attenuated by the pretreatment with RAGE-Ab or JNK inhibitor SP600125 in Western blot analysis.	pyrazolanthrone	147-155	high mobility group box 1	Homo sapiens	13-18
23737485-6	2013	CatmAb promoted tumor cell death associated with ATP release and strongly synergized with oxaliplatin for the exposure of the three hallmarks of immunogenic cell death (calreticulin, HMGB1, and ATP).	Oxaliplatin	90-101	high mobility group box 1	Homo sapiens	183-188
23207101-5	2013	Notably, only one of the redox forms of HMGB1, the one where all cysteines are reduced (all-thiol), can bind CXCL12.	Sulfhydryl Compounds	92-97	high mobility group box 1	Homo sapiens	40-45
23207101-6	2013	Both HMGB1 containing a disulfide bond between C23 and C45, which induces chemokine and cytokine release by activating TLR4, and HMGB1 terminally oxidized to contain a cysteine sulfonate are inactive in recruiting leukocytes.	Disulfides	24-33	high mobility group box 1	Homo sapiens	5-10
23207101-6	2013	Both HMGB1 containing a disulfide bond between C23 and C45, which induces chemokine and cytokine release by activating TLR4, and HMGB1 terminally oxidized to contain a cysteine sulfonate are inactive in recruiting leukocytes.	cysteine sulfonate	168-186	high mobility group box 1	Homo sapiens	129-134
23835906-0	2013	Carbenoxolone blocks endotoxin-induced protein kinase R (PKR) activation and high mobility group box 1 (HMGB1) release.	Carbenoxolone	0-13	high mobility group box 1	Homo sapiens	77-102
23835906-7	2013	Collectively, these results suggested that CBX blocks LPS-induced HMGB1 release possibly through impairing PKR activation, supporting the involvement of PKR in the regulation of HMGB1 release.	Carbenoxolone	43-46	high mobility group box 1	Homo sapiens	66-71
23835906-0	2013	Carbenoxolone blocks endotoxin-induced protein kinase R (PKR) activation and high mobility group box 1 (HMGB1) release.	Carbenoxolone	0-13	high mobility group box 1	Homo sapiens	104-109
23835906-7	2013	Collectively, these results suggested that CBX blocks LPS-induced HMGB1 release possibly through impairing PKR activation, supporting the involvement of PKR in the regulation of HMGB1 release.	Carbenoxolone	43-46	high mobility group box 1	Homo sapiens	178-183
23835906-1	2013	The pathogen- and damage-associated molecular patterns (for example, bacterial endotoxin and adenosine 5"-triphosphate [ATP]) activate the double-stranded RNA-activated protein kinase R (PKR) to trigger the inflammasome-dependent high mobility group box 1 (HMGB1) release.	Adenosine Triphosphate	93-118	high mobility group box 1	Homo sapiens	230-255
23835906-1	2013	The pathogen- and damage-associated molecular patterns (for example, bacterial endotoxin and adenosine 5"-triphosphate [ATP]) activate the double-stranded RNA-activated protein kinase R (PKR) to trigger the inflammasome-dependent high mobility group box 1 (HMGB1) release.	Adenosine Triphosphate	93-118	high mobility group box 1	Homo sapiens	257-262
23835906-1	2013	The pathogen- and damage-associated molecular patterns (for example, bacterial endotoxin and adenosine 5"-triphosphate [ATP]) activate the double-stranded RNA-activated protein kinase R (PKR) to trigger the inflammasome-dependent high mobility group box 1 (HMGB1) release.	Adenosine Triphosphate	120-123	high mobility group box 1	Homo sapiens	230-255
23835906-1	2013	The pathogen- and damage-associated molecular patterns (for example, bacterial endotoxin and adenosine 5"-triphosphate [ATP]) activate the double-stranded RNA-activated protein kinase R (PKR) to trigger the inflammasome-dependent high mobility group box 1 (HMGB1) release.	Adenosine Triphosphate	120-123	high mobility group box 1	Homo sapiens	257-262
23711070-5	2013	There was a positive relationship between the BEBSS and HMGB1 levels (r = 0.54, P = 0.004).	bebss	46-51	high mobility group box 1	Homo sapiens	56-61
23576640-6	2013	Glucose (11.2 mM) maximally increased TLR2 and 4 expression, HMGB1 release, and NF-kappaB activation with increased expression of cytokines.	Glucose	0-7	high mobility group box 1	Homo sapiens	61-66
23576640-10	2013	Therefore, short-term moderate increases in glucose in vitro increase HMGB1, which mediates NF-kappaB activation through both TLR2 and 4.	Glucose	44-51	high mobility group box 1	Homo sapiens	70-75
23421467-7	2013	The LMWH significantly inhibited HMGB1-induced NFkappaB activation through RAGE using an NFkappaB-dependent luciferase reporter assay and the HT1080 cell lines.	Heparin, Low-Molecular-Weight	4-8	high mobility group box 1	Homo sapiens	33-38
23446148-3	2013	HMGB1 contains three conserved redox-sensitive cysteines (C23, C45, and C106); modification of these cysteines determines the bioactivity of extracellular HMGB1.	Cysteine	47-56	high mobility group box 1	Homo sapiens	0-5
23446148-3	2013	HMGB1 contains three conserved redox-sensitive cysteines (C23, C45, and C106); modification of these cysteines determines the bioactivity of extracellular HMGB1.	Cysteine	47-56	high mobility group box 1	Homo sapiens	155-160
23446148-3	2013	HMGB1 contains three conserved redox-sensitive cysteines (C23, C45, and C106); modification of these cysteines determines the bioactivity of extracellular HMGB1.	Cysteine	101-110	high mobility group box 1	Homo sapiens	0-5
23446148-3	2013	HMGB1 contains three conserved redox-sensitive cysteines (C23, C45, and C106); modification of these cysteines determines the bioactivity of extracellular HMGB1.	Cysteine	101-110	high mobility group box 1	Homo sapiens	155-160
23446148-4	2013	Firstly, the cytokine-stimulating activity of HMGB1 requires C23 and C45 to be in a disulfide linkage, at the same time that C106 must remain in its reduced form as a thiol.	Disulfides	84-93	high mobility group box 1	Homo sapiens	46-51
23446148-4	2013	Firstly, the cytokine-stimulating activity of HMGB1 requires C23 and C45 to be in a disulfide linkage, at the same time that C106 must remain in its reduced form as a thiol.	Sulfhydryl Compounds	167-172	high mobility group box 1	Homo sapiens	46-51
23446148-6	2013	Secondly, for HMGB1 to act as a chemotactic mediator, all three cysteines must be in the reduced form.	Cysteine	64-73	high mobility group box 1	Homo sapiens	14-19
23446148-7	2013	This all-thiol HMGB1 exerts its chemotactic activity to initiate inflammation by forming a heterocomplex with CXCL12; that complex binds exclusively to CXCR4 to initiate chemotaxis.	Sulfhydryl Compounds	9-14	high mobility group box 1	Homo sapiens	15-20
23446148-8	2013	Thirdly, binding of the HMGB1 to CXCR4 or to TLR4 is completely prevented by all-cysteine oxidation.	all-cysteine	77-89	high mobility group box 1	Homo sapiens	24-29
23446148-10	2013	Lastly, post-translational acetylation of key lysine residues within NLSs of HMGB1 affects HMGB1 to promote inflammation; hyperacetylation of HMGB1 shifts its equilibrium from a predominant nuclear location toward a cytosolic and subsequent extracellular presence.	Lysine	46-52	high mobility group box 1	Homo sapiens	77-82
23446148-10	2013	Lastly, post-translational acetylation of key lysine residues within NLSs of HMGB1 affects HMGB1 to promote inflammation; hyperacetylation of HMGB1 shifts its equilibrium from a predominant nuclear location toward a cytosolic and subsequent extracellular presence.	Lysine	46-52	high mobility group box 1	Homo sapiens	91-96
23446148-10	2013	Lastly, post-translational acetylation of key lysine residues within NLSs of HMGB1 affects HMGB1 to promote inflammation; hyperacetylation of HMGB1 shifts its equilibrium from a predominant nuclear location toward a cytosolic and subsequent extracellular presence.	Lysine	46-52	high mobility group box 1	Homo sapiens	91-96
23042518-0	2013	Barrier protective effects of rosmarinic acid on HMGB1-induced inflammatory responses in vitro and in vivo.	rosmarinic acid	30-45	high mobility group box 1	Homo sapiens	49-54
23508573-1	2013	High mobility group box 1 (HMGB1) is a DNA-binding protein that possesses cytokinelike, proinflammatory properties when released extracellularly in the C23-C45 disulfide form.	Disulfides	160-169	high mobility group box 1	Homo sapiens	0-25
23508573-1	2013	High mobility group box 1 (HMGB1) is a DNA-binding protein that possesses cytokinelike, proinflammatory properties when released extracellularly in the C23-C45 disulfide form.	Disulfides	160-169	high mobility group box 1	Homo sapiens	27-32
23508573-6	2013	TLR4 and MD2 are recruited into CD14-containing lipid rafts of RAW264.7 macrophages after stimulation with HMGB1, and TLR4 interacts closely with the lipid raft protein GM1.	G(M1) Ganglioside	169-172	high mobility group box 1	Homo sapiens	107-112
23628898-7	2013	One of the mechanisms underlying these activating effects of ICs on human endothelial cells involves cell signaling by high-mobility group box 1 protein (HMGB1)-RAGE axis, as these effects can be partially blocked by HMGB1 A-box, soluble RAGE (sRAGE), SB203580, PD98059, Bay 117082 (P&lt;0.05) and co-treatment with these agents (P&lt;0.05).	SB 203580	252-260	high mobility group box 1	Homo sapiens	119-144
23628898-7	2013	One of the mechanisms underlying these activating effects of ICs on human endothelial cells involves cell signaling by high-mobility group box 1 protein (HMGB1)-RAGE axis, as these effects can be partially blocked by HMGB1 A-box, soluble RAGE (sRAGE), SB203580, PD98059, Bay 117082 (P&lt;0.05) and co-treatment with these agents (P&lt;0.05).	SB 203580	252-260	high mobility group box 1	Homo sapiens	154-159
23628898-7	2013	One of the mechanisms underlying these activating effects of ICs on human endothelial cells involves cell signaling by high-mobility group box 1 protein (HMGB1)-RAGE axis, as these effects can be partially blocked by HMGB1 A-box, soluble RAGE (sRAGE), SB203580, PD98059, Bay 117082 (P&lt;0.05) and co-treatment with these agents (P&lt;0.05).	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	262-269	high mobility group box 1	Homo sapiens	119-144
23628898-7	2013	One of the mechanisms underlying these activating effects of ICs on human endothelial cells involves cell signaling by high-mobility group box 1 protein (HMGB1)-RAGE axis, as these effects can be partially blocked by HMGB1 A-box, soluble RAGE (sRAGE), SB203580, PD98059, Bay 117082 (P&lt;0.05) and co-treatment with these agents (P&lt;0.05).	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	262-269	high mobility group box 1	Homo sapiens	154-159
23628898-7	2013	One of the mechanisms underlying these activating effects of ICs on human endothelial cells involves cell signaling by high-mobility group box 1 protein (HMGB1)-RAGE axis, as these effects can be partially blocked by HMGB1 A-box, soluble RAGE (sRAGE), SB203580, PD98059, Bay 117082 (P&lt;0.05) and co-treatment with these agents (P&lt;0.05).	3-(4-methylphenylsulfonyl)-2-propenenitrile	271-281	high mobility group box 1	Homo sapiens	119-144
23628898-7	2013	One of the mechanisms underlying these activating effects of ICs on human endothelial cells involves cell signaling by high-mobility group box 1 protein (HMGB1)-RAGE axis, as these effects can be partially blocked by HMGB1 A-box, soluble RAGE (sRAGE), SB203580, PD98059, Bay 117082 (P&lt;0.05) and co-treatment with these agents (P&lt;0.05).	3-(4-methylphenylsulfonyl)-2-propenenitrile	271-281	high mobility group box 1	Homo sapiens	154-159
23042518-2	2013	Rosmarinic acid (RA) is an important component of the leaves of Perilla frutescens and has neuroprotective, anti-microbial, anti-oxidant, and anti-cancer effects but little is known of its effects on HMGB1-mediated inflammatory response.	rosmarinic acid	17-19	high mobility group box 1	Homo sapiens	200-205
23042518-3	2013	Here, we investigated this issue by monitoring the effects of RA on the lipopolysaccharide (LPS) or cecal ligation and puncture (CLP)-mediated release of HMGB1 and HMGB1-mediated modulation of inflammatory responses.	rosmarinic acid	62-64	high mobility group box 1	Homo sapiens	154-159
23042518-4	2013	RA potently inhibited the release of HMGB1 and down-regulated HMGB1-dependent inflammatory responses in human endothelial cells.	rosmarinic acid	0-2	high mobility group box 1	Homo sapiens	37-42
23042518-4	2013	RA potently inhibited the release of HMGB1 and down-regulated HMGB1-dependent inflammatory responses in human endothelial cells.	rosmarinic acid	0-2	high mobility group box 1	Homo sapiens	62-67
23042518-6	2013	Furthermore, RA reduced CLP-induced HMGB1 release and sepsis-related mortality.	rosmarinic acid	13-15	high mobility group box 1	Homo sapiens	36-41
23042518-7	2013	Given these results, RA should be viewed as a candidate therapeutic agent for the treatment of various inflammatory diseases via inhibition of the HMGB1 signaling pathway.	rosmarinic acid	21-23	high mobility group box 1	Homo sapiens	147-152
22939552-0	2013	Dexmedetomidine inhibits the secretion of high mobility group box 1 from lipopolysaccharide-activated macrophages in vitro.	Dexmedetomidine	0-15	high mobility group box 1	Homo sapiens	42-67
22939552-4	2013	In this study, we explored the effect of dexmedetomidine on the expression and secretion of HMGB1 from lipopolysaccharide (LPS)-activated macrophages.	Dexmedetomidine	41-56	high mobility group box 1	Homo sapiens	92-97
22939552-10	2013	RESULTS: Dexmedetomidine inhibited the translocation of HMGB1 from the nucleus to the cytoplasm and its extracellular secretion in LPS-activated macrophages while suppressing the expression of HMGB1 mRNA.	Dexmedetomidine	9-24	high mobility group box 1	Homo sapiens	56-61
22939552-10	2013	RESULTS: Dexmedetomidine inhibited the translocation of HMGB1 from the nucleus to the cytoplasm and its extracellular secretion in LPS-activated macrophages while suppressing the expression of HMGB1 mRNA.	Dexmedetomidine	9-24	high mobility group box 1	Homo sapiens	193-198
22939552-13	2013	CONCLUSIONS: Our study demonstrates that dexmedetomidine inhibits the translocation of HMGB1 from the nucleus to the cytoplasm and the expression of HMGB1 mRNA at clinically relevant dosages.	Dexmedetomidine	41-56	high mobility group box 1	Homo sapiens	87-92
22939552-13	2013	CONCLUSIONS: Our study demonstrates that dexmedetomidine inhibits the translocation of HMGB1 from the nucleus to the cytoplasm and the expression of HMGB1 mRNA at clinically relevant dosages.	Dexmedetomidine	41-56	high mobility group box 1	Homo sapiens	149-154
23488692-0	2013	IL-1beta/HMGB1 complexes promote The PGE2 biosynthesis pathway in synovial fibroblasts.	Dinoprostone	37-41	high mobility group box 1	Homo sapiens	9-14
23488692-6	2013	We aimed to investigate the effects of IL-1beta/HMGB1 complexes on mPGES-1 and other enzymes of the PGE2 pathway in synovial fibroblasts (SFs) from patients with arthritis.	Dinoprostone	100-104	high mobility group box 1	Homo sapiens	48-53
23488692-8	2013	Stimulation of SFs with HMGB1 in complex with suboptimal amounts of IL-1beta significantly increased mPGES-1 and COX-2 expressions as well as PGE2 production, as compared to treatment with HMGB1 or IL-1beta alone.	SFS	15-18	high mobility group box 1	Homo sapiens	24-29
23488692-8	2013	Stimulation of SFs with HMGB1 in complex with suboptimal amounts of IL-1beta significantly increased mPGES-1 and COX-2 expressions as well as PGE2 production, as compared to treatment with HMGB1 or IL-1beta alone.	SFS	15-18	high mobility group box 1	Homo sapiens	189-194
23488692-8	2013	Stimulation of SFs with HMGB1 in complex with suboptimal amounts of IL-1beta significantly increased mPGES-1 and COX-2 expressions as well as PGE2 production, as compared to treatment with HMGB1 or IL-1beta alone.	Dinoprostone	142-146	high mobility group box 1	Homo sapiens	24-29
23488692-9	2013	Furthermore, NS-398 reduced the production of IL-6 and IL-8, thus indicating that IL-1beta/HMGB1 complexes modulate cytokine production in part through prostanoid synthesis.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	13-19	high mobility group box 1	Homo sapiens	91-96
23488692-9	2013	Furthermore, NS-398 reduced the production of IL-6 and IL-8, thus indicating that IL-1beta/HMGB1 complexes modulate cytokine production in part through prostanoid synthesis.	Prostaglandins	152-162	high mobility group box 1	Homo sapiens	91-96
23488692-11	2013	IL-1beta/HMGB1 complexes promote the induction of mPGES-1, COX-2 and PGE2 in SF.	Dinoprostone	69-73	high mobility group box 1	Homo sapiens	9-14
23488692-12	2013	The amplification of the PGE2 biosynthesis pathway by HMGB1 might constitute an important pathogenic mechanism perpetuating inflammatory and destructive activities in rheumatoid arthritis.	Dinoprostone	25-29	high mobility group box 1	Homo sapiens	54-59
23985250-2	2013	METHODS: HMGB1 gene targeting siRNA was designed and synthesized, and HMGB1 siRNA oligonucleotides were transfected into the MGC-803 cells with Lipofectamine 2000.	Oligonucleotides	82-98	high mobility group box 1	Homo sapiens	70-75
23447529-4	2013	Using a unique NMR-based approach, we have investigated the kinetics of HMGB1 oxidation and the half-lives of all-thiol and disulfide HMGB1 species in serum, saliva, and cell culture medium.	Disulfides	124-133	high mobility group box 1	Homo sapiens	134-139
23447529-5	2013	In this approach, salt-free lyophilized (15)N-labeled all-thiol HMGB1 was dissolved in actual extracellular fluids, and the oxidation and clearance kinetics were monitored in situ by recording a series of heteronuclear (1)H-(15)N correlation spectra.	Salts	18-22	high mobility group box 1	Homo sapiens	64-69
23447529-5	2013	In this approach, salt-free lyophilized (15)N-labeled all-thiol HMGB1 was dissolved in actual extracellular fluids, and the oxidation and clearance kinetics were monitored in situ by recording a series of heteronuclear (1)H-(15)N correlation spectra.	Sulfhydryl Compounds	58-63	high mobility group box 1	Homo sapiens	64-69
23447529-7	2013	For example, the half-life of all-thiol HMGB1 ranged from ~17 min (in human serum and saliva) to 3 h (in prostate cancer cell culture medium).	Sulfhydryl Compounds	34-39	high mobility group box 1	Homo sapiens	40-45
23447529-8	2013	Furthermore, the binding of ligands (glycyrrhizin and heparin) to HMGB1 significantly modulated the oxidation kinetics.	Glycyrrhizic Acid	37-49	high mobility group box 1	Homo sapiens	66-71
23447529-8	2013	Furthermore, the binding of ligands (glycyrrhizin and heparin) to HMGB1 significantly modulated the oxidation kinetics.	Heparin	54-61	high mobility group box 1	Homo sapiens	66-71
23447529-9	2013	Thus, the balance between the roles of all-thiol and disulfide HMGB1 proteins depends significantly on the extracellular environment and can also be artificially modulated by ligands.	Disulfides	53-62	high mobility group box 1	Homo sapiens	63-68
22911316-4	2013	Persicarin potently inhibited the release of HMGB1 and down-regulated HMGB1-dependent inflammatory responses in human endothelial cells, and inhibited HMGB1-mediated hyperpermeability and leukocyte migration in mice.	persicarin	0-10	high mobility group box 1	Homo sapiens	45-50
22911316-4	2013	Persicarin potently inhibited the release of HMGB1 and down-regulated HMGB1-dependent inflammatory responses in human endothelial cells, and inhibited HMGB1-mediated hyperpermeability and leukocyte migration in mice.	persicarin	0-10	high mobility group box 1	Homo sapiens	70-75
22911316-4	2013	Persicarin potently inhibited the release of HMGB1 and down-regulated HMGB1-dependent inflammatory responses in human endothelial cells, and inhibited HMGB1-mediated hyperpermeability and leukocyte migration in mice.	persicarin	0-10	high mobility group box 1	Homo sapiens	70-75
23617783-9	2013	We demonstrated that patients with MPM had significantly higher serum levels of HMGB1 than the population who had been exposed to asbestos but had not developed MPM.	Asbestos	130-138	high mobility group box 1	Homo sapiens	80-85
23403945-0	2013	Insulin infusion suppresses while glucose infusion induces Toll-like receptors and high-mobility group-B1 protein expression in mononuclear cells of type 1 diabetes patients.	Glucose	34-41	high mobility group box 1	Homo sapiens	83-105
23403945-4	2013	Glucose infusion led to an increase in plasma glucose concentration from 115 (fasting) to 215 (at 4 and 6 h) mg/dl and to an increase in ROS generation, the expression of TLR-4, TLR-2, TLR-1, HMGB1, p38 MAP kinase, and JNK-1, and plasma concentrations of HMGB1.	Glucose	0-7	high mobility group box 1	Homo sapiens	192-197
23403945-4	2013	Glucose infusion led to an increase in plasma glucose concentration from 115 (fasting) to 215 (at 4 and 6 h) mg/dl and to an increase in ROS generation, the expression of TLR-4, TLR-2, TLR-1, HMGB1, p38 MAP kinase, and JNK-1, and plasma concentrations of HMGB1.	Glucose	0-7	high mobility group box 1	Homo sapiens	255-260
23206318-5	2013	Postmortem human alcoholic brain also showed increased HMGB1, TLR2, TLR3, and TLR4 +IR cells that correlated with lifetime alcohol consumption, as well as each other.	Alcohols	17-24	high mobility group box 1	Homo sapiens	55-60
24250621-9	2013	5-FU also induced HMGB1 secretion, Cas3 and PARP activity and these effects were stronger in cells expressing WT TLR4 than the other cells.	Fluorouracil	0-4	high mobility group box 1	Homo sapiens	18-23
23352503-0	2013	Inhibitory effects of epi-sesamin on HMGB1-induced vascular barrier disruptive responses in vitro and in vivo.	sesamin	22-33	high mobility group box 1	Homo sapiens	37-42
23384711-9	2013	At multivariate analysis, HMGB1 was found to be independently correlated with BMI, IL23, IL6, free triiodothyronine, HDL, and HOMA-IR.	Triiodothyronine	99-115	high mobility group box 1	Homo sapiens	26-31
23410002-0	2013	Plasma HMGB-1 after the initial dose of epirubicin/docetaxel in cancer.	Epirubicin	40-50	high mobility group box 1	Homo sapiens	7-13
23410002-6	2013	RESULTS: Treatment of HCC1143 cells with epirubicin/docetaxel resulted in a significant HMGB-1 release in vitro.	Epirubicin	41-51	high mobility group box 1	Homo sapiens	88-94
23410002-0	2013	Plasma HMGB-1 after the initial dose of epirubicin/docetaxel in cancer.	Docetaxel	51-60	high mobility group box 1	Homo sapiens	7-13
23410002-6	2013	RESULTS: Treatment of HCC1143 cells with epirubicin/docetaxel resulted in a significant HMGB-1 release in vitro.	Docetaxel	52-61	high mobility group box 1	Homo sapiens	88-94
23410002-3	2013	We hypothesized that the initial dose of NCT with epirubicin/docetaxel induces changes in plasma HMGB-1 which could allow for an early prediction of response to therapy.	Epirubicin	50-60	high mobility group box 1	Homo sapiens	97-103
23410002-3	2013	We hypothesized that the initial dose of NCT with epirubicin/docetaxel induces changes in plasma HMGB-1 which could allow for an early prediction of response to therapy.	Docetaxel	61-70	high mobility group box 1	Homo sapiens	97-103
23410002-4	2013	MATERIALS AND METHODS: First, we analysed whether epirubicin/docetaxel releases HMGB-1 from HCC1143 breast cancer cells in vitro.	Epirubicin	50-60	high mobility group box 1	Homo sapiens	80-86
23410002-4	2013	MATERIALS AND METHODS: First, we analysed whether epirubicin/docetaxel releases HMGB-1 from HCC1143 breast cancer cells in vitro.	Docetaxel	61-70	high mobility group box 1	Homo sapiens	80-86
23222484-7	2013	Importantly, priming through surface TLRs but not endosomal TLRs during pyroptosis leads to the release of a new TLR4-agonist cysteine redox isoform of HMGB1.	Cysteine	126-134	high mobility group box 1	Homo sapiens	152-157
23808169-0	2013	[The structure of the complexes of DNA with nonhistone chromosomal protein HMGB1 and the histone H1 in the presence of manganese ions.	Manganese	119-128	high mobility group box 1	Homo sapiens	75-80
23808169-3	2013	Complexes of DNA with nonhistone chromosomal protein HMGB1 and histone H1 in the presence of manganese ions were studied using absorption and circular dichroism spectroscopy in infrared region.	Manganese	93-102	high mobility group box 1	Homo sapiens	53-58
23808169-5	2013	It was also shown that the manganese ions are able to coordinate to the chemical groups of DNA as well as to the carboxylic amino acid residues of the protein HMGB1.	Manganese	27-36	high mobility group box 1	Homo sapiens	159-164
23808169-5	2013	It was also shown that the manganese ions are able to coordinate to the chemical groups of DNA as well as to the carboxylic amino acid residues of the protein HMGB1.	carboxylic amino acid	113-134	high mobility group box 1	Homo sapiens	159-164
23325855-2	2013	HMGB1/2 play a critical, although poorly understood, role in vitro in the assembly of functional RAG-RSS complexes, into which HMGB1/2 stably incorporate.	rag-rss	97-104	high mobility group box 1	Homo sapiens	0-5
23325855-2	2013	HMGB1/2 play a critical, although poorly understood, role in vitro in the assembly of functional RAG-RSS complexes, into which HMGB1/2 stably incorporate.	rag-rss	97-104	high mobility group box 1	Homo sapiens	127-132
23325855-4	2013	Here, we report data demonstrating only a weak HMGB1-RAG1 interaction in the absence of DNA in several assays, including fluorescence anisotropy experiments using a novel Alexa488-labeled HMGB1 protein.	alexa488	171-179	high mobility group box 1	Homo sapiens	188-193
23333393-0	2013	Inhibitory effects of berberine on lipopolysaccharide-induced inducible nitric oxide synthase and the high-mobility group box 1 release in macrophages.	Berberine	22-31	high mobility group box 1	Homo sapiens	102-127
23333393-1	2013	We investigated the molecular mechanism by which berberine reduces nitric oxide (NO) expression and high-mobility group box 1 (HMGB1) release in lipopolysaccharide (LPS)-induced macrophages.	Berberine	49-58	high mobility group box 1	Homo sapiens	100-125
23333393-1	2013	We investigated the molecular mechanism by which berberine reduces nitric oxide (NO) expression and high-mobility group box 1 (HMGB1) release in lipopolysaccharide (LPS)-induced macrophages.	Berberine	49-58	high mobility group box 1	Homo sapiens	127-132
23333393-2	2013	Berberine significantly inhibited the LPS-stimulated NO production and HMGB1 release in macrophages.	Berberine	0-9	high mobility group box 1	Homo sapiens	71-76
23333393-4	2013	The inhibitory effect of berberine on LPS-stimulated NO and HMGB1 release was reversed by siRNA-Nrf2, SB203580 (p38 MAPK inhibitor) and zinc protoporphyrin (ZnPP; HO-1 inhibitor) within macrophages.	Berberine	25-34	high mobility group box 1	Homo sapiens	60-65
23333393-4	2013	The inhibitory effect of berberine on LPS-stimulated NO and HMGB1 release was reversed by siRNA-Nrf2, SB203580 (p38 MAPK inhibitor) and zinc protoporphyrin (ZnPP; HO-1 inhibitor) within macrophages.	SB 203580	102-110	high mobility group box 1	Homo sapiens	60-65
23333393-4	2013	The inhibitory effect of berberine on LPS-stimulated NO and HMGB1 release was reversed by siRNA-Nrf2, SB203580 (p38 MAPK inhibitor) and zinc protoporphyrin (ZnPP; HO-1 inhibitor) within macrophages.	zinc protoporphyrin	136-155	high mobility group box 1	Homo sapiens	60-65
23333393-4	2013	The inhibitory effect of berberine on LPS-stimulated NO and HMGB1 release was reversed by siRNA-Nrf2, SB203580 (p38 MAPK inhibitor) and zinc protoporphyrin (ZnPP; HO-1 inhibitor) within macrophages.	zinc protoporphyrin	157-161	high mobility group box 1	Homo sapiens	60-65
23303669-5	2013	HMGB1 directly interacted with polyQ on immunofluorescence and coimmunoprecipitation assay, whereas the overexpression of HMGB1 or exogenous administration of recombinant HMGB1 protein remarkably reduced polyQ aggregates in SHSY5Y cells and hmgb1(-/-) mouse embryonic fibroblasts upon filter trap and immunofluorescence assay.	polyglutamine	31-36	high mobility group box 1	Homo sapiens	0-5
23303669-5	2013	HMGB1 directly interacted with polyQ on immunofluorescence and coimmunoprecipitation assay, whereas the overexpression of HMGB1 or exogenous administration of recombinant HMGB1 protein remarkably reduced polyQ aggregates in SHSY5Y cells and hmgb1(-/-) mouse embryonic fibroblasts upon filter trap and immunofluorescence assay.	polyglutamine	204-209	high mobility group box 1	Homo sapiens	0-5
23303669-5	2013	HMGB1 directly interacted with polyQ on immunofluorescence and coimmunoprecipitation assay, whereas the overexpression of HMGB1 or exogenous administration of recombinant HMGB1 protein remarkably reduced polyQ aggregates in SHSY5Y cells and hmgb1(-/-) mouse embryonic fibroblasts upon filter trap and immunofluorescence assay.	polyglutamine	204-209	high mobility group box 1	Homo sapiens	122-127
23303669-5	2013	HMGB1 directly interacted with polyQ on immunofluorescence and coimmunoprecipitation assay, whereas the overexpression of HMGB1 or exogenous administration of recombinant HMGB1 protein remarkably reduced polyQ aggregates in SHSY5Y cells and hmgb1(-/-) mouse embryonic fibroblasts upon filter trap and immunofluorescence assay.	polyglutamine	204-209	high mobility group box 1	Homo sapiens	122-127
23241947-6	2013	Our results suggest that PEF suppresses LPC-induced inflammatory factor production through inhibition of the HMGB1-RAGE/TLR-2/TLR-4-NF-kappaB pathway.	Lysophosphatidylcholines	40-43	high mobility group box 1	Homo sapiens	109-114
23414442-7	2013	RA 50 mg/kg attenuated histopathological damage, decreased brain edema, inhibited NF-kappaB activation and reduced HMGB1 expression.	rosmarinic acid	0-2	high mobility group box 1	Homo sapiens	115-120
23414442-8	2013	CONCLUSION: These data show that RA protects the brain against I/R injury with a favorable therapeutic time-window by alleviating diabetic cerebral I/R injury and attenuating blood-brain barrier (BBB) breakdown, and its protective effects may involve HMGB1 and the NF-kappaB signaling pathway.	rosmarinic acid	33-35	high mobility group box 1	Homo sapiens	251-256
24148794-9	2013	Moreover, H2 treatment dose-dependently attenuated the increased levels of pro-inflammatory cytokines (TNF-alpha, IL-1beta, HMGB1), but further increased the level of anti-inflammatory cytokine IL-10 at 3 h, 6 h, 12 h and 24 h after LPS stimulation.	Hydrogen	10-12	high mobility group box 1	Homo sapiens	124-129
24289579-10	2013	Methylation of HMGB1 at lysine 112 in ccRCC was detected by MS. Bioinformatics analysis showed that post-translational modification might affect the binding ability to DNA and mediate its translocation.	Lysine	24-30	high mobility group box 1	Homo sapiens	15-20
24289579-12	2013	Methylation of HMGB1 at lysine 112 might the redistribution of this cofactor protein.	Lysine	24-30	high mobility group box 1	Homo sapiens	15-20
24191125-6	2013	The UA-HMGB1 level in the BHT (-) group did not differ significantly from reference values, but was significantly increased 24 hours after birth.	Butylated Hydroxytoluene	26-29	high mobility group box 1	Homo sapiens	7-12
23036589-0	2013	Evidence for the binding affinity of daunomycin to HMGB1 protein in chromatin and in solution.	Daunorubicin	37-47	high mobility group box 1	Homo sapiens	51-56
23036589-1	2013	In this study the interaction of daunomycin with HMGB1 nonhistone chromatin protein in the chromatin context using hydroxyapatite (HAP) column chromatography and free in solution was investigated employing fluorescence, circular dichroism spectroscopy and thermal denaturation techniques.	Daunorubicin	33-43	high mobility group box 1	Homo sapiens	49-54
23036589-1	2013	In this study the interaction of daunomycin with HMGB1 nonhistone chromatin protein in the chromatin context using hydroxyapatite (HAP) column chromatography and free in solution was investigated employing fluorescence, circular dichroism spectroscopy and thermal denaturation techniques.	Durapatite	115-129	high mobility group box 1	Homo sapiens	49-54
23036589-2	2013	The results demonstrate that HMGB1 fraction eluted from HAP column contained the most amount of daunomycin.	Daunorubicin	96-106	high mobility group box 1	Homo sapiens	29-34
23036589-3	2013	Upon addition of daunomycin to HMGB1 solution, fluorescence emission intensity was dependent on the drug concentration used whereas the ellipticity in CD spectra was decreased at both 205 and 220 nm extremes implying that quenching of the drug with the HMGB1 chromospheres alters secondary structure of the protein.	Daunorubicin	17-27	high mobility group box 1	Homo sapiens	31-36
23036589-3	2013	Upon addition of daunomycin to HMGB1 solution, fluorescence emission intensity was dependent on the drug concentration used whereas the ellipticity in CD spectra was decreased at both 205 and 220 nm extremes implying that quenching of the drug with the HMGB1 chromospheres alters secondary structure of the protein.	Daunorubicin	17-27	high mobility group box 1	Homo sapiens	253-258
23036589-3	2013	Upon addition of daunomycin to HMGB1 solution, fluorescence emission intensity was dependent on the drug concentration used whereas the ellipticity in CD spectra was decreased at both 205 and 220 nm extremes implying that quenching of the drug with the HMGB1 chromospheres alters secondary structure of the protein.	Cadmium	151-153	high mobility group box 1	Homo sapiens	253-258
23036589-4	2013	Although daunomycin slightly increased the melting point of HMGB1, but exhibited a significant hyperchromicity at low concentrations and hypochromicity at higher concentrations of daunomycin.	Daunorubicin	9-19	high mobility group box 1	Homo sapiens	60-65
23036589-5	2013	The results suggest that daunomycin binds to HMGB1 protein which may influence its interaction with DNA in nucleosomes and other cellular processes.	Daunorubicin	25-35	high mobility group box 1	Homo sapiens	45-50
23073660-4	2012	Reduced all-thiol-HMGB1 has sole chemokine activity, whereas disulfide-HMGB1 has only cytokine activity, and oxidized, denatured HMGB1 has neither.	Sulfhydryl Compounds	12-17	high mobility group box 1	Homo sapiens	18-23
23042506-11	2013	Knockdown of HMGB1 downregulated the expression of p-AKT, Ki-67             and MMP-2, inhibited the proliferative activities and metastatic potential of             SMMC-7721 cells, induced cell cycle arrest and apoptosis, and slowed the growth             of xenograft tumors.	smmc	166-170	high mobility group box 1	Homo sapiens	13-18
22487382-0	2013	Magnesium sulfate inhibits the secretion of high mobility group box 1 from lipopolysaccharide-activated RAW264.7 macrophages in vitro.	Magnesium Sulfate	0-17	high mobility group box 1	Homo sapiens	44-69
22487382-4	2013	In the present study, we explored the effect of magnesium sulfate on the expression and release of HMGB1 in lipopolysaccharide (LPS)-activated macrophages.	Magnesium Sulfate	48-65	high mobility group box 1	Homo sapiens	99-104
22487382-11	2013	RESULTS: We found that magnesium sulfate inhibited translocation of HMGB1 from the nucleus to the cytoplasm and its extracellular release in LPS-activated macrophages and also suppressed the expression of HMGB1 mRNA.	Magnesium Sulfate	23-40	high mobility group box 1	Homo sapiens	68-73
22487382-11	2013	RESULTS: We found that magnesium sulfate inhibited translocation of HMGB1 from the nucleus to the cytoplasm and its extracellular release in LPS-activated macrophages and also suppressed the expression of HMGB1 mRNA.	Magnesium Sulfate	23-40	high mobility group box 1	Homo sapiens	205-210
22487382-13	2013	CONCLUSIONS: Our study has demonstrated that magnesium sulfate inhibits the translocation of HMGB1 from the nucleus to the cytoplasm and the expression of HMGB1 mRNA in a dose-dependent manner.	Magnesium Sulfate	45-62	high mobility group box 1	Homo sapiens	93-98
22487382-13	2013	CONCLUSIONS: Our study has demonstrated that magnesium sulfate inhibits the translocation of HMGB1 from the nucleus to the cytoplasm and the expression of HMGB1 mRNA in a dose-dependent manner.	Magnesium Sulfate	45-62	high mobility group box 1	Homo sapiens	155-160
24302816-7	2013	Furthermore, both NF- kappa B inhibitor Bay11-7085 and p38 inhibitor SB203580 significantly suppressed the enhanced production of IL-6 and MMPs induced by HMGB1-LPS.	BAY 11-7085	40-50	high mobility group box 1	Homo sapiens	155-160
24302816-7	2013	Furthermore, both NF- kappa B inhibitor Bay11-7085 and p38 inhibitor SB203580 significantly suppressed the enhanced production of IL-6 and MMPs induced by HMGB1-LPS.	SB 203580	69-77	high mobility group box 1	Homo sapiens	155-160
23073660-4	2012	Reduced all-thiol-HMGB1 has sole chemokine activity, whereas disulfide-HMGB1 has only cytokine activity, and oxidized, denatured HMGB1 has neither.	Disulfides	61-70	high mobility group box 1	Homo sapiens	71-76
23073660-4	2012	Reduced all-thiol-HMGB1 has sole chemokine activity, whereas disulfide-HMGB1 has only cytokine activity, and oxidized, denatured HMGB1 has neither.	Disulfides	61-70	high mobility group box 1	Homo sapiens	71-76
23226786-0	2012	Atorvastatin reduces serum HMGB1 levels in patients with hyperlipidemia.	Atorvastatin	0-12	high mobility group box 1	Homo sapiens	27-32
23022229-0	2012	Tanshinone IIA sodium sulfonate facilitates endocytic HMGB1 uptake.	tanshinone II A sodium sulfonate	0-31	high mobility group box 1	Homo sapiens	54-59
23022229-2	2012	We previously reported that a major Danshen ingredient, tanshinone IIA sodium sulfonate (TSN-SS), selectively inhibited endotoxin-induced HMGB1 release and conferred protection against lethal endotoxemia and sepsis.	tanshinone II A sodium sulfonate	56-87	high mobility group box 1	Homo sapiens	138-143
23022229-2	2012	We previously reported that a major Danshen ingredient, tanshinone IIA sodium sulfonate (TSN-SS), selectively inhibited endotoxin-induced HMGB1 release and conferred protection against lethal endotoxemia and sepsis.	tanshinone II A sodium sulfonate	89-95	high mobility group box 1	Homo sapiens	138-143
23022229-3	2012	To investigate the underlying mechanisms by which TSN-SS effectively inhibits HMGB1 release, we examined whether TSN-SS stimulates HMGB1 uptake by macrophages and whether genetic depletion of HMGB1 receptors [e.g., toll-like receptors (TLR)2, TLR4, or the receptor for advanced glycation end product (RAGE)] or pharmacological inhibition of endocytosis impairs TSN-SS-facilitated HMGB1 cellular uptake.	tanshinone II A sodium sulfonate	50-56	high mobility group box 1	Homo sapiens	78-83
23022229-4	2012	TSN-SS stimulated internalization of exogenous HMGB1 protein into macrophage cytoplasmic vesicles that subsequently co-localized with microtubule-associated protein light chain 3 (LC3)-positive punctate structures (likely amphisomes).	trichostatin A	0-3	high mobility group box 1	Homo sapiens	47-52
23022229-8	2012	Taken together, these findings suggest that TSN-SS may facilitate HMGB1 endocytic uptake, and subsequently delivered it to LC3-positive vacuoles (possibly amphisomes) for degradation via a lysosome-dependent pathway.	tanshinone II A sodium sulfonate	44-50	high mobility group box 1	Homo sapiens	66-71
23226786-2	2012	This study investigated the effect of atorvastatin on serum HMGB1 levels in patients with hyperlipidemia.	Atorvastatin	38-50	high mobility group box 1	Homo sapiens	60-65
23226786-9	2012	Serum HMGB1 levels are increased in patients with hyperlipidemia which could be reduced by atorvastatin.	Atorvastatin	91-103	high mobility group box 1	Homo sapiens	6-11
22862965-5	2012	The number of CD34-positive cells was negatively correlated with the serum levels of glucose and hemoglobin A1c, whereas the HMGB-1-positive area was positively correlated with the levels of serum glucose.	Glucose	197-204	high mobility group box 1	Homo sapiens	125-131
22941653-2	2012	We show that HMGB1 alters the structure and stability of the canonical nucleosome (N) in a nonenzymatic, ATP-independent manner.	Adenosine Triphosphate	105-108	high mobility group box 1	Homo sapiens	13-18
23298486-0	2012	Ethyl pyruvate administration suppresses growth and invasion of gallbladder cancer cells via downregulation of HMGB1-RAGE axis.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	111-116
23298486-2	2012	Some studies have confirmed that Ethyl pyruvate (EP), a potent inhibitor of HMGB1, exerts the therapeutic effects on metastatic live tumor from gastric cancer.	ethyl pyruvate	33-47	high mobility group box 1	Homo sapiens	76-81
23298486-2	2012	Some studies have confirmed that Ethyl pyruvate (EP), a potent inhibitor of HMGB1, exerts the therapeutic effects on metastatic live tumor from gastric cancer.	ethyl pyruvate	49-51	high mobility group box 1	Homo sapiens	76-81
23019417-0	2012	Apicidin and docetaxel combination treatment drives CTCFL expression and HMGB1 release acting as potential antitumor immune response inducers in metastatic breast cancer cells.	apicidin	0-8	high mobility group box 1	Homo sapiens	73-78
22759395-5	2012	Ethyl pyruvate (EP) treatment blocked H(2)O(2) (oxidative stress)-induced HMGB1 release from human umbilical vein endothelial cells in vitro, and in vivo resulted in nuclear retention and significant blunting of HMGB1 release into the circulation after IRI.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	74-79
22759395-5	2012	Ethyl pyruvate (EP) treatment blocked H(2)O(2) (oxidative stress)-induced HMGB1 release from human umbilical vein endothelial cells in vitro, and in vivo resulted in nuclear retention and significant blunting of HMGB1 release into the circulation after IRI.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	212-217
22759395-5	2012	Ethyl pyruvate (EP) treatment blocked H(2)O(2) (oxidative stress)-induced HMGB1 release from human umbilical vein endothelial cells in vitro, and in vivo resulted in nuclear retention and significant blunting of HMGB1 release into the circulation after IRI.	ethyl pyruvate	16-18	high mobility group box 1	Homo sapiens	74-79
22759395-5	2012	Ethyl pyruvate (EP) treatment blocked H(2)O(2) (oxidative stress)-induced HMGB1 release from human umbilical vein endothelial cells in vitro, and in vivo resulted in nuclear retention and significant blunting of HMGB1 release into the circulation after IRI.	ethyl pyruvate	16-18	high mobility group box 1	Homo sapiens	212-217
22759395-5	2012	Ethyl pyruvate (EP) treatment blocked H(2)O(2) (oxidative stress)-induced HMGB1 release from human umbilical vein endothelial cells in vitro, and in vivo resulted in nuclear retention and significant blunting of HMGB1 release into the circulation after IRI.	Water	38-43	high mobility group box 1	Homo sapiens	74-79
22759395-5	2012	Ethyl pyruvate (EP) treatment blocked H(2)O(2) (oxidative stress)-induced HMGB1 release from human umbilical vein endothelial cells in vitro, and in vivo resulted in nuclear retention and significant blunting of HMGB1 release into the circulation after IRI.	Water	38-43	high mobility group box 1	Homo sapiens	212-217
22782142-0	2012	IGF-1 alleviates ox-LDL-induced inflammation via reducing HMGB1 release in HAECs.	ox-ldl	17-23	high mobility group box 1	Homo sapiens	58-63
22782142-13	2012	In conclusion, IGF-1 can alleviate ox-LDL-induced inflammation by reducing HMGB1 release, suggesting an unexpected beneficial role of IGF-1 in inflammatory disease.	ox-ldl	35-41	high mobility group box 1	Homo sapiens	75-80
23019417-0	2012	Apicidin and docetaxel combination treatment drives CTCFL expression and HMGB1 release acting as potential antitumor immune response inducers in metastatic breast cancer cells.	Docetaxel	13-22	high mobility group box 1	Homo sapiens	73-78
22931605-0	2012	[Hydrogen peroxide induces high mobility group box 1 release in human bronchial epithelial cells].	Hydrogen Peroxide	1-18	high mobility group box 1	Homo sapiens	27-60
22901013-4	2012	The binding affinities of the two individual DNA-binding domains of HMGB4 to DNA carrying a cisplatin 1,2-intrastrand d(GpG) cross-link are weaker than those of the DNA-binding domains of HMGB1.	Cisplatin	92-101	high mobility group box 1	Homo sapiens	188-193
22901013-6	2012	The residue Phe37 plays a critical role in stabilizing the binding complex of HMGB4 with the cisplatin-modified DNA, as it does for HMGB1.	Cisplatin	93-102	high mobility group box 1	Homo sapiens	132-137
22869893-5	2012	A nonoxidizable HMGB1 mutant in which serines replace all cysteines (3S-HMGB1) does not promote cytokine production, but is more effective than wild-type HMGB1 in recruiting leukocytes in vivo.	Cysteine	58-67	high mobility group box 1	Homo sapiens	72-77
22869893-5	2012	A nonoxidizable HMGB1 mutant in which serines replace all cysteines (3S-HMGB1) does not promote cytokine production, but is more effective than wild-type HMGB1 in recruiting leukocytes in vivo.	3s	69-71	high mobility group box 1	Homo sapiens	16-21
22869893-5	2012	A nonoxidizable HMGB1 mutant in which serines replace all cysteines (3S-HMGB1) does not promote cytokine production, but is more effective than wild-type HMGB1 in recruiting leukocytes in vivo.	3s	69-71	high mobility group box 1	Homo sapiens	72-77
22869893-5	2012	A nonoxidizable HMGB1 mutant in which serines replace all cysteines (3S-HMGB1) does not promote cytokine production, but is more effective than wild-type HMGB1 in recruiting leukocytes in vivo.	3s	69-71	high mobility group box 1	Homo sapiens	72-77
22869893-3	2012	Reduced cysteines make HMGB1 a chemoattractant, whereas a disulfide bond makes it a proinflammatory cytokine and further cysteine oxidation to sulfonates by reactive oxygen species abrogates both activities.	Cysteine	8-17	high mobility group box 1	Homo sapiens	23-28
22869893-3	2012	Reduced cysteines make HMGB1 a chemoattractant, whereas a disulfide bond makes it a proinflammatory cytokine and further cysteine oxidation to sulfonates by reactive oxygen species abrogates both activities.	Cysteine	8-16	high mobility group box 1	Homo sapiens	23-28
22869893-5	2012	A nonoxidizable HMGB1 mutant in which serines replace all cysteines (3S-HMGB1) does not promote cytokine production, but is more effective than wild-type HMGB1 in recruiting leukocytes in vivo.	Serine	38-45	high mobility group box 1	Homo sapiens	16-21
22869893-5	2012	A nonoxidizable HMGB1 mutant in which serines replace all cysteines (3S-HMGB1) does not promote cytokine production, but is more effective than wild-type HMGB1 in recruiting leukocytes in vivo.	Serine	38-45	high mobility group box 1	Homo sapiens	72-77
22869893-5	2012	A nonoxidizable HMGB1 mutant in which serines replace all cysteines (3S-HMGB1) does not promote cytokine production, but is more effective than wild-type HMGB1 in recruiting leukocytes in vivo.	Serine	38-45	high mobility group box 1	Homo sapiens	72-77
22869893-5	2012	A nonoxidizable HMGB1 mutant in which serines replace all cysteines (3S-HMGB1) does not promote cytokine production, but is more effective than wild-type HMGB1 in recruiting leukocytes in vivo.	Cysteine	58-67	high mobility group box 1	Homo sapiens	16-21
22869893-5	2012	A nonoxidizable HMGB1 mutant in which serines replace all cysteines (3S-HMGB1) does not promote cytokine production, but is more effective than wild-type HMGB1 in recruiting leukocytes in vivo.	Cysteine	58-67	high mobility group box 1	Homo sapiens	72-77
22931605-1	2012	OBJECTIVE: To investigate the effect of hydrogen dioxide (H(2)O(2)) on the release and translocation of high mobility group box 1 release (HMGB1) from normal human bronchiolar epithelial cells (HBE).	Hydrogen Peroxide	40-56	high mobility group box 1	Homo sapiens	104-137
22931605-1	2012	OBJECTIVE: To investigate the effect of hydrogen dioxide (H(2)O(2)) on the release and translocation of high mobility group box 1 release (HMGB1) from normal human bronchiolar epithelial cells (HBE).	Hydrogen Peroxide	40-56	high mobility group box 1	Homo sapiens	139-144
22931605-9	2012	CONCLUSION: H(2)O(2) can induce HMGB1 translocation and release in human bronchial epithelial cells, suggesting the involvement of HMGB1 in airway oxidative stress in chronic inflammatory diseases such as asthma and COPD.	Hydrogen Peroxide	12-20	high mobility group box 1	Homo sapiens	32-37
22931605-9	2012	CONCLUSION: H(2)O(2) can induce HMGB1 translocation and release in human bronchial epithelial cells, suggesting the involvement of HMGB1 in airway oxidative stress in chronic inflammatory diseases such as asthma and COPD.	Hydrogen Peroxide	12-20	high mobility group box 1	Homo sapiens	131-136
22549180-6	2012	Up-regulation of Mfn2 attenuated the suppressive effect of HMGB1 on CD4(+) T lymphocytes, which was associated with profound elevation of intracellular calcium concentration ([Ca(2+)](i)) and nuclear factor of activated T cells (NFAT) activity.	Calcium	152-159	high mobility group box 1	Homo sapiens	59-64
22750245-7	2012	The serine residues at S39, S53 and S181 of HMGB1 were related to enhancing HMGB1 secretion.	Serine	4-10	high mobility group box 1	Homo sapiens	44-49
22750245-7	2012	The serine residues at S39, S53 and S181 of HMGB1 were related to enhancing HMGB1 secretion.	Serine	4-10	high mobility group box 1	Homo sapiens	76-81
22750245-9	2012	Our findings suggest that PKC-zeta is involved in the phosphorylation of HMGB1, and the phosphorylation of specific serine residues in the nuclear localization signal regions is related to enhanced HMGB1 secretion in colon cancer cells.	Serine	116-122	high mobility group box 1	Homo sapiens	198-203
22634181-4	2012	In wild-type mice, recombinant human HMGB1 aggravated indomethacin-induced small intestinal damage; enhanced the mRNA expression levels of tumor necrosis factor alpha (TNF-alpha), monocyte chemotactic protein 1, and KC; activated nuclear factor kappa B; and stimulated phosphorylation of the mitogen-activated protein kinases p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK).	Indomethacin	54-66	high mobility group box 1	Homo sapiens	37-42
22617774-0	2012	HMGB1 was a pivotal synergistic effecor for CpG oligonucleotide to enhance the progression of human lung cancer cells.	effecor	32-39	high mobility group box 1	Homo sapiens	0-5
22617774-0	2012	HMGB1 was a pivotal synergistic effecor for CpG oligonucleotide to enhance the progression of human lung cancer cells.	Oligonucleotides	48-63	high mobility group box 1	Homo sapiens	0-5
22617774-5	2012	We further showed that blockade of extracellular HMGB1 using A box peptide and ethyl pyruvate significantly abrogated the CpG ODN enhanced progression of 95D cells.	ethyl pyruvate	79-93	high mobility group box 1	Homo sapiens	49-54
22504532-0	2012	Vascular barrier protective effects of phlorotannins on HMGB1-mediated proinflammatory responses in vitro and in vivo.	phlorotannins	39-52	high mobility group box 1	Homo sapiens	56-61
22655796-5	2012	Enforced expression of HMGB1-3 or HMGB4 by adenoviral-vector-mediated gene transfer resulted in significant inhibition of breast cancer cell proliferation through an LXCXE- or LXCXD-dependent mechanism and an increased radiosensitivity through an LXCXE- or LXCXD-independent mechanism.	lxcxe	166-171	high mobility group box 1	Homo sapiens	23-28
22655796-5	2012	Enforced expression of HMGB1-3 or HMGB4 by adenoviral-vector-mediated gene transfer resulted in significant inhibition of breast cancer cell proliferation through an LXCXE- or LXCXD-dependent mechanism and an increased radiosensitivity through an LXCXE- or LXCXD-independent mechanism.	lxcxd	176-181	high mobility group box 1	Homo sapiens	23-28
22655796-5	2012	Enforced expression of HMGB1-3 or HMGB4 by adenoviral-vector-mediated gene transfer resulted in significant inhibition of breast cancer cell proliferation through an LXCXE- or LXCXD-dependent mechanism and an increased radiosensitivity through an LXCXE- or LXCXD-independent mechanism.	lxcxe	247-252	high mobility group box 1	Homo sapiens	23-28
22655796-5	2012	Enforced expression of HMGB1-3 or HMGB4 by adenoviral-vector-mediated gene transfer resulted in significant inhibition of breast cancer cell proliferation through an LXCXE- or LXCXD-dependent mechanism and an increased radiosensitivity through an LXCXE- or LXCXD-independent mechanism.	lxcxd	257-262	high mobility group box 1	Homo sapiens	23-28
22429818-0	2012	Inhibitory effects of lycopene on HMGB1-mediated pro-inflammatory responses in both cellular and animal models.	Lycopene	22-30	high mobility group box 1	Homo sapiens	34-39
22429818-3	2012	The potential anti-inflammatory roles of lycopene in HMGB1-mediated proinflammatory responses in both primary human umbilical vein endothelial cells (HUVECs) and animal were investigated.	Lycopene	41-49	high mobility group box 1	Homo sapiens	53-58
22429818-6	2012	Lycopene inhibited lipopolysaccharide (LPS)-mediated release of HMGB1, expression of HMGB1-mediated tumor necrosis factor (TNF)-secretory phospholipase A2 (sPLA2)-IIA, and HMGB1-mediated pro-inflammatory signaling responses in endothelial cells.	Lycopene	0-8	high mobility group box 1	Homo sapiens	64-69
22429818-6	2012	Lycopene inhibited lipopolysaccharide (LPS)-mediated release of HMGB1, expression of HMGB1-mediated tumor necrosis factor (TNF)-secretory phospholipase A2 (sPLA2)-IIA, and HMGB1-mediated pro-inflammatory signaling responses in endothelial cells.	Lycopene	0-8	high mobility group box 1	Homo sapiens	85-90
22429818-6	2012	Lycopene inhibited lipopolysaccharide (LPS)-mediated release of HMGB1, expression of HMGB1-mediated tumor necrosis factor (TNF)-secretory phospholipase A2 (sPLA2)-IIA, and HMGB1-mediated pro-inflammatory signaling responses in endothelial cells.	Lycopene	0-8	high mobility group box 1	Homo sapiens	85-90
22429818-8	2012	These findings suggest that lycopene promotes barrier integrity, inhibits monocyte adhesion and migration to HMGB1 activating HUVECs by blocking activation of proinflammatory cytokines and expression of CAMs and HMGB1 receptors, thereby showing its usefulness as a therapy for vascular inflammatory diseases.	Lycopene	28-36	high mobility group box 1	Homo sapiens	109-114
22561332-0	2012	Barrier protective effects of withaferin A in HMGB1-induced inflammatory responses in both cellular and animal models.	withaferin A	30-42	high mobility group box 1	Homo sapiens	46-51
22561332-4	2012	We found that WFA inhibited lipopolysaccharide (LPS)-induced HMGB1 release and HMGB1-mediated barrier disruption, expression of cell adhesion molecules (CAMs) and adhesion/transendothelial migration of leukocytes to human endothelial cells.	withaferin A	14-17	high mobility group box 1	Homo sapiens	61-66
22561332-4	2012	We found that WFA inhibited lipopolysaccharide (LPS)-induced HMGB1 release and HMGB1-mediated barrier disruption, expression of cell adhesion molecules (CAMs) and adhesion/transendothelial migration of leukocytes to human endothelial cells.	withaferin A	14-17	high mobility group box 1	Homo sapiens	79-84
22561332-6	2012	Further studies revealed that WFA suppressed the production of interleukin 6, tumor necrosis factor-alpha (TNF-alpha) and activation of nuclear factor-kappaB (NF-kappaB) by HMGB1.	withaferin A	30-33	high mobility group box 1	Homo sapiens	173-178
22467309-8	2012	In activated HAEC, OSS amplified HMGB1-induced VCAM-1 (3-fold) and RAGE (1.6-fold) expression and proportionally enhanced monocyte adhesion to HAEC in a RAGE-dependent manner, while HSS mitigated these increases to the level of TNF-alpha alone.	OSS	19-22	high mobility group box 1	Homo sapiens	33-38
22467309-8	2012	In activated HAEC, OSS amplified HMGB1-induced VCAM-1 (3-fold) and RAGE (1.6-fold) expression and proportionally enhanced monocyte adhesion to HAEC in a RAGE-dependent manner, while HSS mitigated these increases to the level of TNF-alpha alone.	hepatic stimulator substance	182-185	high mobility group box 1	Homo sapiens	33-38
22429818-8	2012	These findings suggest that lycopene promotes barrier integrity, inhibits monocyte adhesion and migration to HMGB1 activating HUVECs by blocking activation of proinflammatory cytokines and expression of CAMs and HMGB1 receptors, thereby showing its usefulness as a therapy for vascular inflammatory diseases.	Lycopene	28-36	high mobility group box 1	Homo sapiens	212-217
22504532-3	2012	The protective activities of the phlorotannins were determined by measuring permeability, leukocyte adhesion and migration, and the activations of pro-inflammatory proteins in HMGB1-activated HUVECs.	phlorotannins	33-46	high mobility group box 1	Homo sapiens	176-181
22504532-4	2012	We found that the phlorotannins inhibited; lipopolysaccharide (LPS)-induced HMGB1 release, HMGB1-mediated barrier disruption, the expressions of cell adhesion molecules (CAMs), and the adhesion/transendothelial migration of leukocytes to human endothelial cells.	phlorotannins	18-31	high mobility group box 1	Homo sapiens	76-81
22504532-4	2012	We found that the phlorotannins inhibited; lipopolysaccharide (LPS)-induced HMGB1 release, HMGB1-mediated barrier disruption, the expressions of cell adhesion molecules (CAMs), and the adhesion/transendothelial migration of leukocytes to human endothelial cells.	phlorotannins	18-31	high mobility group box 1	Homo sapiens	91-96
22475723-8	2012	Further bioinformatic analysis shows that proteins modulated by curcumin are implicated in protein folding (such as heat-shock protein PPP2R1A; RNA splicing proteins RBM17, DDX39; cell death proteins HMGB1 and NPM1; proteins involved in androgen receptor signaling, NPM1 and FKBP4/FKBP52), and that this compound could have an impact on miR-141, miR-152, and miR-183 expression.	Curcumin	64-72	high mobility group box 1	Homo sapiens	200-205
21932058-2	2012	The study was tested in a fecal peritonitis-induced septic shock model, we observed that levosimendan combined with arginine vasopressin supplemented with norepinephrine therapy resulted in lower mean pulmonary artery pressure, lactate concentrations, arterial total nitrate/nitrite, and high-mobility group box 1 levels; decreased lung wet/dry ratio, and pulmonary levels of interleukin-6, total histological scores, and improved pulmonary gas exchange when compared with norepinephrine group.	Simendan	89-101	high mobility group box 1	Homo sapiens	288-313
21932058-2	2012	The study was tested in a fecal peritonitis-induced septic shock model, we observed that levosimendan combined with arginine vasopressin supplemented with norepinephrine therapy resulted in lower mean pulmonary artery pressure, lactate concentrations, arterial total nitrate/nitrite, and high-mobility group box 1 levels; decreased lung wet/dry ratio, and pulmonary levels of interleukin-6, total histological scores, and improved pulmonary gas exchange when compared with norepinephrine group.	Norepinephrine	155-169	high mobility group box 1	Homo sapiens	288-313
22394598-4	2012	In vitro and in vivo, HMGB-1 inhibition achieved by glycyrrhizin treatment led to a drastic reduction in ALK(+) cell invasiveness.	Glycyrrhizic Acid	52-64	high mobility group box 1	Homo sapiens	22-28
22521432-5	2012	Furthermore, HMGB1 increased the production of intracellular reactive oxygen species (ROS).	Reactive Oxygen Species	61-84	high mobility group box 1	Homo sapiens	13-18
22521432-5	2012	Furthermore, HMGB1 increased the production of intracellular reactive oxygen species (ROS).	Reactive Oxygen Species	86-89	high mobility group box 1	Homo sapiens	13-18
22521432-7	2012	Taken together, our results suggest that HMGB1 induces MUC8 expression in a JNK and PI3K/Akt signaling pathway-dependent manner but that HMGB1 acts in an ROS-independent manner.	Reactive Oxygen Species	154-157	high mobility group box 1	Homo sapiens	137-142
22593488-6	2012	HMGB1 levels were found to be considerably lower in EDTA plasma as compared to serum samples.	Edetic Acid	52-56	high mobility group box 1	Homo sapiens	0-5
22204001-0	2012	Poly(ADP-ribosyl)ation of high mobility group box 1 (HMGB1) protein enhances inhibition of efferocytosis.	poly(adp-ribosyl)	0-17	high mobility group box 1	Homo sapiens	26-51
22204001-0	2012	Poly(ADP-ribosyl)ation of high mobility group box 1 (HMGB1) protein enhances inhibition of efferocytosis.	poly(adp-ribosyl)	0-17	high mobility group box 1	Homo sapiens	53-58
22386814-0	2012	Anti-inflammatory activities of oleanolic acid on HMGB1 activated HUVECs.	Oleanolic Acid	32-46	high mobility group box 1	Homo sapiens	50-55
22386814-3	2012	Oleanolic acid (OA), a triterpenoid known for its anti-inflammatory and anti-cancer properties, is commonly present in several medicinal plants but the effects of OA on HMGB1-mediated pro-inflammatory responses of human endothelial cells is not well-studied.	Oleanolic Acid	0-14	high mobility group box 1	Homo sapiens	169-174
22266604-0	2012	Molecular forms of HMGB1 and keratin-18 as mechanistic biomarkers for mode of cell death and prognosis during clinical acetaminophen hepatotoxicity.	Acetaminophen	119-132	high mobility group box 1	Homo sapiens	19-24
22266604-4	2012	METHODS: HMGB1 (total, acetylated) and K18 (apoptotic, necrotic) were identified and quantified by novel LC-MS/MS assays in APAP overdose patients (n=78).	Acetaminophen	124-128	high mobility group box 1	Homo sapiens	9-14
22366983-10	2012	The present study showed that patients who received sivelestat had reduced release of HMGB1, and that IL-6 levels decreased more rapidly in patients treated with sivelestat than in those who received the placebo.	sivelestat	52-62	high mobility group box 1	Homo sapiens	86-91
22246223-0	2012	Inhibitory effects of ethyl pyruvate administration on human gastric             cancer growth via regulation of the HMGB1-RAGE and Akt pathways in vitro and in             vivo.	ethyl pyruvate	22-36	high mobility group box 1	Homo sapiens	117-122
22246223-2	2012	Ethyl pyruvate (EP), a potent inhibitor             of HMGB1 release, can exert antitumor effects on the growth of gastric cancer.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	55-60
22246223-2	2012	Ethyl pyruvate (EP), a potent inhibitor             of HMGB1 release, can exert antitumor effects on the growth of gastric cancer.	ethyl pyruvate	16-18	high mobility group box 1	Homo sapiens	55-60
22246807-0	2012	Heat shock transcription factor 1 inhibits H2O2-induced cardiomyocyte death through suppression of high-mobility group box 1.	Hydrogen Peroxide	43-47	high mobility group box 1	Homo sapiens	99-124
22248244-8	2012	CONCLUSION: Serum HMGB1 levels are increased in pSS patients and more specifically in patients with SSA autoantibodies.	pss	48-51	high mobility group box 1	Homo sapiens	18-23
22178603-0	2012	Inhibitory effects of kaempferol-3-O-sophoroside on HMGB1-mediated proinflammatory responses.	kaempferol 3-O-sophoroside	22-48	high mobility group box 1	Homo sapiens	52-57
22189943-2	2012	UA, which is significantly increased in the circulation following renal ischemia-reperfusion injury (IRI), was used both in vitro and in vivo as an early response-signaling molecule to determine its ability to induce the secretion of HMGB1 from endothelial cells.	Uric Acid	0-2	high mobility group box 1	Homo sapiens	234-239
22189943-4	2012	Treatment of HUVEC with UA and a calcium mobilization inhibitor (TMB-8) or a MEK/Erk pathway inhibitor (U0126) prevented translocation of HMGB1 from the nucleus, resulting in reduced cytoplasmic and circulating levels of HMGB1.	Uric Acid	24-26	high mobility group box 1	Homo sapiens	138-143
22189943-4	2012	Treatment of HUVEC with UA and a calcium mobilization inhibitor (TMB-8) or a MEK/Erk pathway inhibitor (U0126) prevented translocation of HMGB1 from the nucleus, resulting in reduced cytoplasmic and circulating levels of HMGB1.	Uric Acid	24-26	high mobility group box 1	Homo sapiens	221-226
22189943-4	2012	Treatment of HUVEC with UA and a calcium mobilization inhibitor (TMB-8) or a MEK/Erk pathway inhibitor (U0126) prevented translocation of HMGB1 from the nucleus, resulting in reduced cytoplasmic and circulating levels of HMGB1.	Calcium	33-40	high mobility group box 1	Homo sapiens	138-143
22189943-4	2012	Treatment of HUVEC with UA and a calcium mobilization inhibitor (TMB-8) or a MEK/Erk pathway inhibitor (U0126) prevented translocation of HMGB1 from the nucleus, resulting in reduced cytoplasmic and circulating levels of HMGB1.	8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate	65-70	high mobility group box 1	Homo sapiens	138-143
22189943-4	2012	Treatment of HUVEC with UA and a calcium mobilization inhibitor (TMB-8) or a MEK/Erk pathway inhibitor (U0126) prevented translocation of HMGB1 from the nucleus, resulting in reduced cytoplasmic and circulating levels of HMGB1.	8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate	65-70	high mobility group box 1	Homo sapiens	221-226
22189943-4	2012	Treatment of HUVEC with UA and a calcium mobilization inhibitor (TMB-8) or a MEK/Erk pathway inhibitor (U0126) prevented translocation of HMGB1 from the nucleus, resulting in reduced cytoplasmic and circulating levels of HMGB1.	U 0126	104-109	high mobility group box 1	Homo sapiens	138-143
22189943-4	2012	Treatment of HUVEC with UA and a calcium mobilization inhibitor (TMB-8) or a MEK/Erk pathway inhibitor (U0126) prevented translocation of HMGB1 from the nucleus, resulting in reduced cytoplasmic and circulating levels of HMGB1.	U 0126	104-109	high mobility group box 1	Homo sapiens	221-226
22189943-7	2012	In summary, UA after IRI mediates the acetylation and release of HMGB1 from endothelial cells by mechanisms that involve calcium mobilization, the MEK/Erk pathway, and activation of TLR4.	Calcium	121-128	high mobility group box 1	Homo sapiens	65-70
21743489-0	2012	NAC1 modulates sensitivity of ovarian cancer cells to cisplatin by altering the HMGB1-mediated autophagic response.	Cisplatin	54-63	high mobility group box 1	Homo sapiens	80-85
22047946-5	2012	Peripheral whole blood samples obtained immediately after admission were determined for HMGB1 production in response to ex vivo lipopolysaccharide (LPS) stimulation.	ex vivo lipopolysaccharide	120-146	high mobility group box 1	Homo sapiens	88-93
22065079-8	2012	Asbestos induces cell necrosis, causing the release of HMGB1, which in turn may activate Nalp3 inflammasome, a process that is enhanced by asbestos-induced production of reactive oxygen species.	Asbestos	0-8	high mobility group box 1	Homo sapiens	55-60
22363140-0	2012	Glycyrrhizin attenuates HMGB1-induced hepatocyte apoptosis by inhibiting the p38-dependent mitochondrial pathway.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	24-29
22363140-5	2012	It is also tried to identify hepatocyte apoptosis affected by the HMGB1 inhibitor, GL.	Glycyrrhizic Acid	83-85	high mobility group box 1	Homo sapiens	66-71
22363140-9	2012	HMGB1-induced caspase 3 activation was significantly attenuated by the p38 inhibitor SB203580.	SB 203580	85-93	high mobility group box 1	Homo sapiens	0-5
22363140-10	2012	GL significantly attenuated HMGB1-induced hepatocyte apoptosis.	Glycyrrhizic Acid	0-2	high mobility group box 1	Homo sapiens	28-33
22363140-11	2012	GL also prevented HMGB1-induced cytochrome c release and p38 activation in Huh-BAT cells.	Glycyrrhizic Acid	0-2	high mobility group box 1	Homo sapiens	18-23
22363140-13	2012	In addition, GL had an anti-apoptotic effect on HMGB1-treated hepatocytes.	Glycyrrhizic Acid	13-15	high mobility group box 1	Homo sapiens	48-53
22065079-8	2012	Asbestos induces cell necrosis, causing the release of HMGB1, which in turn may activate Nalp3 inflammasome, a process that is enhanced by asbestos-induced production of reactive oxygen species.	Asbestos	139-147	high mobility group box 1	Homo sapiens	55-60
22065079-8	2012	Asbestos induces cell necrosis, causing the release of HMGB1, which in turn may activate Nalp3 inflammasome, a process that is enhanced by asbestos-induced production of reactive oxygen species.	Reactive Oxygen Species	170-193	high mobility group box 1	Homo sapiens	55-60
22293756-3	2012	The activity of HMGB1 varies with the redox states of the cysteine residues, which are required for binding to TLR4.	Cysteine	58-66	high mobility group box 1	Homo sapiens	16-21
21864037-5	2012	While the use of autophagy inhibitor, 3-methyladenine (3-MA), blocked the autophagic reaction and increased leukemia cell sensitivity to chemotherapy, enhancing HMGB1 expression decreased this sensitivity.	3-methyladenine	38-53	high mobility group box 1	Homo sapiens	161-166
21494799-4	2012	We found that HMGB1 increased human umbilical vein endothelial cell permeability to FITC-dextran 40 kDa in a time- and concentration-dependent manner.	fluorescein isothiocyanate dextran	84-96	high mobility group box 1	Homo sapiens	14-19
22085682-0	2012	Tricin 7-glucoside protects against experimental cerebral ischemia by reduction of NF-kappaB and HMGB1 expression.	Tricin 7-glucoside	0-18	high mobility group box 1	Homo sapiens	97-102
22277195-9	2012	Treatment with DT attenuated the expression of TLR2, TLR4, IRAK1 and Hmgb1, all genes involved in the TLR-mediated signaling pathway associated with classical microglia activation.	3,6'-dithiothalidomide	15-17	high mobility group box 1	Homo sapiens	69-74
22085682-5	2012	For in vivo experiment, rats were subjected to middle cerebral artery occlusion (MACO) for 1h, then followed by reperfusion for 23 h. Treatment of SH-SY5Y cells with Tricin 7-glucoside reduced the OGD-induced apoptosis and cytotoxicity, blocked TNF-alpha-induced NF-kappaB and IkappaB-alpha phosphorylation, and decreased HMGB1 expression.	Tricin 7-glucoside	166-184	high mobility group box 1	Homo sapiens	322-327
22085682-8	2012	Tricin 7-glucoside 100mg/kg attenuated histopathological damage, decreased brain edema, inhibited NF-kappaB activation and reduced HMGB1 expression.	Tricin 7-glucoside	0-18	high mobility group box 1	Homo sapiens	131-136
22085682-9	2012	These data show that Tricin 7-glucoside protects brain against I/R injury with a favorable therapeutic time-window by alleviating cerebral I/R injury and attenuating blood-brain barrier (BBB) breakdown, and its protective effects may involve HMGB1 and NF-kappaB signaling pathway.	Tricin 7-glucoside	21-39	high mobility group box 1	Homo sapiens	242-247
21861984-8	2012	IL-1beta promotes HMGB1 production in human gingival epithelial cells in a nitric oxide-dependent manner.	Nitric Oxide	75-87	high mobility group box 1	Homo sapiens	18-23
22068710-6	2012	The effect of sodium reduction in: (i) Normotensives: Caucasians: systolic BP (SBP) -1.27 mm Hg (95% confidence interval (CI): -1.88, -0.66; P = 0.0001), diastolic BP (DBP) -0.05 mm Hg (95% CI: -0.51, 0.42; P = 0.85).	Sodium	14-20	high mobility group box 1	Homo sapiens	66-86
21760473-9	2012	However, the decreases in UAE, serum HMGB1 and serum IL-6 were significantly greater in the telmisartan group than in the enalapril group at 6 months (P &lt; 0.05, P &lt; 0.01 and P &lt; 0.01, respectively) and 12 months (all, P &lt; 0.05).	Telmisartan	92-103	high mobility group box 1	Homo sapiens	37-42
22108005-0	2012	Autophagy-mediated HMGB1 release antagonizes apoptosis of gastric cancer cells induced by vincristine via transcriptional regulation of Mcl-1.	Vincristine	90-101	high mobility group box 1	Homo sapiens	19-24
22799333-4	2012	HMGB1 was also found significantly enhanced the activity of ATP to induce IL-1beta and IL-18 by the induction of increased expression of pro-IL-1beta and pro-IL-18.	Adenosine Triphosphate	60-63	high mobility group box 1	Homo sapiens	0-5
22108005-3	2012	We show in this study that HMGB1 released into the extracellular space protects gastric cancer cells from apoptosis induced by the microtubule-targeting drug vincristine through transcriptional upregulation of Mcl-1.	Vincristine	158-169	high mobility group box 1	Homo sapiens	27-32
22108005-9	2012	Taken together, these results identify HMGB1-mediated upregulation of Mcl-1 transcription as an important mechanism by which autophagy protects gastric cancer cells from apoptosis induced by vincristine.	Vincristine	191-202	high mobility group box 1	Homo sapiens	39-44
22038506-3	2012	METHODS: We synthesized three specific small interfering RNAs of HMGB1 (HMGB1-siRNAs) and transfected these into HCCLM3 cells by use of Lipofectamine 2000.	Lipofectamine	136-154	high mobility group box 1	Homo sapiens	65-70
23275711-0	2012	Structural insight into the ligand-receptor interaction between glycyrrhetinic acid (GA) and the high-mobility group protein B1 (HMGB1)-DNA complex.	Glycyrrhetinic Acid	64-83	high mobility group box 1	Homo sapiens	97-127
23275711-0	2012	Structural insight into the ligand-receptor interaction between glycyrrhetinic acid (GA) and the high-mobility group protein B1 (HMGB1)-DNA complex.	Glycyrrhetinic Acid	64-83	high mobility group box 1	Homo sapiens	129-134
23275711-0	2012	Structural insight into the ligand-receptor interaction between glycyrrhetinic acid (GA) and the high-mobility group protein B1 (HMGB1)-DNA complex.	Glycyrrhetinic Acid	85-87	high mobility group box 1	Homo sapiens	97-127
23275711-0	2012	Structural insight into the ligand-receptor interaction between glycyrrhetinic acid (GA) and the high-mobility group protein B1 (HMGB1)-DNA complex.	Glycyrrhetinic Acid	85-87	high mobility group box 1	Homo sapiens	129-134
23275711-1	2012	UNLABELLED: Structural analysis of the high-mobility group protein B1 (HMGB1)-DNA complex and a docking simulation between glycyrrhetinic acid (GA) and the HMGB1-DNA complex were performed with a software package the Molecular Operating Environment (MOE).	Glycyrrhetinic Acid	123-142	high mobility group box 1	Homo sapiens	156-161
23275711-1	2012	UNLABELLED: Structural analysis of the high-mobility group protein B1 (HMGB1)-DNA complex and a docking simulation between glycyrrhetinic acid (GA) and the HMGB1-DNA complex were performed with a software package the Molecular Operating Environment (MOE).	Glycyrrhetinic Acid	144-146	high mobility group box 1	Homo sapiens	156-161
23275711-4	2012	The docking simulation revealed that GA possibly inhibits functions of HMGB1 interfering with Lys(90), Arg(91), Ser(101), Tyr(149), C(230) and C(231) in the HMGB1-DNA complex.	Glycyrrhetinic Acid	37-39	high mobility group box 1	Homo sapiens	71-76
23275711-4	2012	The docking simulation revealed that GA possibly inhibits functions of HMGB1 interfering with Lys(90), Arg(91), Ser(101), Tyr(149), C(230) and C(231) in the HMGB1-DNA complex.	Glycyrrhetinic Acid	37-39	high mobility group box 1	Homo sapiens	157-162
23275711-4	2012	The docking simulation revealed that GA possibly inhibits functions of HMGB1 interfering with Lys(90), Arg(91), Ser(101), Tyr(149), C(230) and C(231) in the HMGB1-DNA complex.	Lysine	94-97	high mobility group box 1	Homo sapiens	71-76
23275711-4	2012	The docking simulation revealed that GA possibly inhibits functions of HMGB1 interfering with Lys(90), Arg(91), Ser(101), Tyr(149), C(230) and C(231) in the HMGB1-DNA complex.	Lysine	94-97	high mobility group box 1	Homo sapiens	157-162
23275711-4	2012	The docking simulation revealed that GA possibly inhibits functions of HMGB1 interfering with Lys(90), Arg(91), Ser(101), Tyr(149), C(230) and C(231) in the HMGB1-DNA complex.	Arginine	103-106	high mobility group box 1	Homo sapiens	71-76
23275711-4	2012	The docking simulation revealed that GA possibly inhibits functions of HMGB1 interfering with Lys(90), Arg(91), Ser(101), Tyr(149), C(230) and C(231) in the HMGB1-DNA complex.	Arginine	103-106	high mobility group box 1	Homo sapiens	157-162
23275711-4	2012	The docking simulation revealed that GA possibly inhibits functions of HMGB1 interfering with Lys(90), Arg(91), Ser(101), Tyr(149), C(230) and C(231) in the HMGB1-DNA complex.	Serine	112-115	high mobility group box 1	Homo sapiens	71-76
23275711-4	2012	The docking simulation revealed that GA possibly inhibits functions of HMGB1 interfering with Lys(90), Arg(91), Ser(101), Tyr(149), C(230) and C(231) in the HMGB1-DNA complex.	Serine	112-115	high mobility group box 1	Homo sapiens	157-162
23275711-4	2012	The docking simulation revealed that GA possibly inhibits functions of HMGB1 interfering with Lys(90), Arg(91), Ser(101), Tyr(149), C(230) and C(231) in the HMGB1-DNA complex.	Tyrosine	122-125	high mobility group box 1	Homo sapiens	71-76
23275711-4	2012	The docking simulation revealed that GA possibly inhibits functions of HMGB1 interfering with Lys(90), Arg(91), Ser(101), Tyr(149), C(230) and C(231) in the HMGB1-DNA complex.	Tyrosine	122-125	high mobility group box 1	Homo sapiens	157-162
22102692-4	2012	Anticancer agents including doxorubicin, cisplatin, and methotrexate each induced HMGB1 upregulation in human osteosarcoma cells, and RNA interference-mediated knockdown of HMGB1 restored the chemosensitivity of osteosarcoma cells in vivo and in vitro.	Doxorubicin	28-39	high mobility group box 1	Homo sapiens	82-87
22102692-4	2012	Anticancer agents including doxorubicin, cisplatin, and methotrexate each induced HMGB1 upregulation in human osteosarcoma cells, and RNA interference-mediated knockdown of HMGB1 restored the chemosensitivity of osteosarcoma cells in vivo and in vitro.	Doxorubicin	28-39	high mobility group box 1	Homo sapiens	173-178
22102692-4	2012	Anticancer agents including doxorubicin, cisplatin, and methotrexate each induced HMGB1 upregulation in human osteosarcoma cells, and RNA interference-mediated knockdown of HMGB1 restored the chemosensitivity of osteosarcoma cells in vivo and in vitro.	Cisplatin	41-50	high mobility group box 1	Homo sapiens	82-87
22102692-4	2012	Anticancer agents including doxorubicin, cisplatin, and methotrexate each induced HMGB1 upregulation in human osteosarcoma cells, and RNA interference-mediated knockdown of HMGB1 restored the chemosensitivity of osteosarcoma cells in vivo and in vitro.	Cisplatin	41-50	high mobility group box 1	Homo sapiens	173-178
22102692-4	2012	Anticancer agents including doxorubicin, cisplatin, and methotrexate each induced HMGB1 upregulation in human osteosarcoma cells, and RNA interference-mediated knockdown of HMGB1 restored the chemosensitivity of osteosarcoma cells in vivo and in vitro.	Methotrexate	56-68	high mobility group box 1	Homo sapiens	82-87
22102692-4	2012	Anticancer agents including doxorubicin, cisplatin, and methotrexate each induced HMGB1 upregulation in human osteosarcoma cells, and RNA interference-mediated knockdown of HMGB1 restored the chemosensitivity of osteosarcoma cells in vivo and in vitro.	Methotrexate	56-68	high mobility group box 1	Homo sapiens	173-178
21967802-7	2012	Inhibition of HMGB1 with glycyrrhizin increased the pro-inflammatory response, increasing cell death and up regulating chemokine and TLR4 mRNA expression.	Glycyrrhizic Acid	25-37	high mobility group box 1	Homo sapiens	14-19
21953494-9	2012	Furthermore, HMGB1 silencing sensitized cells to apoptosis that was induced by oxaliplatin and mediated by the caspase-3 pathway.	Oxaliplatin	79-90	high mobility group box 1	Homo sapiens	13-18
22038506-9	2012	MTT assay demonstrated that the growth of cells transfected with HMGB1-siRNA-1 was significantly lower than that of control cells (P &lt; 0.01).	monooxyethylene trimethylolpropane tristearate	0-3	high mobility group box 1	Homo sapiens	65-70
22038506-11	2012	FCM revealed that apoptosis was significantly increased in HMGB1-siRNA-1-transfected cells compared with control cells (P &lt; 0.01).	Fosfomycin	0-3	high mobility group box 1	Homo sapiens	59-64
21944908-13	2012	Inhibition of autophagy with 3MA or chloroquine abrogated tube formation, whereas its induction with rapamycin enhanced tubing and promoted HMGB1 translocation.	Sirolimus	101-110	high mobility group box 1	Homo sapiens	140-145
22082188-2	2012	In this study, we stimulated primary keratinocytes with the TLR3-ligand polyI:C. This induced a toxic effect shown by up-regulation of the alarmin high-mobility group protein B1 and reduced responses in a MTT-assay.	Poly I	72-77	high mobility group box 1	Homo sapiens	147-177
21947243-6	2012	(2)HMGB1 incubation induced ERK1/2 activation in a time- and dose-dependent manner, which could be completely blocked by U0126 (MEK1/2 inhibitor) and partially reversed by RAGE knockdown.	U 0126	121-126	high mobility group box 1	Homo sapiens	3-8
22514737-4	2012	We hypothesized that oxidation of HMGB1 may reduce its pro-inflammatory potential and could take place during prolonged ischemia and upon reperfusion.Liver grafts were cold preserved for 24 h and flushed with saline in hourly intervals to collect the effluent.	Sodium Chloride	209-215	high mobility group box 1	Homo sapiens	34-39
25215057-7	2012	Anti-HMGB1 treatment, such as anti-HMGB1 polyclonal or monoclonal antibodies, inhibitors (e.g., ethyl pyruvate) and antagonists (e.g., A box), can protect against sepsis lethality and give a wider window for the treatment opportunity.	ethyl pyruvate	96-110	high mobility group box 1	Homo sapiens	5-10
22607100-7	2012	After 10-h treatment with CPFA, the MAP and oxygen index (PaO(2)/FiO(2)) were significantly higher than those at 0 h. Furthermore, the serum levels of HMGB-1, ICAM-1, and TNF-alpha decreased after 10 h of CPFA (p &lt; 0.05), while the serum levels of HMGB-1 declined at 5 h of HVHF, but rebounded at 10 h, and the serum levels of TNF-alpha and ICAM-1 were no significant change after treatment with HVHF.	cpfa	26-30	high mobility group box 1	Homo sapiens	251-257
22607100-7	2012	After 10-h treatment with CPFA, the MAP and oxygen index (PaO(2)/FiO(2)) were significantly higher than those at 0 h. Furthermore, the serum levels of HMGB-1, ICAM-1, and TNF-alpha decreased after 10 h of CPFA (p &lt; 0.05), while the serum levels of HMGB-1 declined at 5 h of HVHF, but rebounded at 10 h, and the serum levels of TNF-alpha and ICAM-1 were no significant change after treatment with HVHF.	cpfa	205-209	high mobility group box 1	Homo sapiens	151-157
22607100-7	2012	After 10-h treatment with CPFA, the MAP and oxygen index (PaO(2)/FiO(2)) were significantly higher than those at 0 h. Furthermore, the serum levels of HMGB-1, ICAM-1, and TNF-alpha decreased after 10 h of CPFA (p &lt; 0.05), while the serum levels of HMGB-1 declined at 5 h of HVHF, but rebounded at 10 h, and the serum levels of TNF-alpha and ICAM-1 were no significant change after treatment with HVHF.	hvhf	277-281	high mobility group box 1	Homo sapiens	151-157
22607100-7	2012	After 10-h treatment with CPFA, the MAP and oxygen index (PaO(2)/FiO(2)) were significantly higher than those at 0 h. Furthermore, the serum levels of HMGB-1, ICAM-1, and TNF-alpha decreased after 10 h of CPFA (p &lt; 0.05), while the serum levels of HMGB-1 declined at 5 h of HVHF, but rebounded at 10 h, and the serum levels of TNF-alpha and ICAM-1 were no significant change after treatment with HVHF.	hvhf	399-403	high mobility group box 1	Homo sapiens	151-157
22607100-7	2012	After 10-h treatment with CPFA, the MAP and oxygen index (PaO(2)/FiO(2)) were significantly higher than those at 0 h. Furthermore, the serum levels of HMGB-1, ICAM-1, and TNF-alpha decreased after 10 h of CPFA (p &lt; 0.05), while the serum levels of HMGB-1 declined at 5 h of HVHF, but rebounded at 10 h, and the serum levels of TNF-alpha and ICAM-1 were no significant change after treatment with HVHF.	cpfa	26-30	high mobility group box 1	Homo sapiens	151-157
25215057-7	2012	Anti-HMGB1 treatment, such as anti-HMGB1 polyclonal or monoclonal antibodies, inhibitors (e.g., ethyl pyruvate) and antagonists (e.g., A box), can protect against sepsis lethality and give a wider window for the treatment opportunity.	ethyl pyruvate	96-110	high mobility group box 1	Homo sapiens	35-40
22113336-4	2011	The data revealed that, in the atherosclerotic animal model, the protein HMGB1 and its gene expression were increased and that fluvastatin treatment significantly reduced the release of HMGB1 into the extracellular space.	Fluvastatin	127-138	high mobility group box 1	Homo sapiens	186-191
21922289-0	2011	Vascular anti-inflammatory effects of curcumin on HMGB1-mediated responses in vitro.	Curcumin	38-46	high mobility group box 1	Homo sapiens	50-55
22014880-6	2011	MAIN OUTCOME MEASURE(S): TLR4 in the immortalized progesterone receptor-expressing human endometrial epithelial cell line, EM-PR, was activated with lipopolysaccharide and high-mobility group box 1 (LPS/HMGB1) in the presence or absence of the synthetic progestin dienogest or endogenous progesterone.	dienogest	264-273	high mobility group box 1	Homo sapiens	172-197
22014880-6	2011	MAIN OUTCOME MEASURE(S): TLR4 in the immortalized progesterone receptor-expressing human endometrial epithelial cell line, EM-PR, was activated with lipopolysaccharide and high-mobility group box 1 (LPS/HMGB1) in the presence or absence of the synthetic progestin dienogest or endogenous progesterone.	Progesterone	50-62	high mobility group box 1	Homo sapiens	172-197
22014880-6	2011	MAIN OUTCOME MEASURE(S): TLR4 in the immortalized progesterone receptor-expressing human endometrial epithelial cell line, EM-PR, was activated with lipopolysaccharide and high-mobility group box 1 (LPS/HMGB1) in the presence or absence of the synthetic progestin dienogest or endogenous progesterone.	Progesterone	50-62	high mobility group box 1	Homo sapiens	203-208
21922289-4	2011	However, the effects of curcumin on HMGB1-mediated proinflammatory responses have not been studied.	Curcumin	24-32	high mobility group box 1	Homo sapiens	36-41
21922289-5	2011	METHODS: The anti-inflammatory activities of curcumin were determined by measuring solute flux, leukocyte adhesion and migration and activation of proinflammatory proteins in HMGB1-activated human umbilical vein endothelial cells.	Curcumin	45-53	high mobility group box 1	Homo sapiens	175-180
21922289-6	2011	RESULTS: Curcumin inhibited the release of HMGB1 by lipopolysaccharide (LPS)- and HMGB1-mediated barrier disruption, neutrophil adhesion and migration, and expression of cell adhesion molecules.	Curcumin	9-17	high mobility group box 1	Homo sapiens	43-48
21922289-6	2011	RESULTS: Curcumin inhibited the release of HMGB1 by lipopolysaccharide (LPS)- and HMGB1-mediated barrier disruption, neutrophil adhesion and migration, and expression of cell adhesion molecules.	Curcumin	9-17	high mobility group box 1	Homo sapiens	82-87
21922289-7	2011	Further studies revealed that curcumin down-regulated the cell surface receptor of HMGB1 in human endothelial cells.	Curcumin	30-38	high mobility group box 1	Homo sapiens	83-88
21922289-8	2011	CONCLUSION: These findings suggest that curcumin exerts anti-inflammatory effects in HMGB1-mediated proinflammatory responses, endorsing its usefulness as therapy for vascular inflammatory diseases.	Curcumin	40-48	high mobility group box 1	Homo sapiens	85-90
21273029-3	2011	We investigated here the effects of endotoxin removal by polymyxin B-immobilized polystyrene fiber (PMX-F) treatment on circulating levels of HMGB1, soluble RAGE (sRAGE), and interleukin-6 (IL-6) in septic shock patients.	Polystyrenes	81-92	high mobility group box 1	Homo sapiens	142-147
21273029-3	2011	We investigated here the effects of endotoxin removal by polymyxin B-immobilized polystyrene fiber (PMX-F) treatment on circulating levels of HMGB1, soluble RAGE (sRAGE), and interleukin-6 (IL-6) in septic shock patients.	pmx-f	100-105	high mobility group box 1	Homo sapiens	142-147
21273029-9	2011	The changes in endotoxin obtained by PMX-F treatment were correlated with those in HMGB1, sRAGE, and IL-6.	pmx-f	37-42	high mobility group box 1	Homo sapiens	83-88
22071811-6	2011	MAIN RESULTS: A total of 167 studies were included in this 2011 update.The effect of sodium reduction in normotensive Caucasians was SBP -1.27 mmHg (95% CI: -1.88, -0.66; p=0.0001), DBP -0.05 mmHg (95% CI: -0.51, 0.42; p=0.85).	Sodium	85-91	high mobility group box 1	Homo sapiens	133-139
21273029-11	2011	CONCLUSIONS: Our present study suggests that PMX-F treatment could block the HMGB1-RAGE axis in patients with septic shock via removal of endotoxin-induced inflammatory reactions.	pmx-f	45-50	high mobility group box 1	Homo sapiens	77-82
22169720-4	2011	The molecular weight and identity of HMGB1 was confirmed by SDS-PAGE and Western blot.	Sodium Dodecyl Sulfate	60-63	high mobility group box 1	Homo sapiens	37-42
22169720-5	2011	RESULTS: A sharp stained protein band with a molecular weight of about 26 kD was obtained by SDS-PAGE analysis and shown to be HMGB1 confirmed by Western blot.	Sodium Dodecyl Sulfate	93-96	high mobility group box 1	Homo sapiens	127-132
21294652-8	2011	HMGB1, a protein thiol, weakly expressed in healthy muscles, increases during regeneration in parallel with the antioxidant response in both fibers and leukocytes.	Sulfhydryl Compounds	17-22	high mobility group box 1	Homo sapiens	0-5
21922361-9	2011	Serum levels of tumor necrosis factor-alpha, interleukin-6, and high-mobility group box 1 were higher in the CT group than in the IIT group.	ct	109-111	high mobility group box 1	Homo sapiens	64-89
21691146-8	2011	Loss of either HMGB1 or HSPB1 results in a phenotypically similar deficiency in mitophagy typified by mitochondrial fragmentation with decreased aerobic respiration and adenosine triphosphate (ATP) production.	Adenosine Triphosphate	169-191	high mobility group box 1	Homo sapiens	15-20
21691146-8	2011	Loss of either HMGB1 or HSPB1 results in a phenotypically similar deficiency in mitophagy typified by mitochondrial fragmentation with decreased aerobic respiration and adenosine triphosphate (ATP) production.	Adenosine Triphosphate	193-196	high mobility group box 1	Homo sapiens	15-20
21617575-0	2011	Peroxisome proliferator-activated receptor gamma agonist troglitazone inhibits high mobility group box 1 expression in endothelial cells via suppressing transcriptional activity of nuclear factor kappaB and activator protein 1.	Troglitazone	57-69	high mobility group box 1	Homo sapiens	79-104
21756977-8	2011	Curculigoside A 20 mg/kg attenuated histopathological damage, decreased cerebral Evans Blue extravasation, inhibited NF-kappaB activation and reduced HMGB1 expression.	curculigoside	0-15	high mobility group box 1	Homo sapiens	150-155
21756977-9	2011	These data show that Curculigoside A protects brain against I/R injury with a favorable therapeutic time-window by alleviating cerebral I/R injury and attenuating blood-brain barrier (BBB) breakdown, and its protective effects may involve HMGB1 and NF-kappaB signaling pathway.	curculigoside	21-36	high mobility group box 1	Homo sapiens	239-244
21457762-0	2011	CKD712, (S)-1-(alpha-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, inhibits the lipopolysaccharide-stimulated secretion of HMGB1 by inhibiting PI3K and classical protein kinase C. CKD712, (S)-1-(alpha-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, was considered as a new effective drug candidate to sepsis, based on its anti-inflammatory activity.	YS 49	8-81	high mobility group box 1	Homo sapiens	139-144
21457762-3	2011	CKD712 can reduce Gram-negative lipopolysaccharide (LPS)- and Gram-positive lipoteichoic acid (LTA)-stimulated HMGB1 secretion in RAW264.7 and human peripheral blood monocytes (PBMo), and also reduce LPS-induced nucleocytoplasmic translocation of HMGB1 1h before or after LPS treatment.	positive	67-75	high mobility group box 1	Homo sapiens	111-116
21457762-3	2011	CKD712 can reduce Gram-negative lipopolysaccharide (LPS)- and Gram-positive lipoteichoic acid (LTA)-stimulated HMGB1 secretion in RAW264.7 and human peripheral blood monocytes (PBMo), and also reduce LPS-induced nucleocytoplasmic translocation of HMGB1 1h before or after LPS treatment.	lipoteichoic acid	76-93	high mobility group box 1	Homo sapiens	111-116
21457762-3	2011	CKD712 can reduce Gram-negative lipopolysaccharide (LPS)- and Gram-positive lipoteichoic acid (LTA)-stimulated HMGB1 secretion in RAW264.7 and human peripheral blood monocytes (PBMo), and also reduce LPS-induced nucleocytoplasmic translocation of HMGB1 1h before or after LPS treatment.	lipoteichoic acid	95-98	high mobility group box 1	Homo sapiens	111-116
21457762-3	2011	CKD712 can reduce Gram-negative lipopolysaccharide (LPS)- and Gram-positive lipoteichoic acid (LTA)-stimulated HMGB1 secretion in RAW264.7 and human peripheral blood monocytes (PBMo), and also reduce LPS-induced nucleocytoplasmic translocation of HMGB1 1h before or after LPS treatment.	lipoteichoic acid	95-98	high mobility group box 1	Homo sapiens	247-252
21696758-7	2011	Furthermore, there was a negative correlation between the serum HMGB-1 levels and PaO2/FiO2 ratio on POD3.	pao2	82-86	high mobility group box 1	Homo sapiens	64-70
21696758-7	2011	Furthermore, there was a negative correlation between the serum HMGB-1 levels and PaO2/FiO2 ratio on POD3.	fio2	87-91	high mobility group box 1	Homo sapiens	64-70
21617575-4	2011	Herein, we provide evidence that PPARgamma agonist troglitazone, a member of the TZD class, modulates HMGB1 expression in the endothelial cell line EA.hy926 and propose a potential mechanism for that.	Troglitazone	51-63	high mobility group box 1	Homo sapiens	102-107
21617575-4	2011	Herein, we provide evidence that PPARgamma agonist troglitazone, a member of the TZD class, modulates HMGB1 expression in the endothelial cell line EA.hy926 and propose a potential mechanism for that.	2,4-thiazolidinedione	81-84	high mobility group box 1	Homo sapiens	102-107
21617575-6	2011	Troglitazone inhibited the basal and LPS-stimulated HMGB1 expression at the mRNA level and protein level.	Troglitazone	0-12	high mobility group box 1	Homo sapiens	52-57
21617575-7	2011	A luciferase reporter assay showed that troglitazone inhibited not only the transcriptional activation of the HMGB1 promoter but also activities of heterologous promoters driven by nuclear factor kappaB (NF-kappaB) or activator protein 1 (AP-1) response elements.	Troglitazone	40-52	high mobility group box 1	Homo sapiens	110-115
21617575-8	2011	Altogether, these data suggest that NF-kappaB and AP-1 may participate in the inhibitory effect on HMGB1 transcription induced by troglitazone.	Troglitazone	130-142	high mobility group box 1	Homo sapiens	99-104
21617575-9	2011	Activation of PPARgamma by troglitazone is effective for HMGB1 inhibition via suppressing NF-kappaB and AP-1 transcriptional activity in endothelial cells, which provides a new potential strategy to suppress excessive HMGB1 in inflammatory diseases.	Troglitazone	27-39	high mobility group box 1	Homo sapiens	57-62
21617575-9	2011	Activation of PPARgamma by troglitazone is effective for HMGB1 inhibition via suppressing NF-kappaB and AP-1 transcriptional activity in endothelial cells, which provides a new potential strategy to suppress excessive HMGB1 in inflammatory diseases.	Troglitazone	27-39	high mobility group box 1	Homo sapiens	218-223
21617575-3	2011	Because many proinflammatory cytokines expression were suppressed by thiazolidinediones (TZDs), agonists for nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma), whether TZDs can inhibit HMGB1 expression and function is of great interest, however, it remains unknown.	Thiazolidinediones	196-200	high mobility group box 1	Homo sapiens	213-218
21116767-0	2011	Extracellular HMGB1 released by NMDA treatment confers neuronal apoptosis via RAGE-p38 MAPK/ERK signaling pathway.	N-Methylaspartate	32-36	high mobility group box 1	Homo sapiens	14-19
21487246-5	2011	Hydrogen peroxide (H 2O 2) and loss of superoxide dismutase 1 (SOD1)-mediated oxidative stress promotes cytosolic HMGB1 expression and extracellular release.	Hydrogen Peroxide	0-17	high mobility group box 1	Homo sapiens	114-119
21487246-5	2011	Hydrogen peroxide (H 2O 2) and loss of superoxide dismutase 1 (SOD1)-mediated oxidative stress promotes cytosolic HMGB1 expression and extracellular release.	Water	19-23	high mobility group box 1	Homo sapiens	114-119
21740486-0	2011	Synergistic requirement of orphan nonamer-like elements and DNA bending enhanced by HMGB1 for RAG-mediated nicking at cryptic 12-RSS but not authentic 12-RSS.	12-rss	126-132	high mobility group box 1	Homo sapiens	84-89
21740486-5	2011	The cryptic nicking site within the TEL fragment was cleaved by RAG proteins essentially depending on a 12-RSS framework, and the nicking activity was enhanced synergistically by both HMGB1 and orphan nonamer-like (NL) sequences, which do not possess counterpart heptamers.	RSS	107-110	high mobility group box 1	Homo sapiens	184-189
21740486-7	2011	Collectively, we would propose the mechanism of HMGB1-dependent enhancement of RAG-mediated nicking at a cryptic RSS through enhanced DNA bending.	RSS	113-116	high mobility group box 1	Homo sapiens	48-53
21520052-6	2011	Pretreatment with c-Src inhibitor (PP2), Akt inhibitor and NF-kappaB inhibitor (pyrrolidine dithiocarbamate and L-1-tosylamido-2-phenylenylethyl chloromethyl ketone) also inhibited the potentiating action of HMGB-1.	l-1-tosylamido-2-phenylenylethyl chloromethyl ketone	112-164	high mobility group box 1	Homo sapiens	208-214
21116767-8	2011	A series of RAGE and HMGB1 co-immunoprecipitation experiments in the presence of SB203580 and PD98059 (p38 MAPK and ERK inhibitors, respectively) demonstrated that RAGE-p38 MAPK and RAGE-ERK pathway might underlie extracellular HMGB1-mediated neuronal apoptosis.	SB 203580	81-89	high mobility group box 1	Homo sapiens	21-26
21116767-8	2011	A series of RAGE and HMGB1 co-immunoprecipitation experiments in the presence of SB203580 and PD98059 (p38 MAPK and ERK inhibitors, respectively) demonstrated that RAGE-p38 MAPK and RAGE-ERK pathway might underlie extracellular HMGB1-mediated neuronal apoptosis.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	94-101	high mobility group box 1	Homo sapiens	21-26
21116767-4	2011	HMGB1 was found to be accumulated in NMDA-treated primary cortical culture media, and media collected from these cultures were able to induce neuronal cell death when added to fresh primary cortical cultures.	N-Methylaspartate	37-41	high mobility group box 1	Homo sapiens	0-5
21116767-5	2011	However, HMGB1-depleted NMDA-conditioned media produced by HMGB1 siRNA transfection or by preincubation with anti-HMGB1 antibody or with HMGB1 A box failed to induce neuronal cell death.	N-Methylaspartate	24-28	high mobility group box 1	Homo sapiens	9-14
21116767-5	2011	However, HMGB1-depleted NMDA-conditioned media produced by HMGB1 siRNA transfection or by preincubation with anti-HMGB1 antibody or with HMGB1 A box failed to induce neuronal cell death.	N-Methylaspartate	24-28	high mobility group box 1	Homo sapiens	59-64
21116767-5	2011	However, HMGB1-depleted NMDA-conditioned media produced by HMGB1 siRNA transfection or by preincubation with anti-HMGB1 antibody or with HMGB1 A box failed to induce neuronal cell death.	N-Methylaspartate	24-28	high mobility group box 1	Homo sapiens	59-64
21116767-5	2011	However, HMGB1-depleted NMDA-conditioned media produced by HMGB1 siRNA transfection or by preincubation with anti-HMGB1 antibody or with HMGB1 A box failed to induce neuronal cell death.	N-Methylaspartate	24-28	high mobility group box 1	Homo sapiens	59-64
21116767-6	2011	Furthermore, siRNA-mediated HMGB1 knockdown substantially suppressed NMDA- or Zn(2+)-induced cell death.	N-Methylaspartate	69-73	high mobility group box 1	Homo sapiens	28-33
21116767-6	2011	Furthermore, siRNA-mediated HMGB1 knockdown substantially suppressed NMDA- or Zn(2+)-induced cell death.	Zinc	78-84	high mobility group box 1	Homo sapiens	28-33
21426233-0	2011	18beta-glycyrrhetic acid inhibits immune activation triggered by HMGB1, a pro-inflammatory protein found in the tear fluid during conjunctivitis and blepharitis.	Glycyrrhetinic Acid	0-24	high mobility group box 1	Homo sapiens	65-70
21884474-6	2011	Among the four membranes, surface-treated polyacrylonitrile (AN69ST) showed the highest capacity to adsorb HMGB1; it adsorbed nearly 100 microg of HMGB1 in the initial 60 min and showed a markedly high clearance rate (60.8 +- 5.0 mL/min) at 15 min.	polyacrylonitrile	42-59	high mobility group box 1	Homo sapiens	107-112
21884474-6	2011	Among the four membranes, surface-treated polyacrylonitrile (AN69ST) showed the highest capacity to adsorb HMGB1; it adsorbed nearly 100 microg of HMGB1 in the initial 60 min and showed a markedly high clearance rate (60.8 +- 5.0 mL/min) at 15 min.	polyacrylonitrile	42-59	high mobility group box 1	Homo sapiens	147-152
21884474-8	2011	Although the highest sieving coefficient for HMGB1 was obtained with the high cut-off polyarylethersulfone membrane, which correlated with a constant filtrate clearance rate, albumin loss was observed.	polyarylethersulfone	86-106	high mobility group box 1	Homo sapiens	45-50
21602432-5	2011	We found that only anthracyclines induced a rapid translocation of calreticulin, HSP70, and HSP90 to the cell surface and the release of HMGB1 12 hours after the treatment.	Anthracyclines	19-33	high mobility group box 1	Homo sapiens	137-142
21642542-5	2011	Short hairpin RNA-mediated knockdown of HMGB1 (HMGB1 KD) in tumor cells did not affect tumor cell growth but uncovered naturally acquired long-lasting tumor-specific IFN-gamma- or TNF-alpha-producing CD8 T cell responses and attenuated their ability to induce Treg, leading to naturally acquired CD8 T cell- or IFN-gamma-dependent tumor rejection.	treg	260-264	high mobility group box 1	Homo sapiens	40-45
21642542-5	2011	Short hairpin RNA-mediated knockdown of HMGB1 (HMGB1 KD) in tumor cells did not affect tumor cell growth but uncovered naturally acquired long-lasting tumor-specific IFN-gamma- or TNF-alpha-producing CD8 T cell responses and attenuated their ability to induce Treg, leading to naturally acquired CD8 T cell- or IFN-gamma-dependent tumor rejection.	treg	260-264	high mobility group box 1	Homo sapiens	47-52
21610098-6	2011	In addition, HMGB-1 prevents the pro-neurotoxic effect of tPA, by blocking its interaction with N-methyl-D-aspartate (NMDA) receptors and the attendant potentiation of NMDA-induced neuronal Ca2+ influx.	N-Methylaspartate	118-122	high mobility group box 1	Homo sapiens	13-19
21565414-0	2011	Fluvastatin reduces the high mobility group box 1 protein expression in hyperlipidemia.	Fluvastatin	0-11	high mobility group box 1	Homo sapiens	24-49
21426233-6	2011	The authors also report that 18beta-glycyrrhetic acid impairs antibody recognition of HMGB1, suggesting direct binding to the protein.	Glycyrrhetinic Acid	29-53	high mobility group box 1	Homo sapiens	86-91
21426233-7	2011	Accordingly, 18beta-glycyrrhetic acid prevented HMGB1-dependent COX2 expression and cluster formation in primary cultures of human macrophages.	Glycyrrhetinic Acid	13-37	high mobility group box 1	Homo sapiens	48-53
21355578-1	2011	HMGB1, one of the most abundant nuclear proteins, has a strong binding affinity for cisplatin-modified DNA.	Cisplatin	84-93	high mobility group box 1	Homo sapiens	0-5
21294273-0	2011	HMGB1-carbenoxolone interactions: dynamics insights from combined nuclear magnetic resonance and molecular dynamics.	Carbenoxolone	6-19	high mobility group box 1	Homo sapiens	0-5
21294273-3	2011	Herein, we have combined NMR relaxation experiments and residual dipolar coupling (RDC) measurements with molecular dynamics (MD) simulations to study the effects of the anti-inflammatory drug carbenoxolone (CBNX) on the conformational properties and on the internal dynamics of a subdomain (box A) of high-mobility group B protein (HMGB1).	Carbenoxolone	193-206	high mobility group box 1	Homo sapiens	333-338
21294273-3	2011	Herein, we have combined NMR relaxation experiments and residual dipolar coupling (RDC) measurements with molecular dynamics (MD) simulations to study the effects of the anti-inflammatory drug carbenoxolone (CBNX) on the conformational properties and on the internal dynamics of a subdomain (box A) of high-mobility group B protein (HMGB1).	Carbenoxolone	208-212	high mobility group box 1	Homo sapiens	333-338
21443191-3	2011	NMR structures of two bent DNA oligomers, only one of which binds strongly to HMGB1, revealed that the presence of a pocket structure on the minor groove is crucial for strong binding through penetration of a phenylalanine residue.	Phenylalanine	209-222	high mobility group box 1	Homo sapiens	78-83
21355578-2	2011	It has been proposed that HMGB1 enhances the anticancer efficacy of cisplatin by shielding platinated DNA lesions from repair.	Cisplatin	68-77	high mobility group box 1	Homo sapiens	26-31
21355578-3	2011	Two cysteine residues in HMGB1 domain A form a reversible disulfide bond under mildly oxidizing conditions.	Cysteine	4-12	high mobility group box 1	Homo sapiens	25-30
21355578-3	2011	Two cysteine residues in HMGB1 domain A form a reversible disulfide bond under mildly oxidizing conditions.	Disulfides	58-67	high mobility group box 1	Homo sapiens	25-30
21355578-5	2011	The binding affinities of singly and doubly mutated HMGB1 domain A, respectively deficient in one or both cysteine residues that form the disulfide bond, are unaffected by changes in external redox conditions.	Cysteine	106-114	high mobility group box 1	Homo sapiens	52-57
21355578-5	2011	The binding affinities of singly and doubly mutated HMGB1 domain A, respectively deficient in one or both cysteine residues that form the disulfide bond, are unaffected by changes in external redox conditions.	Disulfides	138-147	high mobility group box 1	Homo sapiens	52-57
21355578-6	2011	The redox-dependent nature of the binding of HMGB1 domain A to cisplatin-modified DNA suggests that formation of the intradomain disulfide bond induces a conformational change that disfavors binding to cisplatin-modified DNA.	Cisplatin	63-72	high mobility group box 1	Homo sapiens	45-50
21355578-6	2011	The redox-dependent nature of the binding of HMGB1 domain A to cisplatin-modified DNA suggests that formation of the intradomain disulfide bond induces a conformational change that disfavors binding to cisplatin-modified DNA.	Disulfides	129-138	high mobility group box 1	Homo sapiens	45-50
21355578-6	2011	The redox-dependent nature of the binding of HMGB1 domain A to cisplatin-modified DNA suggests that formation of the intradomain disulfide bond induces a conformational change that disfavors binding to cisplatin-modified DNA.	Cisplatin	202-211	high mobility group box 1	Homo sapiens	45-50
21355578-8	2011	The results of this study reveal that the cellular redox environment can influence the interaction of HMGB1 with the platinated DNA and suggest that the redox state of the A domain is a potential factor in regulating the role of the protein in modulating the activity of cisplatin as an anticancer drug.	Cisplatin	271-280	high mobility group box 1	Homo sapiens	102-107
21634123-6	2011	Lysine-rich histone H1 facilitates the binding of the HMGB1 with DNA by screening the negatively charged groups of the sugar-phosphate backbone of DNA and dicarboxylic amino-acid residues in the C-terminal domain of the HMGB1 protein.	Lysine	0-6	high mobility group box 1	Homo sapiens	54-59
20969478-6	2011	HMGB1 causes activation of nicotinamide adenine dinucleotide phosphate oxidase and increased reactive oxygen species production in neutrophils.	Reactive Oxygen Species	93-116	high mobility group box 1	Homo sapiens	0-5
20969478-8	2011	Antioxidants such as ethyl pyruvate, quercetin, green tea, N-acetylcysteine, and curcumin are protective in the setting of experimental infection/sepsis and injury including ischemia-reperfusion, partly through attenuating HMGB1 release and systemic accumulation.	Acetylcysteine	59-75	high mobility group box 1	Homo sapiens	223-228
20969478-8	2011	Antioxidants such as ethyl pyruvate, quercetin, green tea, N-acetylcysteine, and curcumin are protective in the setting of experimental infection/sepsis and injury including ischemia-reperfusion, partly through attenuating HMGB1 release and systemic accumulation.	Curcumin	81-89	high mobility group box 1	Homo sapiens	223-228
21186276-0	2011	Endogenous HMGB1 contributes to ischemia-reperfusion-induced myocardial apoptosis by potentiating the effect of TNF-&amp;alpha;/JNK.	Adenosine Monophosphate	117-120	high mobility group box 1	Homo sapiens	11-16
21634123-0	2011	[The structure of the complexes of DNA with chromosomal protein HMGB1 and histone H1 in the presence of manganese ions.	Manganese	104-113	high mobility group box 1	Homo sapiens	64-69
21186276-13	2011	Furthermore, inhibition of JNK (SP-600125) prevented the myocyte apoptosis induced by a TNF-alpha/HMGB1 cocktail.	pyrazolanthrone	32-41	high mobility group box 1	Homo sapiens	98-103
21634123-6	2011	Lysine-rich histone H1 facilitates the binding of the HMGB1 with DNA by screening the negatively charged groups of the sugar-phosphate backbone of DNA and dicarboxylic amino-acid residues in the C-terminal domain of the HMGB1 protein.	Lysine	0-6	high mobility group box 1	Homo sapiens	220-225
21634123-6	2011	Lysine-rich histone H1 facilitates the binding of the HMGB1 with DNA by screening the negatively charged groups of the sugar-phosphate backbone of DNA and dicarboxylic amino-acid residues in the C-terminal domain of the HMGB1 protein.	Sugar Phosphates	119-134	high mobility group box 1	Homo sapiens	54-59
21634123-6	2011	Lysine-rich histone H1 facilitates the binding of the HMGB1 with DNA by screening the negatively charged groups of the sugar-phosphate backbone of DNA and dicarboxylic amino-acid residues in the C-terminal domain of the HMGB1 protein.	Sugar Phosphates	119-134	high mobility group box 1	Homo sapiens	220-225
21634123-9	2011	Manganese ions significantly modify the character of interactions between the components in the triple DNA-HMGB1-H1 complex.	Manganese	0-9	high mobility group box 1	Homo sapiens	107-112
21248133-11	2011	The treatment of microglia with HMGB1 led to membrane translocation of p47(phox) (a cytosolic subunit of NADPH oxidase) and consequent superoxide release, which required the presence of Mac1.	Superoxides	135-145	high mobility group box 1	Homo sapiens	32-37
21149855-5	2011	Butyric acid, an extracellular metabolite from periodontopathic bacteria populating the periodontal pocket, induced the passive release of HMGB1 as a result of eliciting necrosis in the human gingival epithelial cell line.	Butyric Acid	0-12	high mobility group box 1	Homo sapiens	139-144
20739958-0	2011	Synergistic anti-tumor effects between oncolytic vaccinia virus and paclitaxel are mediated by the IFN response and HMGB1.	Paclitaxel	68-78	high mobility group box 1	Homo sapiens	116-121
21300299-7	2011	In trained patients, decreased HMGB1 levels were significantly associated with the improvement in peak oxygen consumption (beta = -3.879, P = .003) and heart rate recovery (beta = -2.492, P = .002), and with reduced left ventricular end-diastolic volume (beta = 1.412, P = .001) and wall motion score index (beta = 1.138, P = .002).	Oxygen	103-109	high mobility group box 1	Homo sapiens	31-36
21647302-0	2011	The DNA binding and bending activities of truncated tail-less HMGB1 protein are differentially affected by Lys-2 and Lys-81 residues and their acetylation.	Lysine	107-110	high mobility group box 1	Homo sapiens	62-67
21283827-9	2011	These effects were specifically linked to HMGB1 since they were blocked by glycyrrhizin or by a neutralizing anti-HMGB1 antibody, and were mediated through TLR2 and the receptor for Advanced Glycation End-products (RAGE).	Glycyrrhizic Acid	75-87	high mobility group box 1	Homo sapiens	42-47
21167721-8	2011	Expectedly, DR396, which is the most potent and specific inhibitor of DNase gamma, was found to almost completely inhibit both HMGB1 release and internucleosomal DNA cleavage in HeLa S3 cells transfected with DNase gamma expression vector and stably expressing DNase gamma (HeLa S3/gamma cells).	4-(4,6-dichloro-(1,3,5)-triazin-2-ylamino)-2-(6-hydroxy-3-oxo-3H-xanthen-9-yl)benzoic acid	12-17	high mobility group box 1	Homo sapiens	127-132
21647302-1	2011	The role of lysines 2 and 81 as target sites for acetylation in full-length HMGB1 and truncated tail-less protein, respectively, has been studied by mutation analysis for the abilities of these proteins to bind and bend DNA.	Lysine	12-19	high mobility group box 1	Homo sapiens	76-81
21647302-2	2011	The DNA bending ability of truncated tail-less HMGB1 containing Lys-2 mutated to alanine does not differ from that of the wild-type protein, while the same mutation of Lys-81 reduced the bending capacity of the mutant protein.	Lysine	64-67	high mobility group box 1	Homo sapiens	47-52
21647302-3	2011	These data demonstrate that Lys-81 is critical for the DNA bending ability of truncated HMGB1.	Lysine	28-31	high mobility group box 1	Homo sapiens	88-93
21647302-5	2011	On the contrary, the acetylation of Lys-81 in the mutant K2/A2 enhanced the bending potential of HMGB1 C. Regarding the ability of HMGB1 to specifically bind bent DNA, the individual mutations of either K2 or K81 as well as the double mutation of both residues to alanine were found to completely abolish binding of truncated tail-less HMGB1 to cisplatin-modified DNA.	Lysine	36-39	high mobility group box 1	Homo sapiens	97-102
21647302-5	2011	On the contrary, the acetylation of Lys-81 in the mutant K2/A2 enhanced the bending potential of HMGB1 C. Regarding the ability of HMGB1 to specifically bind bent DNA, the individual mutations of either K2 or K81 as well as the double mutation of both residues to alanine were found to completely abolish binding of truncated tail-less HMGB1 to cisplatin-modified DNA.	Lysine	36-39	high mobility group box 1	Homo sapiens	131-136
21647302-5	2011	On the contrary, the acetylation of Lys-81 in the mutant K2/A2 enhanced the bending potential of HMGB1 C. Regarding the ability of HMGB1 to specifically bind bent DNA, the individual mutations of either K2 or K81 as well as the double mutation of both residues to alanine were found to completely abolish binding of truncated tail-less HMGB1 to cisplatin-modified DNA.	Lysine	36-39	high mobility group box 1	Homo sapiens	131-136
21647302-5	2011	On the contrary, the acetylation of Lys-81 in the mutant K2/A2 enhanced the bending potential of HMGB1 C. Regarding the ability of HMGB1 to specifically bind bent DNA, the individual mutations of either K2 or K81 as well as the double mutation of both residues to alanine were found to completely abolish binding of truncated tail-less HMGB1 to cisplatin-modified DNA.	Alanine	264-271	high mobility group box 1	Homo sapiens	131-136
21647302-5	2011	On the contrary, the acetylation of Lys-81 in the mutant K2/A2 enhanced the bending potential of HMGB1 C. Regarding the ability of HMGB1 to specifically bind bent DNA, the individual mutations of either K2 or K81 as well as the double mutation of both residues to alanine were found to completely abolish binding of truncated tail-less HMGB1 to cisplatin-modified DNA.	Alanine	264-271	high mobility group box 1	Homo sapiens	131-136
21647302-5	2011	On the contrary, the acetylation of Lys-81 in the mutant K2/A2 enhanced the bending potential of HMGB1 C. Regarding the ability of HMGB1 to specifically bind bent DNA, the individual mutations of either K2 or K81 as well as the double mutation of both residues to alanine were found to completely abolish binding of truncated tail-less HMGB1 to cisplatin-modified DNA.	Cisplatin	345-354	high mobility group box 1	Homo sapiens	131-136
21647302-5	2011	On the contrary, the acetylation of Lys-81 in the mutant K2/A2 enhanced the bending potential of HMGB1 C. Regarding the ability of HMGB1 to specifically bind bent DNA, the individual mutations of either K2 or K81 as well as the double mutation of both residues to alanine were found to completely abolish binding of truncated tail-less HMGB1 to cisplatin-modified DNA.	Cisplatin	345-354	high mobility group box 1	Homo sapiens	131-136
21647302-6	2011	We conclude that unlike the case with the bending ability of truncated HMGB1, where Lys-81 has a primary function, Lys-2 and Lys-81 are both critical for the protein"s binding to cisplatin-modified DNA.	Lysine	84-87	high mobility group box 1	Homo sapiens	71-76
21647302-6	2011	We conclude that unlike the case with the bending ability of truncated HMGB1, where Lys-81 has a primary function, Lys-2 and Lys-81 are both critical for the protein"s binding to cisplatin-modified DNA.	Lysine	115-118	high mobility group box 1	Homo sapiens	71-76
21647302-6	2011	We conclude that unlike the case with the bending ability of truncated HMGB1, where Lys-81 has a primary function, Lys-2 and Lys-81 are both critical for the protein"s binding to cisplatin-modified DNA.	Cisplatin	179-188	high mobility group box 1	Homo sapiens	71-76
21647302-8	2011	Any further substitutions at the acetylable lysines in the truncated form of HMGB1 do not have an additional effect.	Lysine	44-51	high mobility group box 1	Homo sapiens	77-82
20803525-8	2010	Inhibition of SIRT1 by sirtinol or SIRT1 siRNA blocked the HMGB1-stimulated expression of RANKL and cytokines.	sirtinol	23-31	high mobility group box 1	Homo sapiens	59-64
20845025-8	2010	ETR-P1/fl administration resulted in higher MAP at 6 and 9 h after CLP, less negative BE, lower mean pulmonary arterial pressure (mPAP)/MAP ratio at 9 h after CLP, and lower TNF-alpha, NOx, and HMGB-1 compared to the CLP group.	etr-p1	0-6	high mobility group box 1	Homo sapiens	194-200
20845025-8	2010	ETR-P1/fl administration resulted in higher MAP at 6 and 9 h after CLP, less negative BE, lower mean pulmonary arterial pressure (mPAP)/MAP ratio at 9 h after CLP, and lower TNF-alpha, NOx, and HMGB-1 compared to the CLP group.	fl	7-9	high mobility group box 1	Homo sapiens	194-200
20845025-11	2010	CONCLUSIONS: ETR-P1/fl treatment significantly attenuated the elevation of NOx, TNF-alpha, and HMGB-1, which improved the systemic hypotension, pulmonary hypertension, and blood gases, thereby causing improvement of survival time in a progressive neonatal sepsis CLP model.	etr	13-16	high mobility group box 1	Homo sapiens	95-101
21602594-0	2011	Immunosuppressant cytoprotection correlates with HMGB1 suppression in primary astrocyte cultures exposed to combined oxygen-glucose deprivation.	oxygen-glucose	117-131	high mobility group box 1	Homo sapiens	49-54
21602594-2	2011	Because high-mobility group box 1 (HMGB1) protein has recently been reported to be involved in ischemic brain injury, the purpose of the present study was to determine whether treatment with immunosuppressants could decrease the expression and release of HMGB1 in astrocytes exposed to simulated ischemic conditions (combined oxygen-glucose deprivation, OGD).	oxygen-glucose	326-340	high mobility group box 1	Homo sapiens	35-40
21602594-2	2011	Because high-mobility group box 1 (HMGB1) protein has recently been reported to be involved in ischemic brain injury, the purpose of the present study was to determine whether treatment with immunosuppressants could decrease the expression and release of HMGB1 in astrocytes exposed to simulated ischemic conditions (combined oxygen-glucose deprivation, OGD).	oxygen-glucose	326-340	high mobility group box 1	Homo sapiens	255-260
21602594-7	2011	Our data suggest that HMGB1 release may be partly an active process triggered by oxidative stress because the antioxidant N-acetylcysteine (NAC) clearly attenuated HMGB1 expression and release.	Acetylcysteine	122-138	high mobility group box 1	Homo sapiens	22-27
21602594-7	2011	Our data suggest that HMGB1 release may be partly an active process triggered by oxidative stress because the antioxidant N-acetylcysteine (NAC) clearly attenuated HMGB1 expression and release.	Acetylcysteine	122-138	high mobility group box 1	Homo sapiens	164-169
21602594-7	2011	Our data suggest that HMGB1 release may be partly an active process triggered by oxidative stress because the antioxidant N-acetylcysteine (NAC) clearly attenuated HMGB1 expression and release.	Acetylcysteine	140-143	high mobility group box 1	Homo sapiens	22-27
21602594-7	2011	Our data suggest that HMGB1 release may be partly an active process triggered by oxidative stress because the antioxidant N-acetylcysteine (NAC) clearly attenuated HMGB1 expression and release.	Acetylcysteine	140-143	high mobility group box 1	Homo sapiens	164-169
20163887-7	2010	Additionally, the HMGB1-induced activation of HUVECs was significantly inhibited by anti-RAGE monoclonal antibody and Ethyl pyruvate (EP) that had been shown to be an effective anti-inflammatory agent.	ethyl pyruvate	118-132	high mobility group box 1	Homo sapiens	18-23
20568967-7	2010	One of the cellular cofactors known to play a key role during SB-mediated transposition is the high-mobility group DNA-binding protein-1 (HMGB1).	Antimony	62-64	high mobility group box 1	Homo sapiens	95-136
20714791-8	2010	These findings indicate that atorvastatin attenuates HMGB1-induced vascular endothelial activation.	Atorvastatin	29-41	high mobility group box 1	Homo sapiens	53-58
20714791-3	2010	The aim of our study was to investigate whether atorvastatin inhibits HMGB1-induced vascular endothelial activation, and elucidate the underlying molecular mechanism.	Atorvastatin	48-60	high mobility group box 1	Homo sapiens	70-75
20714791-4	2010	In this study, we found that atorvastatin, at concentrations ranging from 0.1 to 10 muM, effectively and in a dose-dependent manner inhibited HMGB1-induced endothelial cells (ECs) activation.	Atorvastatin	29-41	high mobility group box 1	Homo sapiens	142-147
20714791-5	2010	Incubation of ECs with 10 muM atorvastatin reduced adhesion molecules (ICAM-1 and E-selectin) expression concomitant with a significant inhibition in HMGB1-stimulated leukocyte-endothelial adhesion.	Atorvastatin	30-42	high mobility group box 1	Homo sapiens	150-155
20714791-6	2010	Further experiments showed that atorvastatin markedly suppressed HMGB1-induced Toll like receptor 4 (TLR4) expression, Nuclear factor kappaB (NF-kappaB) nuclear translocation and DNA binding activity in ECs.	Atorvastatin	32-44	high mobility group box 1	Homo sapiens	65-70
20935509-7	2010	Moreover, the intramolecular disulfide bridge (C23/45) of HMGB1 is required for binding to Beclin 1 and sustaining autophagy.	Disulfides	29-38	high mobility group box 1	Homo sapiens	58-63
20568967-7	2010	One of the cellular cofactors known to play a key role during SB-mediated transposition is the high-mobility group DNA-binding protein-1 (HMGB1).	Antimony	62-64	high mobility group box 1	Homo sapiens	138-143
20568967-10	2010	As a result, HSV/SB amplicon virions arrive prearmed with HMGB1 protein at levels sufficient for facilitating SB-mediated transposition in the transduced mammalian cell.	Antimony	17-19	high mobility group box 1	Homo sapiens	58-63
20664360-0	2010	Preconditioning with high mobility group box 1 (HMGB1) induces lipoteichoic acid (LTA) tolerance.	lipoteichoic acid	63-80	high mobility group box 1	Homo sapiens	21-46
20622903-5	2010	Diminished HMGB1 by short hairpin RNA transfection or inhibition of HMGB1 release by ethyl pyruvate or other small molecules led predominantly to apoptosis and decreased autophagy in stressed cancer cells.	ethyl pyruvate	85-99	high mobility group box 1	Homo sapiens	68-73
20622903-6	2010	In this setting, reducible HMGB1 binds to the receptor for advanced glycation end products (RAGEs), but not to Toll-like receptor 4, induces Beclin1-dependent autophagy and promotes tumor resistance to alkylators (melphalan), tubulin disrupting agents (paclitaxel), DNA crosslinkers (ultraviolet light) and DNA intercalators (oxaliplatin or adriamycin).	Paclitaxel	253-263	high mobility group box 1	Homo sapiens	27-32
20622903-6	2010	In this setting, reducible HMGB1 binds to the receptor for advanced glycation end products (RAGEs), but not to Toll-like receptor 4, induces Beclin1-dependent autophagy and promotes tumor resistance to alkylators (melphalan), tubulin disrupting agents (paclitaxel), DNA crosslinkers (ultraviolet light) and DNA intercalators (oxaliplatin or adriamycin).	Oxaliplatin	326-337	high mobility group box 1	Homo sapiens	27-32
20622903-6	2010	In this setting, reducible HMGB1 binds to the receptor for advanced glycation end products (RAGEs), but not to Toll-like receptor 4, induces Beclin1-dependent autophagy and promotes tumor resistance to alkylators (melphalan), tubulin disrupting agents (paclitaxel), DNA crosslinkers (ultraviolet light) and DNA intercalators (oxaliplatin or adriamycin).	Doxorubicin	341-351	high mobility group box 1	Homo sapiens	27-32
20819940-3	2010	Stimuli that enhance reactive oxygen species promote cytosolic translocation of HMGB1 and thereby enhance autophagic flux.	Reactive Oxygen Species	21-44	high mobility group box 1	Homo sapiens	80-85
20819940-5	2010	Mutation of cysteine 106 (C106), but not the vicinal C23 and C45, of HMGB1 promotes cytosolic localization and sustained autophagy.	Cysteine	12-20	high mobility group box 1	Homo sapiens	69-74
20819940-6	2010	Pharmacological inhibition of HMGB1 cytoplasmic translocation by agents such as ethyl pyruvate limits starvation-induced autophagy.	ethyl pyruvate	80-94	high mobility group box 1	Homo sapiens	30-35
20819940-7	2010	Moreover, the intramolecular disulfide bridge (C23/45) of HMGB1 is required for binding to Beclin1 and sustaining autophagy.	Disulfides	29-38	high mobility group box 1	Homo sapiens	58-63
20664360-0	2010	Preconditioning with high mobility group box 1 (HMGB1) induces lipoteichoic acid (LTA) tolerance.	lipoteichoic acid	63-80	high mobility group box 1	Homo sapiens	48-53
20664360-0	2010	Preconditioning with high mobility group box 1 (HMGB1) induces lipoteichoic acid (LTA) tolerance.	lipoteichoic acid	82-85	high mobility group box 1	Homo sapiens	21-46
20664360-0	2010	Preconditioning with high mobility group box 1 (HMGB1) induces lipoteichoic acid (LTA) tolerance.	lipoteichoic acid	82-85	high mobility group box 1	Homo sapiens	48-53
20616036-0	2010	Programmed necrosis induced by asbestos in human mesothelial cells causes high-mobility group box 1 protein release and resultant inflammation.	Asbestos	31-39	high mobility group box 1	Homo sapiens	74-99
20664360-3	2010	We tested the hypothesis that extracellular HMGB1 can induce tolerance to the bacterial product, lipoteichoic acid (LTA).	lipoteichoic acid	97-114	high mobility group box 1	Homo sapiens	44-49
20664360-3	2010	We tested the hypothesis that extracellular HMGB1 can induce tolerance to the bacterial product, lipoteichoic acid (LTA).	lipoteichoic acid	116-119	high mobility group box 1	Homo sapiens	44-49
20664360-5	2010	Denaturation of HMGB1 with boiling water or coincubation with anti-HMGB1 antibody abrogated the induction of tolerance to LTA.	Water	35-40	high mobility group box 1	Homo sapiens	16-21
20664360-7	2010	These findings support the view that the induction of LTA tolerance by HMGB1 was not due to lipopolysaccharide contamination.	lipoteichoic acid	54-57	high mobility group box 1	Homo sapiens	71-76
20182437-0	2010	High-mobility group box-1 protein in tracheal aspirates from premature infants: relationship with bronchopulmonary dysplasia and steroid therapy.	Steroids	129-136	high mobility group box 1	Homo sapiens	0-25
20182437-3	2010	We studied the association between HMGB1 levels in tracheal aspirates (TAs) and adverse outcomes (BPD/death) in ventilated premature infants (VPIs) and modulation of HMGB1 levels with dexamethasone (Dex) use.	Dexamethasone	184-197	high mobility group box 1	Homo sapiens	166-171
20182437-3	2010	We studied the association between HMGB1 levels in tracheal aspirates (TAs) and adverse outcomes (BPD/death) in ventilated premature infants (VPIs) and modulation of HMGB1 levels with dexamethasone (Dex) use.	Dexamethasone	199-202	high mobility group box 1	Homo sapiens	166-171
20386869-5	2010	Pharmacologically relevant doses of dexamethasone, gold sodium thiomalate and chloroquine inhibited the extracellular release of HMGB1 in a dose-dependent mode.	Dexamethasone	36-49	high mobility group box 1	Homo sapiens	129-134
20386869-5	2010	Pharmacologically relevant doses of dexamethasone, gold sodium thiomalate and chloroquine inhibited the extracellular release of HMGB1 in a dose-dependent mode.	Gold Sodium Thiomalate	51-73	high mobility group box 1	Homo sapiens	129-134
20386869-5	2010	Pharmacologically relevant doses of dexamethasone, gold sodium thiomalate and chloroquine inhibited the extracellular release of HMGB1 in a dose-dependent mode.	Chloroquine	78-89	high mobility group box 1	Homo sapiens	129-134
20386869-6	2010	Immunostaining demonstrated that dexamethasone caused intracellular HMGB1 retention.	Dexamethasone	33-46	high mobility group box 1	Homo sapiens	68-73
20386869-9	2010	We conclude that dexamethasone, gold sodium thiomalate and chloroquine share a capacity to inhibit HMGB1 release from activated monocytes.	Dexamethasone	17-30	high mobility group box 1	Homo sapiens	99-104
20386869-9	2010	We conclude that dexamethasone, gold sodium thiomalate and chloroquine share a capacity to inhibit HMGB1 release from activated monocytes.	Gold Sodium Thiomalate	32-54	high mobility group box 1	Homo sapiens	99-104
20386869-9	2010	We conclude that dexamethasone, gold sodium thiomalate and chloroquine share a capacity to inhibit HMGB1 release from activated monocytes.	Chloroquine	59-70	high mobility group box 1	Homo sapiens	99-104
20647757-4	2010	Combining genetic and cell death assays, we demonstrate that elevated FFA concentrations lead to necrotic cell death, as evidenced by loss of membrane integrity and release of nuclear HMGB1.	Fatty Acids, Nonesterified	70-73	high mobility group box 1	Homo sapiens	184-189
20483361-5	2010	HMGB1 treatment for 24h significantly inhibited the current densities of heterologously expressed Kv4.3 and Kv4.2 in COS-7 cells and native I(to) in neonatal rat ventricular myocytes (NRVMs) in a dose-dependent manner.	9-(3-hydroxy-2-phosphonomethoxypropyl)guanine	20-23	high mobility group box 1	Homo sapiens	0-5
20483361-5	2010	HMGB1 treatment for 24h significantly inhibited the current densities of heterologously expressed Kv4.3 and Kv4.2 in COS-7 cells and native I(to) in neonatal rat ventricular myocytes (NRVMs) in a dose-dependent manner.	carbonyl sulfide	117-120	high mobility group box 1	Homo sapiens	0-5
20616036-4	2010	Asbestos-exposed HM activate poly(ADP-ribose) polymerase, secrete H(2)O(2), deplete ATP, and translocate high-mobility group box 1 protein (HMGB1) from the nucleus to the cytoplasm, and into the extracellular space.	Adenosine Triphosphate	84-87	high mobility group box 1	Homo sapiens	140-145
20616036-8	2010	HMGB1 levels in asbestos-exposed individuals were significantly higher than in nonexposed controls (P &lt; 0.0001).	Asbestos	16-24	high mobility group box 1	Homo sapiens	0-5
20616036-10	2010	Chemopreventive approaches aimed at inhibiting the chronic inflammatory response, and especially blocking HMGB1, may decrease the risk of malignant mesothelioma among asbestos-exposed cohorts.	Asbestos	167-175	high mobility group box 1	Homo sapiens	106-111
20616036-4	2010	Asbestos-exposed HM activate poly(ADP-ribose) polymerase, secrete H(2)O(2), deplete ATP, and translocate high-mobility group box 1 protein (HMGB1) from the nucleus to the cytoplasm, and into the extracellular space.	Asbestos	0-8	high mobility group box 1	Homo sapiens	105-130
20616036-4	2010	Asbestos-exposed HM activate poly(ADP-ribose) polymerase, secrete H(2)O(2), deplete ATP, and translocate high-mobility group box 1 protein (HMGB1) from the nucleus to the cytoplasm, and into the extracellular space.	Asbestos	0-8	high mobility group box 1	Homo sapiens	140-145
20514401-7	2010	These results demonstrate that in metabolically stressed cancer cells, ROS induce a specific set of cellular proteins to form insoluble aggregates that are highly toxic to cells and trigger the necrosis-associated membrane rupture and HMGB1 release to promote tumour progression.	Reactive Oxygen Species	71-74	high mobility group box 1	Homo sapiens	235-240
22993577-13	2010	Here, we present Western blotting and immunofluorescence microscopy data indicating that MK615 inhibited the expression of RAGE in SK-MEL28 cells, and suppressed the release of HMGB1 by SK-MEL28 cells.	mk615	89-94	high mobility group box 1	Homo sapiens	177-182
20514411-4	2010	In solid tumours, ROS is produced by metabolic stress due to insufficient oxygen and glucose supply and induces necrosis that is known to promote tumour progression by releasing the proinflammatory cytokine HMGB1.	Reactive Oxygen Species	18-21	high mobility group box 1	Homo sapiens	207-212
20512925-3	2010	We earlier showed that carboxylated glycans on the V-domain of RAGE promote the binding of HMGB1 and S100A8/A9.	Polysaccharides	36-43	high mobility group box 1	Homo sapiens	91-96
20514411-5	2010	We observed that CuZnSOD and MnSOD overexpression prevents metabolic stress-induced necrosis and HMGB1 release by inhibiting mitochondrial ROS and intracellular O2- production in response to glucose depletion in two dimensional cell culture.	Glucose	191-198	high mobility group box 1	Homo sapiens	97-102
20547845-0	2010	A critical cysteine is required for HMGB1 binding to Toll-like receptor 4 and activation of macrophage cytokine release.	Cysteine	11-19	high mobility group box 1	Homo sapiens	36-41
20547845-8	2010	Surface plasmon resonance studies indicate that HMGB1 binds specifically to TLR4, and that this binding requires a cysteine in position 106.	Cysteine	115-123	high mobility group box 1	Homo sapiens	48-53
20547845-10	2010	Inhibition of TLR4 binding with neutralizing anti-HMGB1 mAb or by mutating cysteine 106 prevents HMGB1 activation of cytokine release.	Cysteine	75-83	high mobility group box 1	Homo sapiens	97-102
20928981-4	2010	In addition to advanced glycation end products (AGE), RAGE has other important ligands such as: high mobility group box 1 protein (HMGB1, also termed amphoterin), the group of calcium binding cellular factors S100 (also termed calgranulin), amiloid beta peptides and Mac-1, a beta-2 integrin (CD1lb/CD18).	Calcium	176-183	high mobility group box 1	Homo sapiens	131-136
20928981-4	2010	In addition to advanced glycation end products (AGE), RAGE has other important ligands such as: high mobility group box 1 protein (HMGB1, also termed amphoterin), the group of calcium binding cellular factors S100 (also termed calgranulin), amiloid beta peptides and Mac-1, a beta-2 integrin (CD1lb/CD18).	Calcium	176-183	high mobility group box 1	Homo sapiens	150-160
20618458-6	2010	Extracellular HMGB-1 levels markedly increased after hydrogen peroxide stimulation, but did not change after STS stimulation.	Hydrogen Peroxide	53-70	high mobility group box 1	Homo sapiens	14-20
19906009-3	2010	A growing number of HMGB1 inhibitors ranging from neutralizing antibodies, endogenous hormones, to medicinal herb-derived small molecule HMGB1 inhibitors (such as nicotine, glycyrrhizin, tanshinones, and EGCG) are proven protective against lethal infection and ischemic injury.	Nicotine	163-171	high mobility group box 1	Homo sapiens	20-25
19898867-4	2010	METHODS: In present study, we investigated HMGB1 expression and its prognostic significance in CRC by performing immunohistochemical analysis, using a total of 192 paraffin-embedded archival CRC samples.	Paraffin	164-172	high mobility group box 1	Homo sapiens	43-48
20368109-7	2010	The recombinant protein of human HMGB1 A box was purificated by Ni(2+)-NTA chromatography and the inhibit effection of the purpose protern to the activation of monocyte stimulated by immunocomplex was identified by RT-PCR.	nickel nitrilotriacetic acid	64-74	high mobility group box 1	Homo sapiens	33-38
20368109-9	2010	Western blot showed recombinant protein can specificly reacted with anti-human HMGB1 polyclonal antibody and anti-His-Tag polyclonal antibody.The purpose protein was found more than 90% after purified, and can effectively inhibit the production of BAFF, IFN-gamma and TNF-alpha in monocyte which were induced by IC.	Histidine	114-117	high mobility group box 1	Homo sapiens	79-84
20302902-1	2010	BACKGROUND: High mobility group box 1 (HMGB1) is a highly conserved, ubiquitous protein that functions as an activator for inducing the immune response and can be released from neurons after glutamate excitotoxicity.	Glutamic Acid	191-200	high mobility group box 1	Homo sapiens	12-37
20302902-1	2010	BACKGROUND: High mobility group box 1 (HMGB1) is a highly conserved, ubiquitous protein that functions as an activator for inducing the immune response and can be released from neurons after glutamate excitotoxicity.	Glutamic Acid	191-200	high mobility group box 1	Homo sapiens	39-44
20133931-8	2010	BAL HMGB1 correlated positively with IL-1beta (r(s) = 0.438; P = 0.0006) and negatively with FEV(1) (r(s) = -0.570; P &lt; 0.0001) and transfer factor of the lung for carbon monoxide (r(s) = -0.382; P = 0.0026).	Carbon Monoxide	167-182	high mobility group box 1	Homo sapiens	4-9
20335795-3	2010	It is well known that the cationic portion of HMGB1 binds to heparin, which has abundant sulfates in its structure.	Heparin	61-68	high mobility group box 1	Homo sapiens	46-51
20335795-3	2010	It is well known that the cationic portion of HMGB1 binds to heparin, which has abundant sulfates in its structure.	Sulfates	89-97	high mobility group box 1	Homo sapiens	46-51
20335795-4	2010	In this study, we determined whether spherical sulfated cellulose (SC) efficiently adsorbed HMGB1, as well as other inflammatory mediators, in vitro.	Cellulose	56-65	high mobility group box 1	Homo sapiens	92-97
20510002-2	2010	METHODS: Three specific siRNAs of HMGB1 were designed and synthesized, and were transiently transfected into HepG2 cells by Lipofectamine 2000.	Lipofectamine	124-142	high mobility group box 1	Homo sapiens	34-39
20510002-6	2010	RESULTS: All of these specific HMGB1-siRNAs (1, 2, 3) efficiently and specifically inhibited the expression of the HMGB1 gene, and the levels of HMGB1 mRNA were 1.147+/-0.024, 1.014+/-0.042, 0.435+/-0.055, respectively, in HMGB1-siRNAs transfection group, which were significantly lower than that in Lipofectamine 2000 alone group (1.411+/-0.065, P &lt; 0.01).	Lipofectamine	300-318	high mobility group box 1	Homo sapiens	31-36
20510002-6	2010	RESULTS: All of these specific HMGB1-siRNAs (1, 2, 3) efficiently and specifically inhibited the expression of the HMGB1 gene, and the levels of HMGB1 mRNA were 1.147+/-0.024, 1.014+/-0.042, 0.435+/-0.055, respectively, in HMGB1-siRNAs transfection group, which were significantly lower than that in Lipofectamine 2000 alone group (1.411+/-0.065, P &lt; 0.01).	Lipofectamine	300-318	high mobility group box 1	Homo sapiens	115-120
20510002-6	2010	RESULTS: All of these specific HMGB1-siRNAs (1, 2, 3) efficiently and specifically inhibited the expression of the HMGB1 gene, and the levels of HMGB1 mRNA were 1.147+/-0.024, 1.014+/-0.042, 0.435+/-0.055, respectively, in HMGB1-siRNAs transfection group, which were significantly lower than that in Lipofectamine 2000 alone group (1.411+/-0.065, P &lt; 0.01).	Lipofectamine	300-318	high mobility group box 1	Homo sapiens	115-120
20510002-6	2010	RESULTS: All of these specific HMGB1-siRNAs (1, 2, 3) efficiently and specifically inhibited the expression of the HMGB1 gene, and the levels of HMGB1 mRNA were 1.147+/-0.024, 1.014+/-0.042, 0.435+/-0.055, respectively, in HMGB1-siRNAs transfection group, which were significantly lower than that in Lipofectamine 2000 alone group (1.411+/-0.065, P &lt; 0.01).	Lipofectamine	300-318	high mobility group box 1	Homo sapiens	115-120
20332323-2	2010	Because selenium-binding protein 1 (SELENBP1, SBP1, hSP56) has been shown to bind selenium covalently and selenium deficiency has been associated with esophageal adenocarcinoma (EAC), we examined its role in EAC development and its potential effect on chemosensitivity in the presence of selenium.	Selenium	8-16	high mobility group box 1	Homo sapiens	46-50
20332323-2	2010	Because selenium-binding protein 1 (SELENBP1, SBP1, hSP56) has been shown to bind selenium covalently and selenium deficiency has been associated with esophageal adenocarcinoma (EAC), we examined its role in EAC development and its potential effect on chemosensitivity in the presence of selenium.	Selenium	82-90	high mobility group box 1	Homo sapiens	46-50
20332323-2	2010	Because selenium-binding protein 1 (SELENBP1, SBP1, hSP56) has been shown to bind selenium covalently and selenium deficiency has been associated with esophageal adenocarcinoma (EAC), we examined its role in EAC development and its potential effect on chemosensitivity in the presence of selenium.	Selenium	82-90	high mobility group box 1	Homo sapiens	46-50
20348922-5	2010	The proconvulsant effects of HMGB1, like those of interleukin-1beta (IL-1beta), are partly mediated by ifenprodil-sensitive N-methyl-d-aspartate (NMDA) receptors.	ifenprodil	103-113	high mobility group box 1	Homo sapiens	29-34
19906009-3	2010	A growing number of HMGB1 inhibitors ranging from neutralizing antibodies, endogenous hormones, to medicinal herb-derived small molecule HMGB1 inhibitors (such as nicotine, glycyrrhizin, tanshinones, and EGCG) are proven protective against lethal infection and ischemic injury.	Nicotine	163-171	high mobility group box 1	Homo sapiens	137-142
19906009-3	2010	A growing number of HMGB1 inhibitors ranging from neutralizing antibodies, endogenous hormones, to medicinal herb-derived small molecule HMGB1 inhibitors (such as nicotine, glycyrrhizin, tanshinones, and EGCG) are proven protective against lethal infection and ischemic injury.	epigallocatechin gallate	204-208	high mobility group box 1	Homo sapiens	20-25
19906009-3	2010	A growing number of HMGB1 inhibitors ranging from neutralizing antibodies, endogenous hormones, to medicinal herb-derived small molecule HMGB1 inhibitors (such as nicotine, glycyrrhizin, tanshinones, and EGCG) are proven protective against lethal infection and ischemic injury.	epigallocatechin gallate	204-208	high mobility group box 1	Homo sapiens	137-142
20009166-8	2010	The percentage of GFP-transfected cells and VEGF protein expression level induced by HMGB1/PEG-PEI were 2.6-4.9-fold and 1.4-2.8-fold higher, respectively, than that of a common cationic polymer PEI 25 kDa.	Polymers	187-194	high mobility group box 1	Homo sapiens	85-90
19914413-5	2010	In addition to RAGE, proteoglycans and sulfated carbohydrate epitopes of glycolipids and glycoproteins may play a role as cell surface binding sites of HMGB1, affecting migratory behaviour of cells.	Carbohydrates	48-60	high mobility group box 1	Homo sapiens	152-157
19651408-6	2010	RESULTS: HMGB1 levels were inversely correlated with peak oxygen consumption (VO(2peak)) (r=-0.449, P&lt;0.001), with left ventricular ejection fraction (LVEF) (r=-0.360, P=0.003), and with HRR (r=-0.387, P&lt;0.001).	Oxygen	58-64	high mobility group box 1	Homo sapiens	9-14
19651408-7	2010	In a linear regression analysis adjusted for multiple confounders, we found a significant inverse association between HMGB1 levels and HRR independent of age, gender, body mass index, VO(2peak), slope of increase in ventilation over carbon dioxide output (VE/VCO(2slope)), and presence of diabetes (beta=-0.377, P=0.034).	Carbon Dioxide	233-247	high mobility group box 1	Homo sapiens	118-123
19657355-6	2010	Release of High Mobility Group Box-1 protein by MBEH-treated melanocytes and ultrastructural features further confirmed a necrotic death pathway mediated by MBEH.	hydroquinone	48-52	high mobility group box 1	Homo sapiens	11-36
20123074-4	2010	Directing of base lesion repair to the long-patch sub-pathway can result in trinucleotide repeat instability suggesting an important role of HMGB1 in modulating genome stability.	trinucleotide	76-89	high mobility group box 1	Homo sapiens	141-146
19956840-2	2010	We have previously shown that metabolic stress due to glucose depletion (GD) induces necrosis and HMGB1 release through mitochondrial ROS production in A549 lung adenocarcinoma cells.	Glucose	54-61	high mobility group box 1	Homo sapiens	98-103
19956840-2	2010	We have previously shown that metabolic stress due to glucose depletion (GD) induces necrosis and HMGB1 release through mitochondrial ROS production in A549 lung adenocarcinoma cells.	ros	134-137	high mobility group box 1	Homo sapiens	98-103
19956840-3	2010	In this study, we examined the effects of hypoxia on GD-induced necrosis and show that hypoxia prevented GD-induced mitochondrial ROS production, HMGB1 release, and necrosis and switched the cell death mode to apoptosis that is dependent on caspase-3 and -9.	Gadolinium	105-107	high mobility group box 1	Homo sapiens	146-151
19657355-6	2010	Release of High Mobility Group Box-1 protein by MBEH-treated melanocytes and ultrastructural features further confirmed a necrotic death pathway mediated by MBEH.	hydroquinone	157-161	high mobility group box 1	Homo sapiens	11-36
20936104-9	2010	Meanwhile, heme could stimulate cultured microglia to release large amounts of HMGB1 whereas Fe(2+/3+) ions failed to stimulate HMGB1 production from microglia.	Heme	11-15	high mobility group box 1	Homo sapiens	79-84
19588230-7	2009	The HMGb1-induced increases of cell proliferation, cell migration, and wound closure were abolished by the MEK inhibitor PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	121-128	high mobility group box 1	Homo sapiens	4-9
19943199-7	2009	Targeting HMGB1 using platinum-containing compounds, ethyl pyruvate or glycyrrhizin has also been used to limit autophagy.	Platinum	22-30	high mobility group box 1	Homo sapiens	10-15
19943199-7	2009	Targeting HMGB1 using platinum-containing compounds, ethyl pyruvate or glycyrrhizin has also been used to limit autophagy.	Glycyrrhizic Acid	71-83	high mobility group box 1	Homo sapiens	10-15
19148928-3	2009	The phorbol myristate acetate-dependent effects of the material chemistry on cell activation and degradation were evaluated by adding reactive oxygen species scavengers, catalase plus superoxide dismutase to MDM and assaying possible markers of MDM activation: esterase activity, acid phosphatase activity, and high molecular weight group box 1 protein (HMGB1).	Tetradecanoylphorbol Acetate	4-29	high mobility group box 1	Homo sapiens	354-359
19148928-6	2009	Secretion of HMGB1 from MDM on HDI431 was higher than MDI; however only secretion from MDM on HDI was inhibited by phorbol myristate acetate.	Tetradecanoylphorbol Acetate	115-140	high mobility group box 1	Homo sapiens	13-18
19148928-7	2009	In MDM on HDI, catalase plus superoxide dismutase reduced intracellular HMGB1 levels +/- phorbol myristate acetate; whereas, catalase, superoxide dismutase plus phorbol myristate acetate increased intracellular HMGB1 in MDM on MDI, suggesting that esterase and HMGB1 are more specific markers of activation than acid phosphatase.	Tetradecanoylphorbol Acetate	161-186	high mobility group box 1	Homo sapiens	211-216
19148928-7	2009	In MDM on HDI, catalase plus superoxide dismutase reduced intracellular HMGB1 levels +/- phorbol myristate acetate; whereas, catalase, superoxide dismutase plus phorbol myristate acetate increased intracellular HMGB1 in MDM on MDI, suggesting that esterase and HMGB1 are more specific markers of activation than acid phosphatase.	Tetradecanoylphorbol Acetate	161-186	high mobility group box 1	Homo sapiens	211-216
19265175-0	2009	Quercetin prevents LPS-induced high-mobility group box 1 release and proinflammatory function.	Quercetin	0-9	high mobility group box 1	Homo sapiens	31-56
19265175-5	2009	Quercetin treatment reduced circulating levels of HMGB1 in animals with established endotoxemia.	Quercetin	0-9	high mobility group box 1	Homo sapiens	50-55
19265175-6	2009	In macrophage cultures, quercetin inhibited release as well as the cytokine activities of HMGB1, including limiting the activation of mitogen-activated protein kinase and NF-kappaB, two signaling pathways that are critical for HMGB1-induced subsequent cytokine release.	Quercetin	24-33	high mobility group box 1	Homo sapiens	90-95
19265175-6	2009	In macrophage cultures, quercetin inhibited release as well as the cytokine activities of HMGB1, including limiting the activation of mitogen-activated protein kinase and NF-kappaB, two signaling pathways that are critical for HMGB1-induced subsequent cytokine release.	Quercetin	24-33	high mobility group box 1	Homo sapiens	227-232
19265175-7	2009	Quercetin and autophagic inhibitor, wortmannin, inhibited LPS-induced type-II microtubule-associated protein 1A/1B-light chain 3 production and aggregation, as well as HMGB1 translocation and release, suggesting a potential association between autophagy and HMGB1 release.	Quercetin	0-9	high mobility group box 1	Homo sapiens	168-173
19265175-7	2009	Quercetin and autophagic inhibitor, wortmannin, inhibited LPS-induced type-II microtubule-associated protein 1A/1B-light chain 3 production and aggregation, as well as HMGB1 translocation and release, suggesting a potential association between autophagy and HMGB1 release.	Quercetin	0-9	high mobility group box 1	Homo sapiens	258-263
19265175-7	2009	Quercetin and autophagic inhibitor, wortmannin, inhibited LPS-induced type-II microtubule-associated protein 1A/1B-light chain 3 production and aggregation, as well as HMGB1 translocation and release, suggesting a potential association between autophagy and HMGB1 release.	Wortmannin	36-46	high mobility group box 1	Homo sapiens	168-173
19265175-7	2009	Quercetin and autophagic inhibitor, wortmannin, inhibited LPS-induced type-II microtubule-associated protein 1A/1B-light chain 3 production and aggregation, as well as HMGB1 translocation and release, suggesting a potential association between autophagy and HMGB1 release.	Wortmannin	36-46	high mobility group box 1	Homo sapiens	258-263
19265175-8	2009	Quercetin delivery, a strategy to pharmacologically inhibit HMGB1 release that is effective at clinically achievable concentrations, now warrants further evaluation in sepsis and other systemic inflammatory disorders.	Quercetin	0-9	high mobility group box 1	Homo sapiens	60-65
19295481-0	2009	Edaravone, a novel free radical scavenger, reduces high-mobility group box 1 and prolongs survival in a neonatal sepsis model.	Edaravone	0-9	high mobility group box 1	Homo sapiens	51-76
19295481-8	2009	In conclusion, edaravone suppressed free radicals, delayed the TNF-alpha surge, and prevented HMGB1 elevation, thereby maintaining MAP and prolonging survival time in a neonatal sepsis CLP model.	Edaravone	15-24	high mobility group box 1	Homo sapiens	94-99
20193282-13	2009	MTT indicated the growth of HMGB1-siRNA group was significantly inhibited than other two groups.	monooxyethylene trimethylolpropane tristearate	0-3	high mobility group box 1	Homo sapiens	28-33
19786828-3	2009	In addition to demonstrating that cisplatin prevents liver damage associated with liver I/R by sequestering HMGB1 inside the nucleus of ischemic cells, cisplatin also alters cell survival signaling through autophagy.	Cisplatin	34-43	high mobility group box 1	Homo sapiens	108-113
19786011-0	2009	Histidine-rich glycoprotein inhibited high mobility group box 1 in complex with heparin-induced angiogenesis in matrigel plug assay.	Heparin	80-87	high mobility group box 1	Homo sapiens	38-63
19786011-3	2009	Additionally, we reported that high mobility group box 1 (HMGB1) in complex with heparin induces angiogenesis; therefore, we examined the effect of HRG on heparin-dependent HMGB1-induced angiogenesis in the present study.	Heparin	81-88	high mobility group box 1	Homo sapiens	58-63
19786011-3	2009	Additionally, we reported that high mobility group box 1 (HMGB1) in complex with heparin induces angiogenesis; therefore, we examined the effect of HRG on heparin-dependent HMGB1-induced angiogenesis in the present study.	Heparin	155-162	high mobility group box 1	Homo sapiens	58-63
19786011-3	2009	Additionally, we reported that high mobility group box 1 (HMGB1) in complex with heparin induces angiogenesis; therefore, we examined the effect of HRG on heparin-dependent HMGB1-induced angiogenesis in the present study.	Heparin	155-162	high mobility group box 1	Homo sapiens	173-178
19786011-4	2009	HRG completely inhibited angiogenesis induced by HMGB1 in complex with heparin.	Heparin	71-78	high mobility group box 1	Homo sapiens	49-54
19786011-5	2009	HRG inhibited the diffusion of a complex of HMGB1 with heparin from matrigel into surrounding tissue.	Heparin	55-62	high mobility group box 1	Homo sapiens	44-49
19786011-6	2009	HRG also competed with HMGB1 for heparin binding in vitro.	Heparin	33-40	high mobility group box 1	Homo sapiens	23-28
19604520-0	2009	Positive association of serum levels of advanced glycation end products and high mobility group box-1 with asymmetric dimethylarginine in nondiabetic chronic kidney disease patients.	dimethylarginine	118-134	high mobility group box 1	Homo sapiens	76-101
20101991-0	2009	[Analysis of the impact of heparin on the affinity of high mobility group box-1 protein and the receptor of advanced glycation end products by surface plasmon resonance technology].	Heparin	27-34	high mobility group box 1	Homo sapiens	54-79
20101991-1	2009	To investigate the affinity constants of heparin with high mobility group protein 1(HMGB1) and HMGB1 with the receptor of advanced glycation end products (RAGE) and to analyze the impact of heparin on the affinity of HMGB1 and RAGE, the standard BIAcore amine coupling chemistry protocol using EDC and NHS was employed for immobilizing.	Heparin	41-48	high mobility group box 1	Homo sapiens	84-89
20101991-3	2009	Binding analysis was used to investigate the impact of heparin on the affinity of HMGB1 and RAGE.	Heparin	55-62	high mobility group box 1	Homo sapiens	82-87
20101991-7	2009	The highest concentration of 10 000 u x L(-1) of heparin in this experiment did not reach the saturation with HMGB1.	Heparin	49-56	high mobility group box 1	Homo sapiens	110-115
20101991-8	2009	After 50 mg x L(-1) of HMGB1 was mixed with heparin of 50, 100, 1 000, 10 000 u x L(-1), the combining amount of HMGB1 and RAGE declined from 100 to 50 RU.	Heparin	44-51	high mobility group box 1	Homo sapiens	23-28
20101991-8	2009	After 50 mg x L(-1) of HMGB1 was mixed with heparin of 50, 100, 1 000, 10 000 u x L(-1), the combining amount of HMGB1 and RAGE declined from 100 to 50 RU.	Heparin	44-51	high mobility group box 1	Homo sapiens	113-118
20101991-10	2009	It was concluded that heparin can combine with HMGB1 and affect the affinity of HMGB1/RAGE.	Heparin	22-29	high mobility group box 1	Homo sapiens	47-52
20101991-10	2009	It was concluded that heparin can combine with HMGB1 and affect the affinity of HMGB1/RAGE.	Heparin	22-29	high mobility group box 1	Homo sapiens	80-85
19604520-11	2009	The present study demonstrated that AGE and sRAGE levels were correlated with each other and that AGEs and HMGB-1 were independently associated with ADMA in nondiabetic CKD patients.	N,N-dimethylarginine	149-153	high mobility group box 1	Homo sapiens	107-113
19751561-2	2009	METHODS: HepG2 cells were cultured, and purified HMGB1 protein was prepared by chromatography on Ni(2+)-NTA Sepharose column under natural conditions with recombinant expression plasmid pET14b-HMGB1.	nickel nitrilotriacetic acid	97-107	high mobility group box 1	Homo sapiens	49-54
19751561-2	2009	METHODS: HepG2 cells were cultured, and purified HMGB1 protein was prepared by chromatography on Ni(2+)-NTA Sepharose column under natural conditions with recombinant expression plasmid pET14b-HMGB1.	Sepharose	108-117	high mobility group box 1	Homo sapiens	49-54
19545550-5	2009	RESULTS: HMGB1 level in USAP group was higher than that in control and SAP group.	usap	24-28	high mobility group box 1	Homo sapiens	9-14
19727205-9	2009	These results suggested that heparin"s anti-inflammatory effects can be partly explained by its blocking of the interaction between HMGB1 or S100A12 and RAGE.	Heparin	29-36	high mobility group box 1	Homo sapiens	132-137
19387923-0	2009	Carbon dioxide, hypoxia and low pH lead to overexpression of c-myc and HMGB-1 oncogenes in neuroblastoma cells.	Carbon Dioxide	0-14	high mobility group box 1	Homo sapiens	71-77
19387923-3	2009	We studied whether exposure to CO (2), hypoxia or acidosis affects the expression of C-MYC and HMGB-1 in neuroblastoma cells.	Carbon Dioxide	31-37	high mobility group box 1	Homo sapiens	95-101
19387923-10	2009	CONCLUSIONS: Exposures mimicking conditions of CO (2) pneumoperitoneum lead to significant overexpression of C-MYC and HMGB-1 in neuroblastoma cells with decreased apoptosis.	Carbon Dioxide	47-53	high mobility group box 1	Homo sapiens	119-125
19506549-3	2009	To simulate the activated state of HMGB1, we mutated serine residues of nuclear localization signals (NLSs) to glutamic acid and performed transfection assays.	Serine	53-59	high mobility group box 1	Homo sapiens	35-40
19506549-6	2009	Concurrent mutations at six serine residues (35, 39, 42, 46, 53, and 181) to glutamic acid induced the nuclear to cytoplasmic transport of HMGB1, which was detected in the culture medium.	Serine	28-34	high mobility group box 1	Homo sapiens	139-144
19506549-6	2009	Concurrent mutations at six serine residues (35, 39, 42, 46, 53, and 181) to glutamic acid induced the nuclear to cytoplasmic transport of HMGB1, which was detected in the culture medium.	Glutamic Acid	77-90	high mobility group box 1	Homo sapiens	139-144
19379716-7	2009	In light of recent observations as well as the good safety profile of minocycline in humans, we propose that minocycline might play a potent neuroprotective role through the inhibition of HMGB1-induced neuronal cell death in cerebral infarction.	Minocycline	109-120	high mobility group box 1	Homo sapiens	188-193
19726280-8	2009	This synergistic effect was significantly inhibited by pretreatment with MAPK signaling kinases inhibitors, especially the p38 MAP kinase inhibitor SB203580, and the cocktail of MAP kinase inhibitors almost totally blocked the expression of these chemokines in HUVECs treated with HMGB1 and LPS.	SB 203580	148-156	high mobility group box 1	Homo sapiens	281-286
19506468-11	2009	These data suggest that HMGB1 and oxidative stress play a role in the pathogenesis of ARDS and that PMX-F treatment may ameliorate increased blood HMGB1 and urinary 8-OHdG levels in patients with ARDS.	pmx-f	100-105	high mobility group box 1	Homo sapiens	147-152
19380828-10	2009	HMGB1 secretion was also induced by the calcium ionophore A23187 and inhibited by the Ca(2+) chelators BAPTA-AM and EGTA.	Calcium	40-47	high mobility group box 1	Homo sapiens	0-5
19401149-0	2009	Native HMGB1 protein inhibits repair of cisplatin-damaged nucleosomes in vitro.	Cisplatin	40-49	high mobility group box 1	Homo sapiens	7-12
19401149-1	2009	The high mobility group box (HMGB) 1 protein, one of the most abundant nuclear non-histone proteins has been known for its inhibitory effect on repair of DNA damaged by the antitumor drug cisplatin.	Cisplatin	188-197	high mobility group box 1	Homo sapiens	4-36
19401149-2	2009	Here, we report the first results that link HMGB1 to repair of cisplatin-treated DNA at nucleosome level.	Cisplatin	63-72	high mobility group box 1	Homo sapiens	44-49
19401149-10	2009	We show that both the repair of cisplatin-damaged nucleosomes and its inhibition by HMGB1 are nucleosome position-dependent events which are accomplished via the acidic tail and modulated by acetylation.	Cisplatin	32-41	high mobility group box 1	Homo sapiens	84-89
18670905-2	2009	Here, we have investigated how the post-synthetic acetylation of HMGB1 affects its interaction with negatively supercoiled DNA by employing monoacetylated at Lys2 protein, isolated from butyrate-treated cells.	Butyrates	186-194	high mobility group box 1	Homo sapiens	65-70
19442462-0	2009	High mobility group box 1 protein enhances polyethylenimine mediated gene delivery in vitro.	Polyethyleneimine	43-59	high mobility group box 1	Homo sapiens	0-25
19442462-7	2009	In MTT assay the results of cell viability suggested lower cytotoxicity for HMGB1/PEI combined carriers.	monooxyethylene trimethylolpropane tristearate	3-6	high mobility group box 1	Homo sapiens	76-81
19380828-0	2009	HMGB1 is phosphorylated by classical protein kinase C and is secreted by a calcium-dependent mechanism.	Calcium	75-82	high mobility group box 1	Homo sapiens	0-5
19380828-4	2009	In this study, we show that HMGB1 is phosphorylated by the classical protein kinase C (cPKC) and is secreted by a calcium-dependent mechanism.	Calcium	114-121	high mobility group box 1	Homo sapiens	28-33
19570774-8	2009	We also showed the killing efficacy of Ad-TK+GCV in human GBM cell lines and GBM primary cultures, which also elicited release of HMGB1.	Ganciclovir	45-48	high mobility group box 1	Homo sapiens	130-135
19811284-8	2009	Moreover, tagging of oxidized cysteine residues by a maleimide moiety linked to polyethylene glycol showed that HMGB1 passively released from primary and secondary necrotic cells was predominantly oxidized.	Cysteine	30-38	high mobility group box 1	Homo sapiens	112-117
19811284-8	2009	Moreover, tagging of oxidized cysteine residues by a maleimide moiety linked to polyethylene glycol showed that HMGB1 passively released from primary and secondary necrotic cells was predominantly oxidized.	maleimide	53-62	high mobility group box 1	Homo sapiens	112-117
19811284-8	2009	Moreover, tagging of oxidized cysteine residues by a maleimide moiety linked to polyethylene glycol showed that HMGB1 passively released from primary and secondary necrotic cells was predominantly oxidized.	Polyethylene Glycols	80-99	high mobility group box 1	Homo sapiens	112-117
19811284-10	2009	In conclusion, HMGB1 undergoes reversible oxidative modifications at cysteine residues during cell death, which may modulate its biological properties.	Cysteine	69-77	high mobility group box 1	Homo sapiens	15-20
19380828-5	2009	For this study, RAW264.7 cells and human peripheral blood monocytes were treated with PI3K inhibitors wortmannin, LY294002, and ZSTK474, resulting in inhibition of LPS-stimulated HMGB1 secretion, whereas inhibitors of NF-kappaB and MAPKs p38 and ERK showed no inhibition.	Wortmannin	102-112	high mobility group box 1	Homo sapiens	179-184
19380828-5	2009	For this study, RAW264.7 cells and human peripheral blood monocytes were treated with PI3K inhibitors wortmannin, LY294002, and ZSTK474, resulting in inhibition of LPS-stimulated HMGB1 secretion, whereas inhibitors of NF-kappaB and MAPKs p38 and ERK showed no inhibition.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	114-122	high mobility group box 1	Homo sapiens	179-184
19380828-10	2009	HMGB1 secretion was also induced by the calcium ionophore A23187 and inhibited by the Ca(2+) chelators BAPTA-AM and EGTA.	Calcimycin	58-64	high mobility group box 1	Homo sapiens	0-5
19380828-10	2009	HMGB1 secretion was also induced by the calcium ionophore A23187 and inhibited by the Ca(2+) chelators BAPTA-AM and EGTA.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	103-111	high mobility group box 1	Homo sapiens	0-5
19380828-10	2009	HMGB1 secretion was also induced by the calcium ionophore A23187 and inhibited by the Ca(2+) chelators BAPTA-AM and EGTA.	Egtazic Acid	116-120	high mobility group box 1	Homo sapiens	0-5
19317908-3	2009	The high mobility group proteins HMGB1 and HMGB2 (HMGB1/2) are highly abundant architectural DNA binding proteins known to promote RAG-mediated synapsis and cleavage of consensus recombination signals in vitro by facilitating RSS binding and bending by the RAG1/2 complex.	RSS	226-229	high mobility group box 1	Homo sapiens	33-38
19372559-2	2009	High-mobility group protein 1 (HMGB1) is a DNA damage sensor responsive to the incorporation of nonnatural nucleosides into DNA; several nuclear and cytosolic proteins are functionally integrated with HMGB1 in the context of DNA damage response.	Nucleosides	107-118	high mobility group box 1	Homo sapiens	31-36
19372559-2	2009	High-mobility group protein 1 (HMGB1) is a DNA damage sensor responsive to the incorporation of nonnatural nucleosides into DNA; several nuclear and cytosolic proteins are functionally integrated with HMGB1 in the context of DNA damage response.	Nucleosides	107-118	high mobility group box 1	Homo sapiens	201-206
19372559-4	2009	Using the cell proliferation assay, we found that knockdown of HMGB1-associated proteins resulted in 8-fold to 50-fold decreased chemosensitivity of A549 cells to cytarabine.	Cytarabine	163-173	high mobility group box 1	Homo sapiens	63-68
19372559-6	2009	Our results dissect the roles of HMGB1-associated proteins in DNA damage response: HMGB1 and HMGB2 facilitate p53 phosphorylation after exposure to genotoxic stress, and PDIA3 has been found essential for H2AX phosphorylation (no gamma-H2AX accumulated after 24-72 hours of incubation with 1 micromol/L of cytarabine in PDIA3 knockdown cells).	Cytarabine	306-316	high mobility group box 1	Homo sapiens	33-38
18715145-4	2009	Forced cytoplasmic overexpression of APE1 profoundly attenuated the upregulation of HMGB1-mediated reactive oxygen species generation, cytokine secretion, and cyclooxygenase-2 expression by primary monocytes and macrophage-like THP-1 cell lines.	Reactive Oxygen Species	99-122	high mobility group box 1	Homo sapiens	84-89
19166815-2	2009	We created mutants at the target sites (lysines 2 and 81) in the tailless HMGB1 modified by the histone acetyltransferase CBP.	Lysine	40-47	high mobility group box 1	Homo sapiens	74-79
19166815-7	2009	In the case of HMGB1DeltaC modified at Lys 2 and Lys 81 prior to PKC treatment background phosphorylation is detected.	Lysine	39-42	high mobility group box 1	Homo sapiens	15-20
19166815-7	2009	In the case of HMGB1DeltaC modified at Lys 2 and Lys 81 prior to PKC treatment background phosphorylation is detected.	Lysine	49-52	high mobility group box 1	Homo sapiens	15-20
19109190-7	2009	We also show that beta-adrenergic receptor activation by catecholamine of macrophages mediates the HS/R-induced release of HMGB1.	Catecholamines	57-70	high mobility group box 1	Homo sapiens	123-128
18515078-5	2008	Results showed that the HMGB1 Mut (102-105), one of the HMGB1 mutants, in which amino acids 102-105 (FFLF) were replaced with two Glys, significantly decreased the full-length HMGB1 protein induced TNF-alpha release in human monocyte cultures.	glys	130-134	high mobility group box 1	Homo sapiens	24-29
18949384-0	2008	Induction of high mobility group box 1 release from serotonin-stimulated human umbilical vein endothelial cells.	Serotonin	52-61	high mobility group box 1	Homo sapiens	13-38
18949384-5	2008	Therefore, we examined whether serotonin (5-HT), a key factor involved in the development of atherosclerosis, induced HMGB1 release in human umbilical vein endothelial cells (HUVECs).	Serotonin	31-40	high mobility group box 1	Homo sapiens	118-123
18949384-7	2008	The p38MAPK inhibitor SB203580 and the 5-HT1B antagonist GR55526 markedly inhibited HMGB1 release from 5-HT-stimulated HUVECs.	SB 203580	22-30	high mobility group box 1	Homo sapiens	84-89
18949384-7	2008	The p38MAPK inhibitor SB203580 and the 5-HT1B antagonist GR55526 markedly inhibited HMGB1 release from 5-HT-stimulated HUVECs.	gr55526	57-64	high mobility group box 1	Homo sapiens	84-89
18949384-11	2008	The PI3-kinase inhibitor LY294002 significantly inhibited VEGF production in HMGB1-stimulated macrophages, while other kinase inhibitors did not.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	25-33	high mobility group box 1	Homo sapiens	77-82
18799030-0	2008	[Role of high mobility group box 1 in adriamycin-induced apoptosis in leukemia K562 cells].	Doxorubicin	38-48	high mobility group box 1	Homo sapiens	9-34
18799030-1	2008	BACKGROUND &amp; OBJECTIVE: High mobility group box l (HMGB1), a nuclear DNA-binding protein, stabilizes the structure and function of chromatin, regulates gene transcription.	Adenosine Monophosphate	12-15	high mobility group box 1	Homo sapiens	55-60
18799030-3	2008	This study was to explore the role of HMGB1 in adriamycin (ADM)-induced apoptosis in leukemia K562 cells.	Doxorubicin	47-57	high mobility group box 1	Homo sapiens	38-43
18799030-3	2008	This study was to explore the role of HMGB1 in adriamycin (ADM)-induced apoptosis in leukemia K562 cells.	Doxorubicin	59-62	high mobility group box 1	Homo sapiens	38-43
18996119-2	2008	We have carried out quantitative investigations of the redox chemistry involving Cys22 and Cys44 of the HMGB1 A-domain, which form an intramolecular disulfide bond.	Disulfides	149-158	high mobility group box 1	Homo sapiens	104-109
19114373-0	2008	[Effect of progesterone on high mobility group Box-1 protein-induced interleukin-6 release by human umbilic vein endothelial cells].	Progesterone	11-23	high mobility group box 1	Homo sapiens	27-52
19114373-2	2008	METHOD: The recombinant expression plasmid pET14b-HMGB1 was constructed and transformed into competent E.coli BL21 cells to obtain HMGB1 protein, which was purified with chromatography on Ni-NTA Sepharose column.	ni-nta	188-194	high mobility group box 1	Homo sapiens	131-136
19114373-2	2008	METHOD: The recombinant expression plasmid pET14b-HMGB1 was constructed and transformed into competent E.coli BL21 cells to obtain HMGB1 protein, which was purified with chromatography on Ni-NTA Sepharose column.	Sepharose	195-204	high mobility group box 1	Homo sapiens	131-136
19114373-5	2008	RESULTS: The IL-6 levels in HUVEC culture medium was slightly decreased after treatment with low-concentration HMGB1 but increased obviously following treatment with high-concentration HMGB1, and these effects could be dose-dependently inhibited by progesterone.	Progesterone	249-261	high mobility group box 1	Homo sapiens	111-116
19114373-5	2008	RESULTS: The IL-6 levels in HUVEC culture medium was slightly decreased after treatment with low-concentration HMGB1 but increased obviously following treatment with high-concentration HMGB1, and these effects could be dose-dependently inhibited by progesterone.	Progesterone	249-261	high mobility group box 1	Homo sapiens	185-190
19114373-7	2008	CONCLUSIONS: Progesterone can dose-dependently inhibit HMGB1-induced IL-6 release from HUVECs, suggesting the protective role of progesterone in endotoxemia.	Progesterone	129-141	high mobility group box 1	Homo sapiens	55-60
18515078-5	2008	Results showed that the HMGB1 Mut (102-105), one of the HMGB1 mutants, in which amino acids 102-105 (FFLF) were replaced with two Glys, significantly decreased the full-length HMGB1 protein induced TNF-alpha release in human monocyte cultures.	glys	130-134	high mobility group box 1	Homo sapiens	56-61
18515078-5	2008	Results showed that the HMGB1 Mut (102-105), one of the HMGB1 mutants, in which amino acids 102-105 (FFLF) were replaced with two Glys, significantly decreased the full-length HMGB1 protein induced TNF-alpha release in human monocyte cultures.	glys	130-134	high mobility group box 1	Homo sapiens	56-61
18682735-5	2008	DNA-protein complexes formed between HMGB1 and radiolabeled hcDNA are analyzed by electrophoresis on nondenaturing polyacrylamide gels using the band-shift assay method.	polyacrylamide	115-129	high mobility group box 1	Homo sapiens	37-42
18682735-6	2008	In addition, using a simple and fast protocol to purify HMGB1 on the basis of its solubility in perchloric acid allowed us to increase the sensitivity by suppressing any nonspecific background.	Perchloric Acid	96-111	high mobility group box 1	Homo sapiens	56-61
19112920-0	2008	[Enhancive effect of HMGB1 gene silence on adriamycin-induced apoptosis in K562/A02 drug resistance leukemia cells].	Doxorubicin	43-53	high mobility group box 1	Homo sapiens	21-26
18715162-5	2008	MSCs exposed to HMGB1 were negative for CD31, CD45, CD80, and HLA-DR, and displayed equal levels of CD73, CD166, and HLA-ABC compared with their counterparts, but HMGB1 profoundly suppressed MSC proliferation in a dose-dependent manner as evaluated by carboxyfluorescein diacetate succinmidyl ester dye dilution assay.	carboxyfluorescein diacetate succinmidyl ester	252-298	high mobility group box 1	Homo sapiens	16-21
18953944-1	2008	OBJECTIVE: To investigate the release and intracellular localization of high mobility group box chromosomal protein 1 (HMGB1) in the peripheral blood monocytes of rheumatoid arthritis (RA) patients and the inhibitive effect of thalidomide.	Thalidomide	227-238	high mobility group box 1	Homo sapiens	119-124
18631454-4	2008	ROS oxidized the potential danger signal high-mobility group box-1 protein (HMGB1) released from dying cells and thereby neutralized its stimulatory activity.	Reactive Oxygen Species	0-3	high mobility group box 1	Homo sapiens	41-66
18631454-4	2008	ROS oxidized the potential danger signal high-mobility group box-1 protein (HMGB1) released from dying cells and thereby neutralized its stimulatory activity.	Reactive Oxygen Species	0-3	high mobility group box 1	Homo sapiens	76-81
18425372-5	2008	While GD induced mostly necrotic death in A549 cells, salicylate suppresssed GD-induced necrosis and HMGB1 release.	Salicylates	54-64	high mobility group box 1	Homo sapiens	101-106
18953944-10	2008	Thalidomide (40 microg/ml) could inhibit the release of HMGB1 in the monocytes from RA patients stimulated with TNFalpha (P &lt; 0.05).	Thalidomide	0-11	high mobility group box 1	Homo sapiens	56-61
18953944-12	2008	Treatment with TNFalpha (100 ng/ml) for 24 hours resulted in a cytoplasmic translocation of HMGB1, which was inhibited significantly by thalidomide.	Thalidomide	136-147	high mobility group box 1	Homo sapiens	92-97
18483013-0	2008	Estradiol 17-beta and progesterone modulate inducible nitric oxide synthase and high mobility group box 1 expression in human endometrium.	Estradiol	0-17	high mobility group box 1	Homo sapiens	80-105
18483013-0	2008	Estradiol 17-beta and progesterone modulate inducible nitric oxide synthase and high mobility group box 1 expression in human endometrium.	Progesterone	22-34	high mobility group box 1	Homo sapiens	80-105
18483013-8	2008	HMGB1 is expressed by human endometrium, and its expression is increased by E2 and decreased by progesterone.	Progesterone	96-108	high mobility group box 1	Homo sapiens	0-5
18483013-9	2008	Incubation with sodium nitroprusside results in a reduction in HMGB1 expression.	Nitroprusside	16-36	high mobility group box 1	Homo sapiens	63-68
18483013-11	2008	HMGB1 is expressed in the human endometrium, and its expression is modulated by E2, progesterone, and nitric oxide.	Progesterone	84-96	high mobility group box 1	Homo sapiens	0-5
18483013-11	2008	HMGB1 is expressed in the human endometrium, and its expression is modulated by E2, progesterone, and nitric oxide.	Nitric Oxide	102-114	high mobility group box 1	Homo sapiens	0-5
18241198-0	2008	A critical role in structure-specific DNA binding for the acetylatable lysine residues in HMGB1.	Lysine	71-77	high mobility group box 1	Homo sapiens	90-95
18241198-1	2008	The structure-specific DNA-binding protein HMGB1 (high-mobility group protein B1) which comprises two tandem HMG boxes (A and B) and an acidic C-terminal tail, is acetylated in vivo at Lys(2) and Lys(11) in the A box.	Lysine	185-188	high mobility group box 1	Homo sapiens	43-48
18241198-1	2008	The structure-specific DNA-binding protein HMGB1 (high-mobility group protein B1) which comprises two tandem HMG boxes (A and B) and an acidic C-terminal tail, is acetylated in vivo at Lys(2) and Lys(11) in the A box.	Lysine	185-188	high mobility group box 1	Homo sapiens	50-80
18241198-1	2008	The structure-specific DNA-binding protein HMGB1 (high-mobility group protein B1) which comprises two tandem HMG boxes (A and B) and an acidic C-terminal tail, is acetylated in vivo at Lys(2) and Lys(11) in the A box.	Lysine	196-199	high mobility group box 1	Homo sapiens	43-48
18241198-1	2008	The structure-specific DNA-binding protein HMGB1 (high-mobility group protein B1) which comprises two tandem HMG boxes (A and B) and an acidic C-terminal tail, is acetylated in vivo at Lys(2) and Lys(11) in the A box.	Lysine	196-199	high mobility group box 1	Homo sapiens	50-80
18241198-8	2008	We conclude that Lys(2) and Lys(11) are critical for binding of the isolated A domain and HMGB1 to distorted DNA substrates.	Lysine	17-20	high mobility group box 1	Homo sapiens	90-95
18241198-8	2008	We conclude that Lys(2) and Lys(11) are critical for binding of the isolated A domain and HMGB1 to distorted DNA substrates.	Lysine	28-31	high mobility group box 1	Homo sapiens	90-95
18953944-13	2008	CONCLUSION: TNFalpha induces the release and cytoplasmic translocation of HMGB1 in the peripheral blood monocytes of RA patients and thalidomide inhibits the release and translocation of HMGB1.	Thalidomide	133-144	high mobility group box 1	Homo sapiens	74-79
18160415-4	2008	In vitro glutathione S-transferase pull-down and in vivo co-immunoprecipitation studies confirmed an interaction between HMGB1 and HNF1alpha.	Glutathione	9-20	high mobility group box 1	Homo sapiens	121-126
18953944-13	2008	CONCLUSION: TNFalpha induces the release and cytoplasmic translocation of HMGB1 in the peripheral blood monocytes of RA patients and thalidomide inhibits the release and translocation of HMGB1.	Thalidomide	133-144	high mobility group box 1	Homo sapiens	187-192
18844116-3	2008	The eukaryotic expression vector carrying human Pgenesil-1/HMGB1 siRNA was constructed and transfected into T3B cells by Lipofectamine 2000 and the positive clones was screened by G418.	Lipofectamine	121-139	high mobility group box 1	Homo sapiens	59-64
18844116-10	2008	The HMGB1 expression of the T3B cells transfected with Pgenesil-1/HMGB1 siRNA was significantly lower than those of the other 2 groups (both P &lt;0.05).	pgenesil-1	55-65	high mobility group box 1	Homo sapiens	4-9
18844116-10	2008	The HMGB1 expression of the T3B cells transfected with Pgenesil-1/HMGB1 siRNA was significantly lower than those of the other 2 groups (both P &lt;0.05).	pgenesil-1	55-65	high mobility group box 1	Homo sapiens	66-71
18380906-5	2008	RESULTS: We show here that single HMG-box domains of HMGB1 stimulate RAG-mediated RSS cleavage in a concentration-dependent manner in the presence of Mn2+, but not Mg2+.	RSS	82-85	high mobility group box 1	Homo sapiens	53-58
18353726-4	2008	It has recently been revealed that the translocation of calreticulin to the plasma membrane in tumor cells and the release of high-mobility-group box 1 (HMGB1) by tumor cells are two key post-transcriptional events required for the immunogenicity of anthracyclines.	Anthracyclines	250-264	high mobility group box 1	Homo sapiens	126-151
18353726-4	2008	It has recently been revealed that the translocation of calreticulin to the plasma membrane in tumor cells and the release of high-mobility-group box 1 (HMGB1) by tumor cells are two key post-transcriptional events required for the immunogenicity of anthracyclines.	Anthracyclines	250-264	high mobility group box 1	Homo sapiens	153-158
18223193-5	2008	The immediate negative inotropic effects of HMGB1 on cell contractility and calcium homeostasis were partially reversible upon washout of HMGB1.	Calcium	76-83	high mobility group box 1	Homo sapiens	44-49
18223193-8	2008	These studies show for the first time that HMGB1 impairs sarcomere shortening by decreasing calcium availability in cardiac myocytes through modulating membrane calcium influx and suggest that HMGB1 maybe acts as a novel myocardial depressant factor during cardiac injury.	Calcium	92-99	high mobility group box 1	Homo sapiens	43-48
18223193-8	2008	These studies show for the first time that HMGB1 impairs sarcomere shortening by decreasing calcium availability in cardiac myocytes through modulating membrane calcium influx and suggest that HMGB1 maybe acts as a novel myocardial depressant factor during cardiac injury.	Calcium	92-99	high mobility group box 1	Homo sapiens	193-198
18223193-8	2008	These studies show for the first time that HMGB1 impairs sarcomere shortening by decreasing calcium availability in cardiac myocytes through modulating membrane calcium influx and suggest that HMGB1 maybe acts as a novel myocardial depressant factor during cardiac injury.	Calcium	161-168	high mobility group box 1	Homo sapiens	43-48
18223193-8	2008	These studies show for the first time that HMGB1 impairs sarcomere shortening by decreasing calcium availability in cardiac myocytes through modulating membrane calcium influx and suggest that HMGB1 maybe acts as a novel myocardial depressant factor during cardiac injury.	Calcium	161-168	high mobility group box 1	Homo sapiens	193-198
18380906-5	2008	RESULTS: We show here that single HMG-box domains of HMGB1 stimulate RAG-mediated RSS cleavage in a concentration-dependent manner in the presence of Mn2+, but not Mg2+.	Manganese(2+)	150-154	high mobility group box 1	Homo sapiens	53-58
18380906-5	2008	RESULTS: We show here that single HMG-box domains of HMGB1 stimulate RAG-mediated RSS cleavage in a concentration-dependent manner in the presence of Mn2+, but not Mg2+.	magnesium ion	164-168	high mobility group box 1	Homo sapiens	53-58
18380906-7	2008	Furthermore, we show that mutant forms of HMGB1 which otherwise fail to stimulate RAG-mediated RSS cleavage in Mg2+ can be substantially rescued when Mg2+ is replaced with Mn2+.	RSS	95-98	high mobility group box 1	Homo sapiens	42-47
18380906-7	2008	Furthermore, we show that mutant forms of HMGB1 which otherwise fail to stimulate RAG-mediated RSS cleavage in Mg2+ can be substantially rescued when Mg2+ is replaced with Mn2+.	magnesium ion	111-115	high mobility group box 1	Homo sapiens	42-47
18380906-7	2008	Furthermore, we show that mutant forms of HMGB1 which otherwise fail to stimulate RAG-mediated RSS cleavage in Mg2+ can be substantially rescued when Mg2+ is replaced with Mn2+.	magnesium ion	150-154	high mobility group box 1	Homo sapiens	42-47
18380906-7	2008	Furthermore, we show that mutant forms of HMGB1 which otherwise fail to stimulate RAG-mediated RSS cleavage in Mg2+ can be substantially rescued when Mg2+ is replaced with Mn2+.	Manganese(2+)	172-176	high mobility group box 1	Homo sapiens	42-47
18380906-9	2008	The observation that single HMG-box domains can promote RAG-mediated 23-RSS cleavage in Mg2+ in the presence, but not absence, of partner RSS suggests that synaptic complex assembly in vitro is associated with conformational changes that alter how the RAG and/or HMGB1 proteins bind and bend DNA in a manner that functionally replaces the role of one of the HMG-box domains in RAG-HMGB1 complexes assembled on a single RSS.	magnesium ion	88-92	high mobility group box 1	Homo sapiens	263-268
18380906-9	2008	The observation that single HMG-box domains can promote RAG-mediated 23-RSS cleavage in Mg2+ in the presence, but not absence, of partner RSS suggests that synaptic complex assembly in vitro is associated with conformational changes that alter how the RAG and/or HMGB1 proteins bind and bend DNA in a manner that functionally replaces the role of one of the HMG-box domains in RAG-HMGB1 complexes assembled on a single RSS.	magnesium ion	88-92	high mobility group box 1	Homo sapiens	381-386
18354232-4	2008	We used ELISA and surface plasmon resonance to show that HMGB1 binds LPS in a concentration-dependent manner and that the binding is stronger to lipid A moiety than to the polysaccharide moiety of LPS.	Lipid A	145-152	high mobility group box 1	Homo sapiens	57-62
18354232-4	2008	We used ELISA and surface plasmon resonance to show that HMGB1 binds LPS in a concentration-dependent manner and that the binding is stronger to lipid A moiety than to the polysaccharide moiety of LPS.	Polysaccharides	172-186	high mobility group box 1	Homo sapiens	57-62
18557992-4	2008	In the previous issue of Arthritis Research &amp; Therapy, Sundberg and colleagues address, for the first time in a prospective cohort study, whether HMGB1 expression is dependent upon tumor necrosis factor activity in patients with RA.	Adenosine Monophosphate	45-48	high mobility group box 1	Homo sapiens	150-155
18090368-10	2008	There was a significant correlation between CSF HMGB1 levels and CSF white blood cell counts and glucose levels in patients with bacterial meningitis.	Glucose	97-104	high mobility group box 1	Homo sapiens	48-53
17979839-7	2007	A TLR4 polymorphism that affects the binding of HMGB1 to TLR4 predicts early relapse after anthracycline-based chemotherapy in breast cancer patients.	Anthracyclines	91-104	high mobility group box 1	Homo sapiens	48-53
17913975-0	2008	Pivotal advance: inhibition of HMGB1 nuclear translocation as a mechanism for the anti-rheumatic effects of gold sodium thiomalate.	Gold Sodium Thiomalate	108-130	high mobility group box 1	Homo sapiens	31-36
17913975-10	2008	Furthermore, gold chloride also inhibited release of HMGB1.	gold chloride	13-26	high mobility group box 1	Homo sapiens	53-58
17667523-6	2007	Rather, we observed that tumor cells incubated with the platinating agent oxaliplatin, retained HMGB1 within the nucleus for significantly longer periods than other agents used at comparable cytotoxic concentrations or even with potent cytolytic cells.	Oxaliplatin	74-85	high mobility group box 1	Homo sapiens	96-101
18049445-4	2007	The "cholinergic anti-inflammatory pathway" mediated by acetylcholine acts by inhibiting the production of tumor necrosis factor, interleukin-1, macrophage migration inhibitory factor, and high mobility group box-1 and suppresses the activation of nuclear factor-kappa B expression.	Acetylcholine	56-69	high mobility group box 1	Homo sapiens	189-214
17984303-0	2007	HMGB1 release induced by liver ischemia involves Toll-like receptor 4 dependent reactive oxygen species production and calcium-mediated signaling.	Reactive Oxygen Species	80-103	high mobility group box 1	Homo sapiens	0-5
17984303-0	2007	HMGB1 release induced by liver ischemia involves Toll-like receptor 4 dependent reactive oxygen species production and calcium-mediated signaling.	Calcium	119-126	high mobility group box 1	Homo sapiens	0-5
17984303-4	2007	HMGB1 release from cultured hepatocytes was found to be an active process regulated by reactive oxygen species (ROS).	Reactive Oxygen Species	87-110	high mobility group box 1	Homo sapiens	0-5
17984303-4	2007	HMGB1 release from cultured hepatocytes was found to be an active process regulated by reactive oxygen species (ROS).	Reactive Oxygen Species	112-115	high mobility group box 1	Homo sapiens	0-5
17984303-7	2007	HMGB1 release induced by oxidative stress was markedly reduced by inhibition of calcium/calmodulin-dependent kinases (CaMKs), a family of proteins involved in a wide range of calcium-linked signaling events.	Calcium	80-87	high mobility group box 1	Homo sapiens	0-5
17984303-9	2007	Collectively, these results demonstrate that hypoxia-induced HMGB1 release by hepatocytes is an active, regulated process that occurs through a mechanism promoted by TLR4-dependent ROS production and downstream CaMK-mediated signaling.	Reactive Oxygen Species	181-184	high mobility group box 1	Homo sapiens	61-66
18073062-11	2007	There were positive correlations between HMGB1 and TBil and negative correlations between HMGB1 and PTA.	tbil	51-55	high mobility group box 1	Homo sapiens	41-46
17885340-8	2007	We observed a relationship between hemodynamic improvement and increase of the serum HMGB-1 levels and between improvement of respiratory functions and increase of the serum 2-AG and PAI-1 levels in septic shock patients treated with DHP-PMX.	dhp-pmx	234-241	high mobility group box 1	Homo sapiens	85-91
17525840-8	2007	A positive correlation was observed between HMGB1 and SOFA score and lactate, and procalcitonin concentrations.	Lactic Acid	69-76	high mobility group box 1	Homo sapiens	44-49
17430886-7	2007	Both full-length HMGB1 and a truncated form of HMGB1 lacking the highly conserved glutamate-rich C-terminal tail can induce macrophage activation and tumor necrosis factor-alpha production.	Glutamic Acid	82-91	high mobility group box 1	Homo sapiens	17-22
17611636-0	2007	Ethyl pyruvate induces necrosis-to-apoptosis switch and inhibits high mobility group box protein 1 release in A549 lung adenocarcinoma cells.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	65-98
17611636-1	2007	Ethyl pyruvate (EP), a stable lipophilic pyruvate derivative, has been shown to exert anti-inflammatory activities through inhibiting the expression of various pro-inflammatory mediators as well as circulating levels of high mobility group box protein 1 (HMGB1) in a variety of in vitro and in vivo model systems.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	220-253
17611636-1	2007	Ethyl pyruvate (EP), a stable lipophilic pyruvate derivative, has been shown to exert anti-inflammatory activities through inhibiting the expression of various pro-inflammatory mediators as well as circulating levels of high mobility group box protein 1 (HMGB1) in a variety of in vitro and in vivo model systems.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	255-260
17611636-1	2007	Ethyl pyruvate (EP), a stable lipophilic pyruvate derivative, has been shown to exert anti-inflammatory activities through inhibiting the expression of various pro-inflammatory mediators as well as circulating levels of high mobility group box protein 1 (HMGB1) in a variety of in vitro and in vivo model systems.	ethyl pyruvate	16-18	high mobility group box 1	Homo sapiens	220-253
17611636-1	2007	Ethyl pyruvate (EP), a stable lipophilic pyruvate derivative, has been shown to exert anti-inflammatory activities through inhibiting the expression of various pro-inflammatory mediators as well as circulating levels of high mobility group box protein 1 (HMGB1) in a variety of in vitro and in vivo model systems.	ethyl pyruvate	16-18	high mobility group box 1	Homo sapiens	255-260
17611636-1	2007	Ethyl pyruvate (EP), a stable lipophilic pyruvate derivative, has been shown to exert anti-inflammatory activities through inhibiting the expression of various pro-inflammatory mediators as well as circulating levels of high mobility group box protein 1 (HMGB1) in a variety of in vitro and in vivo model systems.	Pyruvic Acid	6-14	high mobility group box 1	Homo sapiens	220-253
17611636-1	2007	Ethyl pyruvate (EP), a stable lipophilic pyruvate derivative, has been shown to exert anti-inflammatory activities through inhibiting the expression of various pro-inflammatory mediators as well as circulating levels of high mobility group box protein 1 (HMGB1) in a variety of in vitro and in vivo model systems.	Pyruvic Acid	6-14	high mobility group box 1	Homo sapiens	255-260
17611636-4	2007	Here we show that EP prevented GD-induced necrosis and HMGB1 release and switched the cell death mode to apoptosis through inhibiting GD-induced CuZn superoxide dismutase release and ROS production.	Gadolinium	31-33	high mobility group box 1	Homo sapiens	55-60
17430886-7	2007	Both full-length HMGB1 and a truncated form of HMGB1 lacking the highly conserved glutamate-rich C-terminal tail can induce macrophage activation and tumor necrosis factor-alpha production.	Glutamic Acid	82-91	high mobility group box 1	Homo sapiens	47-52
17430886-8	2007	However, displacement of HMGB1 from the nucleus following PARP activation requires the presence of the glutamate-rich C-terminal tail.	Glutamic Acid	103-112	high mobility group box 1	Homo sapiens	25-30
17515723-3	2007	We investigated the high-mobility group box-1 (HMGB-1) level in septic shock patients treated with DHP-PMX.	dhp-pmx	99-106	high mobility group box 1	Homo sapiens	20-45
17513788-0	2007	Nuclear heat shock protein 72 as a negative regulator of oxidative stress (hydrogen peroxide)-induced HMGB1 cytoplasmic translocation and release.	Hydrogen Peroxide	75-92	high mobility group box 1	Homo sapiens	102-107
17515723-3	2007	We investigated the high-mobility group box-1 (HMGB-1) level in septic shock patients treated with DHP-PMX.	dhp-pmx	99-106	high mobility group box 1	Homo sapiens	47-53
17515723-9	2007	In the E group, only the HMGB-1 levels improved significantly after DHP-PMX.	dhp-pmx	68-75	high mobility group box 1	Homo sapiens	25-31
17515723-10	2007	Present data suggest that the circulation dynamics of septic shock patients can be improved by reducing HMGB-1 levels by using DHP-PMX.	dhp-pmx	127-134	high mobility group box 1	Homo sapiens	104-110
17334246-14	2007	CONCLUSIONS: HMGB1 is elevated in almost all CAP subjects, and higher circulating HMGB1 is associated with mortality.	cap	45-48	high mobility group box 1	Homo sapiens	13-18
17437420-7	2007	The serum HMGB1 level in CSS patients decreased after the steroid therapy, and showed significant positive correlations with several molecules, including soluble interleukin-2 receptor, soluble thrombomodulin, and eosinophil cationic protein in sera.	Steroids	58-65	high mobility group box 1	Homo sapiens	10-15
17697615-13	2007	Inhibitors specific for the JNK (SP600125), MEK (PD98059), and p38 MAPK (SB203580), abrogated HMGB1-induced TNF-alpha secretion.	pyrazolanthrone	33-41	high mobility group box 1	Homo sapiens	94-99
17697615-13	2007	Inhibitors specific for the JNK (SP600125), MEK (PD98059), and p38 MAPK (SB203580), abrogated HMGB1-induced TNF-alpha secretion.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	49-56	high mobility group box 1	Homo sapiens	94-99
17697615-13	2007	Inhibitors specific for the JNK (SP600125), MEK (PD98059), and p38 MAPK (SB203580), abrogated HMGB1-induced TNF-alpha secretion.	SB 203580	73-81	high mobility group box 1	Homo sapiens	94-99
17462578-3	2007	We show that glycyrrhizin, a natural anti-inflammatory and antiviral triterpene in clinical use, inhibits HMGB1 chemoattractant and mitogenic activities, and has a weak inhibitory effect on its intranuclear DNA-binding function.	Glycyrrhizic Acid	13-25	high mobility group box 1	Homo sapiens	106-111
17462578-4	2007	NMR and fluorescence studies indicate that glycyrrhizin binds directly to HMGB1 (K(d) approximately 150 microM), interacting with two shallow concave surfaces formed by the two arms of both HMG boxes.	Glycyrrhizic Acid	43-55	high mobility group box 1	Homo sapiens	74-79
17235565-8	2007	The effect of HMGB-1 was abrogated by RAGE down-regulation by antisense S-oligodeoxynucleic acid.	oligodeoxynucleic acid	74-96	high mobility group box 1	Homo sapiens	14-20
17339485-4	2007	However, several steroid-like pigments (tanshinone I, tanshinone IIA, and cryptotanshinone) of a popular Chinese herb, Danshen (Salvia miltiorrhiza), dose dependently attenuated endotoxin-induced HMGB1 release in macrophage/monocyte cultures.	Steroids	17-24	high mobility group box 1	Homo sapiens	196-201
17339485-4	2007	However, several steroid-like pigments (tanshinone I, tanshinone IIA, and cryptotanshinone) of a popular Chinese herb, Danshen (Salvia miltiorrhiza), dose dependently attenuated endotoxin-induced HMGB1 release in macrophage/monocyte cultures.	cryptotanshinone	74-90	high mobility group box 1	Homo sapiens	196-201
17339485-5	2007	A water-soluble tanshinone IIA sodium sulfonate derivative (TSNIIA-SS), which has been widely used as a Chinese medicine for patients with cardiovascular disorders, selectively abrogated endotoxin-induced HMGB1 cytoplasmic translocation and release in a glucocorticoid receptor-independent manner.	Water	2-7	high mobility group box 1	Homo sapiens	205-210
17339485-5	2007	A water-soluble tanshinone IIA sodium sulfonate derivative (TSNIIA-SS), which has been widely used as a Chinese medicine for patients with cardiovascular disorders, selectively abrogated endotoxin-induced HMGB1 cytoplasmic translocation and release in a glucocorticoid receptor-independent manner.	tanshinone II A sodium sulfonate	16-47	high mobility group box 1	Homo sapiens	205-210
17135572-0	2007	Hydrogen peroxide stimulates macrophages and monocytes to actively release HMGB1.	Hydrogen Peroxide	0-17	high mobility group box 1	Homo sapiens	75-80
17135572-2	2007	Here, we demonstrated that a reactive oxygen species, hydrogen peroxide (H(2)O(2)), induces active and passive HMGB1 release from macrophage and monocyte cultures in a time- and dose-dependent manner.	Reactive Oxygen Species	29-52	high mobility group box 1	Homo sapiens	111-116
17135572-2	2007	Here, we demonstrated that a reactive oxygen species, hydrogen peroxide (H(2)O(2)), induces active and passive HMGB1 release from macrophage and monocyte cultures in a time- and dose-dependent manner.	Hydrogen Peroxide	54-71	high mobility group box 1	Homo sapiens	111-116
17135572-2	2007	Here, we demonstrated that a reactive oxygen species, hydrogen peroxide (H(2)O(2)), induces active and passive HMGB1 release from macrophage and monocyte cultures in a time- and dose-dependent manner.	Hydrogen Peroxide	73-81	high mobility group box 1	Homo sapiens	111-116
17135572-3	2007	At nontoxic doses (e.g., 0.0125-0.125 mM), H(2)O(2) induced HMGB1 cytoplasmic translocation and active release within 3-24 h. At higher concentrations (e.g., 0.25 mM), however, H(2)O(2) exhibited cytotoxicity to macrophage and monocyte cell cultures and consequently, triggered active and passive HMGB1 release.	Hydrogen Peroxide	43-51	high mobility group box 1	Homo sapiens	60-65
17135572-3	2007	At nontoxic doses (e.g., 0.0125-0.125 mM), H(2)O(2) induced HMGB1 cytoplasmic translocation and active release within 3-24 h. At higher concentrations (e.g., 0.25 mM), however, H(2)O(2) exhibited cytotoxicity to macrophage and monocyte cell cultures and consequently, triggered active and passive HMGB1 release.	Hydrogen Peroxide	43-51	high mobility group box 1	Homo sapiens	297-302
17135572-4	2007	In addition, H(2)O(2) stimulated potential interaction of HMGB1 with a nuclear export factor, chromosome region maintenance (CRM1), in macrophage/monocyte cultures.	Hydrogen Peroxide	13-21	high mobility group box 1	Homo sapiens	58-63
17135572-5	2007	Inhibitors specific for the JNK (SP600125) and MEK (PD98059), but not p38 MAPK (SB203580), abrogated H(2)O(2)-induced, active HMGB1 release.	pyrazolanthrone	33-41	high mobility group box 1	Homo sapiens	126-131
17135572-5	2007	Inhibitors specific for the JNK (SP600125) and MEK (PD98059), but not p38 MAPK (SB203580), abrogated H(2)O(2)-induced, active HMGB1 release.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	52-59	high mobility group box 1	Homo sapiens	126-131
17135572-5	2007	Inhibitors specific for the JNK (SP600125) and MEK (PD98059), but not p38 MAPK (SB203580), abrogated H(2)O(2)-induced, active HMGB1 release.	2)o(2)	103-109	high mobility group box 1	Homo sapiens	126-131
17187938-0	2007	Inhibition of HMGB1 by deep ocean water attenuates endotoxin-induced sepsis.	Water	34-39	high mobility group box 1	Homo sapiens	14-19
16968820-7	2007	TRAIL treatment, however, induced HMGB1 release, and it is interesting that this extrinsic pathway-mediated cell death was blocked with the pancaspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone.	Caspase Inhibitor VI	161-211	high mobility group box 1	Homo sapiens	34-39
16980512-3	2007	Mass analyses revealed that recombinant eukaryotic HMGB1 has an intrachain disulphide bond.	disulphide	75-85	high mobility group box 1	Homo sapiens	51-56
16980512-4	2007	In mass analysis of tissue-derived HMGB1, two forms were detected: the carboxyl terminal glutamic acid residue lacking form and a full-length form.	Glutamic Acid	89-102	high mobility group box 1	Homo sapiens	35-40
16980512-5	2007	Cell culture studies indicated that both eukaryotic and bacterial HMGB1 proteins induce TNF-alpha secretion and nitric oxide release from mononuclear cells.	Nitric Oxide	112-124	high mobility group box 1	Homo sapiens	66-71
16980512-7	2007	A soluble proinflammatory substance was separated from the bacterial recombinant HMGB1 by chloroform-methanol treatment.	Chloroform	90-100	high mobility group box 1	Homo sapiens	81-86
16980512-7	2007	A soluble proinflammatory substance was separated from the bacterial recombinant HMGB1 by chloroform-methanol treatment.	Methanol	101-109	high mobility group box 1	Homo sapiens	81-86
17958722-9	2007	Serum NE activities and serum concentrations of IL-1beta, IL-6, and HMGB1 were significantly suppressed in the Sivelestat-treated group.	sivelestat	111-121	high mobility group box 1	Homo sapiens	68-73
17678956-0	2007	The high-mobility group box 1 cytokine induces transporter-mediated release of glutamate from glial subcellular particles (gliosomes) prepared from in situ-matured astrocytes.	Glutamic Acid	79-88	high mobility group box 1	Homo sapiens	4-29
17678956-8	2007	HMGB1-induced release of the stable glutamate analogue [(3)H]d-aspartate and endogenous glutamate form gliosomes, whereas nerve terminals were insensitive to the protein.	Glutamic Acid	36-45	high mobility group box 1	Homo sapiens	0-5
17678956-8	2007	HMGB1-induced release of the stable glutamate analogue [(3)H]d-aspartate and endogenous glutamate form gliosomes, whereas nerve terminals were insensitive to the protein.	Deuterium	8-9	high mobility group box 1	Homo sapiens	0-5
17678956-8	2007	HMGB1-induced release of the stable glutamate analogue [(3)H]d-aspartate and endogenous glutamate form gliosomes, whereas nerve terminals were insensitive to the protein.	Aspartic Acid	63-72	high mobility group box 1	Homo sapiens	0-5
17678956-8	2007	HMGB1-induced release of the stable glutamate analogue [(3)H]d-aspartate and endogenous glutamate form gliosomes, whereas nerve terminals were insensitive to the protein.	Glutamic Acid	88-97	high mobility group box 1	Homo sapiens	0-5
17678956-9	2007	The HMGB1-evoked release of glutamate was independent on modifications of cytosolic Ca(2+) concentration, but it was blocked by dl-threo-beta-benzyloxyaspartate, suggesting the involvement of transporter-mediated release mechanisms.	Glutamic Acid	28-37	high mobility group box 1	Homo sapiens	4-9
17678956-9	2007	The HMGB1-evoked release of glutamate was independent on modifications of cytosolic Ca(2+) concentration, but it was blocked by dl-threo-beta-benzyloxyaspartate, suggesting the involvement of transporter-mediated release mechanisms.	benzyloxyaspartate	128-160	high mobility group box 1	Homo sapiens	4-9
17678956-12	2007	Taken together, these results suggest that the HMGB1 cytokine could act as a modulator of glutamate homeostasis in adult mammalian brain.	Glutamic Acid	90-99	high mobility group box 1	Homo sapiens	47-52
17636313-5	2007	Although HMGB1 stimulates ATP hydrolysis by topo IIalpha, the DNA cleavage is much more enhanced.	Adenosine Triphosphate	26-29	high mobility group box 1	Homo sapiens	9-14
16842881-6	2006	The potential use of PAMAM-Arg was demonstrated by efficient gene knock-down by transfecting HMGB1 shRNA-expressing plasmid.	pamam-arg	21-30	high mobility group box 1	Homo sapiens	93-98
18066803-0	2007	Bent oligonucleotide duplexes as HMGB1 inhibitors: a comparative study.	Oligonucleotides	5-20	high mobility group box 1	Homo sapiens	33-38
18066803-1	2007	In this work we explore the ability of a chimeric LNA/DNA bent duplex, in which the kink is induced by 2 unpaired adenines in the middle of one strand, to bind HMGB1, a protein involved in many inflammatory processes.	Adenine	114-122	high mobility group box 1	Homo sapiens	160-165
16855214-7	2006	Results of these experiments indicate that HMGB1 appears in the media of apoptotic Jurkat cells in a time-dependent manner and that this release can be reduced by Z-VAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	163-172	high mobility group box 1	Homo sapiens	43-48
17114460-5	2006	Phosphorylation of HMGB1 was detected by metabolic labeling and Western blot analysis after treatments with TNF-alpha and okadaic acid, a phosphatase inhibitor.	Okadaic Acid	122-134	high mobility group box 1	Homo sapiens	19-24
17114460-8	2006	We mutated serine residues of either or both NLSs of HMGB1 to glutamic acid to simulate a phosphorylated state and examined the binding of HMGB1 to karyopherin-alpha1, which was identified as the nuclear import protein for HMGB1 in this study.	Serine	11-17	high mobility group box 1	Homo sapiens	53-58
17114460-8	2006	We mutated serine residues of either or both NLSs of HMGB1 to glutamic acid to simulate a phosphorylated state and examined the binding of HMGB1 to karyopherin-alpha1, which was identified as the nuclear import protein for HMGB1 in this study.	Glutamic Acid	62-75	high mobility group box 1	Homo sapiens	53-58
16911580-10	2006	These results suggest that the HMGB1 cytokine could act as a modulator of glutamate homeostasis in adult mammal brain.	Glutamic Acid	74-83	high mobility group box 1	Homo sapiens	31-36
16732569-0	2006	The effect of manganese(II) on the structure of DNA/HMGB1/H1 complexes: electronic and vibrational circular dichroism studies.	Manganese(2+)	14-27	high mobility group box 1	Homo sapiens	52-57
16732569-1	2006	The interactions were studied of DNA with the nonhistone chromatin protein HMGB1 and histone H1 in the presence of manganese(II) ions at different protein to DNA and manganese to DNA phosphate ratios by using absorption and optical activity spectroscopy in the electronic [ultraviolet (UV) and electronic circular dichroism ECD)] and vibrational [infrared (IR) and vibrational circular dichroism (VCD)] regions.	Manganese(2+)	115-128	high mobility group box 1	Homo sapiens	75-80
16732569-3	2006	At the same time, the presence of HMGB1 and H1 also changed the mode of interaction of Mn2+ with DNA, which now takes place mostly in the major groove of DNA involving N7(G), whereas interactions between Mn2+ and DNA phosphate groups are weakened by histone molecules.	Manganese(2+)	87-91	high mobility group box 1	Homo sapiens	34-39
16732569-3	2006	At the same time, the presence of HMGB1 and H1 also changed the mode of interaction of Mn2+ with DNA, which now takes place mostly in the major groove of DNA involving N7(G), whereas interactions between Mn2+ and DNA phosphate groups are weakened by histone molecules.	Manganese(2+)	204-208	high mobility group box 1	Homo sapiens	34-39
16732569-3	2006	At the same time, the presence of HMGB1 and H1 also changed the mode of interaction of Mn2+ with DNA, which now takes place mostly in the major groove of DNA involving N7(G), whereas interactions between Mn2+ and DNA phosphate groups are weakened by histone molecules.	Phosphates	217-226	high mobility group box 1	Homo sapiens	34-39
17060403-6	2006	However, cultured SMCs actively secrete HMGB1 after cholesterol loading.	Cholesterol	52-63	high mobility group box 1	Homo sapiens	40-45
17079940-8	2006	Serum HMGB1 levels were significantly positively correlated with lactate dehydrogenase, C-reactive protein, and total bilirubin.	Bilirubin	118-127	high mobility group box 1	Homo sapiens	6-11
16814517-3	2006	Ethyl pyruvate specifically inhibits tumor necrosis factor-alpha production and decreases circulating levels of high-mobility group box-1 and nuclear factor-kappaB signaling pathways by specifically targeting its p65 subunit in animals with established endotoxemia or sepsis and in macrophage cultures.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	112-137
16842881-7	2006	The numbers of green fluorescent protein (GFP)-positive and HMGB1-negative cells indicated that PAMAM-Arg/shRNA-expressing plasmid complex suppressed target gene expression in over 40% of cells, which is the highest level achieved to date in primary cortical culture by any gene carrier.	Poly(amidoamine)	96-101	high mobility group box 1	Homo sapiens	60-65
16842881-7	2006	The numbers of green fluorescent protein (GFP)-positive and HMGB1-negative cells indicated that PAMAM-Arg/shRNA-expressing plasmid complex suppressed target gene expression in over 40% of cells, which is the highest level achieved to date in primary cortical culture by any gene carrier.	Arginine	102-105	high mobility group box 1	Homo sapiens	60-65
16807371-0	2006	Activation of sPLA2-IIA and PGE2 production by high mobility group protein B1 in vascular smooth muscle cells sensitized by IL-1beta.	Dinoprostone	28-32	high mobility group box 1	Homo sapiens	47-77
16807371-7	2006	The present study investigates the role of HMGB1 in the activation of sPLA2-IIA expression and PGE2 production in VSMCs.	Dinoprostone	95-99	high mobility group box 1	Homo sapiens	43-48
16807371-8	2006	Recombinant HMGB1 slightly activated the sPLA2-IIA, COX-2, and mPGES-1 genes but dramatically stimulated these genes in VSMCs that had been incubated with the proinflammatory cytokine IL-1beta for 24 h. This effect was accompanied by significantly increased PGE2 release.	Dinoprostone	258-262	high mobility group box 1	Homo sapiens	12-17
16282196-0	2006	HMGB1 is secreted by immunostimulated enterocytes and contributes to cytomix-induced hyperpermeability of Caco-2 monolayers.	caco-2	106-112	high mobility group box 1	Homo sapiens	0-5
16775128-6	2006	HMGB1 was found to accumulate in NMDA-treated primary cortical culture media, and supernatants collected from these cultures were found to trigger microglia activation, the hallmark of brain inflammation.	N-Methylaspartate	33-37	high mobility group box 1	Homo sapiens	0-5
16641887-1	2006	Pyruvic acid, an intermediate metabolite of glucose, an effective scavenger of reactive oxygen species (ROS), inhibits tumor necrosis factor-alpha production and NF-kappaB signaling pathways, reduces circulating levels of HMGB1 (high mobility group B1), decreases COX-2 (cyclo-oxygenase-2), iNOS (inducible nitric oxide synthase), and IL-6 (interleukin-6) mRNA expression in liver, ileal mucosa, and colonic mucosa in animal models with endotoxemia.	Pyruvic Acid	0-12	high mobility group box 1	Homo sapiens	222-227
16641887-1	2006	Pyruvic acid, an intermediate metabolite of glucose, an effective scavenger of reactive oxygen species (ROS), inhibits tumor necrosis factor-alpha production and NF-kappaB signaling pathways, reduces circulating levels of HMGB1 (high mobility group B1), decreases COX-2 (cyclo-oxygenase-2), iNOS (inducible nitric oxide synthase), and IL-6 (interleukin-6) mRNA expression in liver, ileal mucosa, and colonic mucosa in animal models with endotoxemia.	Pyruvic Acid	0-12	high mobility group box 1	Homo sapiens	229-251
16641887-1	2006	Pyruvic acid, an intermediate metabolite of glucose, an effective scavenger of reactive oxygen species (ROS), inhibits tumor necrosis factor-alpha production and NF-kappaB signaling pathways, reduces circulating levels of HMGB1 (high mobility group B1), decreases COX-2 (cyclo-oxygenase-2), iNOS (inducible nitric oxide synthase), and IL-6 (interleukin-6) mRNA expression in liver, ileal mucosa, and colonic mucosa in animal models with endotoxemia.	Glucose	44-51	high mobility group box 1	Homo sapiens	222-227
16641887-1	2006	Pyruvic acid, an intermediate metabolite of glucose, an effective scavenger of reactive oxygen species (ROS), inhibits tumor necrosis factor-alpha production and NF-kappaB signaling pathways, reduces circulating levels of HMGB1 (high mobility group B1), decreases COX-2 (cyclo-oxygenase-2), iNOS (inducible nitric oxide synthase), and IL-6 (interleukin-6) mRNA expression in liver, ileal mucosa, and colonic mucosa in animal models with endotoxemia.	Glucose	44-51	high mobility group box 1	Homo sapiens	229-251
16354107-6	2006	In contrast, IL-1 stimulates the release of the immunological adjuvant high mobility group box 1 protein (HMGB1; a biochemical maker of necrosis) in a nitric oxide-dependent manner, while apoptosis inducers fail to stimulate HMGB1 release.	Nitric Oxide	151-163	high mobility group box 1	Homo sapiens	71-96
16697213-5	2006	Dexamethasone, a known inhibitor of NF-kappaB signaling in U1 cells, inhibited HMGB1-induced stimulation of the viral production.	Dexamethasone	0-13	high mobility group box 1	Homo sapiens	79-84
16403427-5	2006	Recombinant Sbp1p modified by Hmt1p in vivo were isolated by affinity chromatography followed by electrophoresis on a polyacrylamide gel and subjected to acid hydrolysis.	polyacrylamide	118-132	high mobility group box 1	Homo sapiens	12-17
16354107-6	2006	In contrast, IL-1 stimulates the release of the immunological adjuvant high mobility group box 1 protein (HMGB1; a biochemical maker of necrosis) in a nitric oxide-dependent manner, while apoptosis inducers fail to stimulate HMGB1 release.	Nitric Oxide	151-163	high mobility group box 1	Homo sapiens	106-111
15994314-5	2005	To identify determinants of HMGB1 required for stimulation of RAG-mediated RSS binding and cleavage, we prepared an extensive panel of mutant HMGB1 proteins and tested their ability to augment RAG-mediated RSS binding and cleavage activity.	RSS	75-78	high mobility group box 1	Homo sapiens	28-33
15912505-6	2005	Histone H1 facilitated binding of HMGB1 to DNA by interacting with the negatively charged groups of the sugar-phosphate backbone and binding of aspartic and glutamic amino acid residues of HMGB1.	Sugar Phosphates	104-119	high mobility group box 1	Homo sapiens	34-39
15912505-6	2005	Histone H1 facilitated binding of HMGB1 to DNA by interacting with the negatively charged groups of the sugar-phosphate backbone and binding of aspartic and glutamic amino acid residues of HMGB1.	aspartic	144-152	high mobility group box 1	Homo sapiens	34-39
15912505-6	2005	Histone H1 facilitated binding of HMGB1 to DNA by interacting with the negatively charged groups of the sugar-phosphate backbone and binding of aspartic and glutamic amino acid residues of HMGB1.	aspartic	144-152	high mobility group box 1	Homo sapiens	189-194
15912505-6	2005	Histone H1 facilitated binding of HMGB1 to DNA by interacting with the negatively charged groups of the sugar-phosphate backbone and binding of aspartic and glutamic amino acid residues of HMGB1.	glutamic amino acid	157-176	high mobility group box 1	Homo sapiens	34-39
15912505-6	2005	Histone H1 facilitated binding of HMGB1 to DNA by interacting with the negatively charged groups of the sugar-phosphate backbone and binding of aspartic and glutamic amino acid residues of HMGB1.	glutamic amino acid	157-176	high mobility group box 1	Homo sapiens	189-194
15922304-2	2005	The domain A of HMGB1 (HMGB1a protein) binds to the adduct formed by the R enantiomer at the CGGA sequence with a similar high affinity as it does to the adduct of antitumor cisplatin, and to the adduct formed by the S enantiomer with a slightly lower affinity.	Cisplatin	174-183	high mobility group box 1	Homo sapiens	16-21
16040616-4	2005	In vitro glutathione S-transferase pull-down and in vivo coimmunoprecipitation studies confirmed an interaction between HMGB1 and both SREBP-1 and -2.	Glutathione	9-20	high mobility group box 1	Homo sapiens	120-125
15823048-0	2005	The inhibitory effect of HMGB-1 protein on the repair of cisplatin-damaged DNA is accomplished through the acidic domain.	Cisplatin	57-66	high mobility group box 1	Homo sapiens	25-31
15823048-5	2005	These findings strongly suggest that the HMGB-1-induced inhibition of cisplatin-DNA adduct repair is accomplished through the acidic domain.	Cisplatin	70-79	high mobility group box 1	Homo sapiens	41-47
15687351-0	2005	Suppression of HMGB1 release by stearoyl lysophosphatidylcholine:an additional mechanism for its therapeutic effects in experimental sepsis.	stearoyl alpha-lysolecithin	32-64	high mobility group box 1	Homo sapiens	15-20
15687351-2	2005	Here, we demonstrate that stearoyl LPC, but not caproyl LPC, significantly attenuates circulating high-mobility group box 1 (HMGB1) levels in endotoxemia and sepsis by suppressing endotoxin-induced HMGB1 release from macrophages/monocytes.	stearoyl alpha-lysolecithin	26-38	high mobility group box 1	Homo sapiens	98-123
15687351-2	2005	Here, we demonstrate that stearoyl LPC, but not caproyl LPC, significantly attenuates circulating high-mobility group box 1 (HMGB1) levels in endotoxemia and sepsis by suppressing endotoxin-induced HMGB1 release from macrophages/monocytes.	stearoyl alpha-lysolecithin	26-38	high mobility group box 1	Homo sapiens	125-130
15687351-2	2005	Here, we demonstrate that stearoyl LPC, but not caproyl LPC, significantly attenuates circulating high-mobility group box 1 (HMGB1) levels in endotoxemia and sepsis by suppressing endotoxin-induced HMGB1 release from macrophages/monocytes.	stearoyl alpha-lysolecithin	26-38	high mobility group box 1	Homo sapiens	198-203
15687351-2	2005	Here, we demonstrate that stearoyl LPC, but not caproyl LPC, significantly attenuates circulating high-mobility group box 1 (HMGB1) levels in endotoxemia and sepsis by suppressing endotoxin-induced HMGB1 release from macrophages/monocytes.	Lysophosphatidylcholines	35-38	high mobility group box 1	Homo sapiens	98-123
15687351-2	2005	Here, we demonstrate that stearoyl LPC, but not caproyl LPC, significantly attenuates circulating high-mobility group box 1 (HMGB1) levels in endotoxemia and sepsis by suppressing endotoxin-induced HMGB1 release from macrophages/monocytes.	Lysophosphatidylcholines	35-38	high mobility group box 1	Homo sapiens	125-130
15687351-2	2005	Here, we demonstrate that stearoyl LPC, but not caproyl LPC, significantly attenuates circulating high-mobility group box 1 (HMGB1) levels in endotoxemia and sepsis by suppressing endotoxin-induced HMGB1 release from macrophages/monocytes.	Lysophosphatidylcholines	35-38	high mobility group box 1	Homo sapiens	198-203
15687351-4	2005	Thus, stearoyl LPC confers protection against lethal experimental sepsis partly by facilitating the elimination of the invading pathogens and partly by inhibiting endotoxin-induced release of a late proinflammatory cytokine, HMGB1.	stearoyl alpha-lysolecithin	6-18	high mobility group box 1	Homo sapiens	225-230
15502843-2	2004	Here we report that the neurotransmitter acetylcholine inhibits HMGB1 release from human macrophages by signaling through a nicotinic acetylcholine receptor.	Acetylcholine	41-54	high mobility group box 1	Homo sapiens	64-69
15943034-3	2005	Production of IL-15 and/or TGF-alpha was also associated with amphoterin mRNA expression in colon cancer tissues with TAM depletion in both Dukes" B and C tumors (P = 0.0167 and P = 0.0062, respectively).	tam	118-121	high mobility group box 1	Homo sapiens	62-72
15584967-5	2004	A nuclear relocation of HMGB1 to the cytoplasm was seen at 4 h. Subsequently, high amounts of HMGB1 could be seen in the supernatants from stimulated cells after 16 h. It was also observed that the pro-inflammatory activity of HMGB1 is sensitive to dexamethasone.	Dexamethasone	249-262	high mobility group box 1	Homo sapiens	24-29
15584967-5	2004	A nuclear relocation of HMGB1 to the cytoplasm was seen at 4 h. Subsequently, high amounts of HMGB1 could be seen in the supernatants from stimulated cells after 16 h. It was also observed that the pro-inflammatory activity of HMGB1 is sensitive to dexamethasone.	Dexamethasone	249-262	high mobility group box 1	Homo sapiens	94-99
15584967-5	2004	A nuclear relocation of HMGB1 to the cytoplasm was seen at 4 h. Subsequently, high amounts of HMGB1 could be seen in the supernatants from stimulated cells after 16 h. It was also observed that the pro-inflammatory activity of HMGB1 is sensitive to dexamethasone.	Dexamethasone	249-262	high mobility group box 1	Homo sapiens	94-99
15584967-6	2004	Interestingly, the HMGB1-induced TNF-alpha release from monocytes could be inhibited by either the A-box of the protein or the p38 inhibitor CNI-1493, but neither had any inhibitory effects on the HMGB1-dependent upregulation of cell-adhesion molecules on HUVEC.	semapimod	141-149	high mobility group box 1	Homo sapiens	19-24
15743787-5	2005	The number of PMA-U937 cells was markedly decreased by co-culture with WiDr cells exposed to HMGB1/amphoterin sense S-oligodeoxynucleotide (ODN) in spheroids or monolayers.	Oligodeoxyribonucleotides	116-138	high mobility group box 1	Homo sapiens	99-109
15743787-5	2005	The number of PMA-U937 cells was markedly decreased by co-culture with WiDr cells exposed to HMGB1/amphoterin sense S-oligodeoxynucleotide (ODN) in spheroids or monolayers.	Oligodeoxyribonucleotides	140-143	high mobility group box 1	Homo sapiens	99-109
15743787-8	2005	Recombinant human HMGB1/amphoterin induced growth inhibition in thioglycollate-induced rat peritoneal macrophages, PMA-U937 cells, and human alveolar macrophages, an effect that was abrogated by absorption with anti-HMGB1 antibody.	Thioglycolates	64-78	high mobility group box 1	Homo sapiens	18-23
15743787-8	2005	Recombinant human HMGB1/amphoterin induced growth inhibition in thioglycollate-induced rat peritoneal macrophages, PMA-U937 cells, and human alveolar macrophages, an effect that was abrogated by absorption with anti-HMGB1 antibody.	Thioglycolates	64-78	high mobility group box 1	Homo sapiens	24-34
15743787-8	2005	Recombinant human HMGB1/amphoterin induced growth inhibition in thioglycollate-induced rat peritoneal macrophages, PMA-U937 cells, and human alveolar macrophages, an effect that was abrogated by absorption with anti-HMGB1 antibody.	Thioglycolates	64-78	high mobility group box 1	Homo sapiens	216-221
15672453-6	2005	Moreover, a group of downregulated genes, with corresponding disappearing proteins (HSP90, 14-3-3 protein, HMGB1) in two-dimensional polyacrylamide gel electrophoresis (2-D PAGE), are good candidates for use as biomarkers of uranium effects.	polyacrylamide	133-147	high mobility group box 1	Homo sapiens	107-112
15612592-0	2004	[The structure of the complexes of DNA with non-histone chromosomal protein HMGB1 in the presence of manganese ions].	Manganese	101-110	high mobility group box 1	Homo sapiens	76-81
15612592-1	2004	The complexes of DNA - HMGB1 protein - manganese ions have been studied using circular dichroism (CD) technique.	Manganese	39-48	high mobility group box 1	Homo sapiens	23-28
15612592-5	2004	The presence of Mn2+ ions prevents formation of the ordered supramolecular structures specific for the HMGB1-DNA complexes.	Manganese(2+)	16-20	high mobility group box 1	Homo sapiens	103-108
15612592-9	2004	Moreover, the changes in local DNA structure induced by manganese ions promote the appearance of new HMGB1 binding sites on the DNA double helix.	Manganese	56-65	high mobility group box 1	Homo sapiens	101-106
15612592-13	2004	Thus, structural changes of the DNA double helix in the three-component DNA-HMGB1-Mn2+ complexes come as a result of the combined and interdependent interactions of DNA with Mn2+ ions and the molecules of HMGB1.	Manganese(2+)	82-86	high mobility group box 1	Homo sapiens	76-81
15612592-13	2004	Thus, structural changes of the DNA double helix in the three-component DNA-HMGB1-Mn2+ complexes come as a result of the combined and interdependent interactions of DNA with Mn2+ ions and the molecules of HMGB1.	Manganese(2+)	82-86	high mobility group box 1	Homo sapiens	205-210
15612592-13	2004	Thus, structural changes of the DNA double helix in the three-component DNA-HMGB1-Mn2+ complexes come as a result of the combined and interdependent interactions of DNA with Mn2+ ions and the molecules of HMGB1.	Manganese(2+)	174-178	high mobility group box 1	Homo sapiens	76-81
15612592-13	2004	Thus, structural changes of the DNA double helix in the three-component DNA-HMGB1-Mn2+ complexes come as a result of the combined and interdependent interactions of DNA with Mn2+ ions and the molecules of HMGB1.	Manganese(2+)	174-178	high mobility group box 1	Homo sapiens	205-210
15502843-3	2004	Nicotine, a selective cholinergic agonist, is more efficient than acetylcholine and inhibits HMGB1 release induced by either endotoxin or tumor necrosis factor-alpha (TNF-alpha).	Nicotine	0-8	high mobility group box 1	Homo sapiens	93-98
15502843-5	2004	In vivo, treatment with nicotine attenuates serum HMGB1 levels and improves survival in experimental models of sepsis, even when treatment is started after the onset of the disease.	Nicotine	24-32	high mobility group box 1	Homo sapiens	50-55
15502843-6	2004	These results reveal acetylcholine as the first known physiological inhibitor of HMGB1 release from human macrophages and suggest that selective nicotinic agonists for the alpha7nAChR might have therapeutic potential for the treatment of sepsis.	Acetylcholine	21-34	high mobility group box 1	Homo sapiens	81-86
15130941-6	2004	Amphoterin was secreted from phorbol ester and interferon-gamma (IFN-gamma)-activated macrophages, and the secretion was inhibited by blocking the adenosine 5"-triphosphate (ATP)-binding cassette transporter-1, a member of the multidrug resistance protein family.	Phorbol Esters	29-42	high mobility group box 1	Homo sapiens	0-10
15469275-8	2004	Combining the (1)H-PRE data with the crystal structure of the HMGB-1 A-box/cisplatin-modified DNA complex allows one to obtain a semiquantitative estimate of the equilibrium populations at the various sites.	Cisplatin	75-84	high mobility group box 1	Homo sapiens	62-68
15130941-6	2004	Amphoterin was secreted from phorbol ester and interferon-gamma (IFN-gamma)-activated macrophages, and the secretion was inhibited by blocking the adenosine 5"-triphosphate (ATP)-binding cassette transporter-1, a member of the multidrug resistance protein family.	Adenosine Triphosphate	147-172	high mobility group box 1	Homo sapiens	0-10
15130941-6	2004	Amphoterin was secreted from phorbol ester and interferon-gamma (IFN-gamma)-activated macrophages, and the secretion was inhibited by blocking the adenosine 5"-triphosphate (ATP)-binding cassette transporter-1, a member of the multidrug resistance protein family.	Adenosine Triphosphate	174-177	high mobility group box 1	Homo sapiens	0-10
15170359-1	2004	We have recently observed that chromatin architectural protein HMGB1 (previously reported to be involved in numerous biological processes such as DNA replication, recombination, repair, tumor growth, and metastasis) could bind with extremely high affinity (K(d) &lt; 1 pM) to a novel DNA structure that forms a DNA loop maintained at its base by a hemicatenane (hcDNA).	hemicatenane	348-360	high mobility group box 1	Homo sapiens	63-68
15274644-5	2004	Transcription stimulation assays using acidic C-tail deletion mutants showed that the five amino acid residues at the C-terminal end of HMGB1, a DDDDE sequence, are essential for the stimulation.	dddde	145-150	high mobility group box 1	Homo sapiens	136-141
15274644-6	2004	The DDDDE sequence was also required for the preferential binding of HMGB1 to nucleosome linker DNA, which is a cognate HMGB1 binding site in chromatin.	dddde	4-9	high mobility group box 1	Homo sapiens	69-74
15274644-6	2004	The DDDDE sequence was also required for the preferential binding of HMGB1 to nucleosome linker DNA, which is a cognate HMGB1 binding site in chromatin.	dddde	4-9	high mobility group box 1	Homo sapiens	120-125
15274644-8	2004	These results strongly suggest that the interaction between the DDDDE sequence of HMGB1 and the H3 N-tail is a key factor for the transcription stimulation by HMGB1 as well as the preferential binding of HMGB1 to chromatin.	dddde	64-69	high mobility group box 1	Homo sapiens	82-87
15274644-8	2004	These results strongly suggest that the interaction between the DDDDE sequence of HMGB1 and the H3 N-tail is a key factor for the transcription stimulation by HMGB1 as well as the preferential binding of HMGB1 to chromatin.	dddde	64-69	high mobility group box 1	Homo sapiens	159-164
15274644-8	2004	These results strongly suggest that the interaction between the DDDDE sequence of HMGB1 and the H3 N-tail is a key factor for the transcription stimulation by HMGB1 as well as the preferential binding of HMGB1 to chromatin.	dddde	64-69	high mobility group box 1	Homo sapiens	159-164
14550538-4	2003	We propose to classify HMGB1 into a new group of proteins unrelated structurally to chemokines but having chemokine-like functions, and to name this class CLF (chemokine-like functions).	Chlorine fluoride	155-158	high mobility group box 1	Homo sapiens	23-28
15146429-9	2004	After treatment with high-dose prednisolone, cytoplasmic and extracellular HMGB-1 expression was significantly reduced, coinciding mainly with a decreased number of infiltrating inflammatory cells.	Prednisolone	31-43	high mobility group box 1	Homo sapiens	75-81
15161015-1	2004	BACKGROUND: The human high mobility group protein B1 (HMGB1) has attracted considerable interest among oncologists because it sensitises cancer cells to the anticancer drug cisplatin by shielding cisplatin-DNA adducts from nucleotide excision repair.	Cisplatin	173-182	high mobility group box 1	Homo sapiens	22-52
15161015-1	2004	BACKGROUND: The human high mobility group protein B1 (HMGB1) has attracted considerable interest among oncologists because it sensitises cancer cells to the anticancer drug cisplatin by shielding cisplatin-DNA adducts from nucleotide excision repair.	Cisplatin	173-182	high mobility group box 1	Homo sapiens	54-59
15161015-1	2004	BACKGROUND: The human high mobility group protein B1 (HMGB1) has attracted considerable interest among oncologists because it sensitises cancer cells to the anticancer drug cisplatin by shielding cisplatin-DNA adducts from nucleotide excision repair.	Cisplatin	196-205	high mobility group box 1	Homo sapiens	22-52
15161015-1	2004	BACKGROUND: The human high mobility group protein B1 (HMGB1) has attracted considerable interest among oncologists because it sensitises cancer cells to the anticancer drug cisplatin by shielding cisplatin-DNA adducts from nucleotide excision repair.	Cisplatin	196-205	high mobility group box 1	Homo sapiens	54-59
14759813-8	2004	When combined with hyperactive transposons and transiently overexpressed HMGB1, a cellular cofactor of SB transposition, hyperactive transposases elevate transposition by almost an order of magnitude compared to the first-generation transposon system.	Antimony	103-105	high mobility group box 1	Homo sapiens	73-78
14999020-5	2004	The multiprotein complex including HMGB1 showed ATP hydrolysis and ATP-dependent chromatin structural modulation activities that increased the susceptibility of chromatin to MNase digestion, while HMGB1 alone had no such activity.	Adenosine Triphosphate	67-70	high mobility group box 1	Homo sapiens	35-40
15051925-9	2004	Infiltration of PMA-treated U937 monocytes through the KM12SM cell layer was increased by pretreatment of KM12SM cells with amphoterin antisense S-oligodeoxynucleotide exposure.	Oligodeoxyribonucleotides	147-167	high mobility group box 1	Homo sapiens	124-134
14632258-4	2004	Multiple transposase binding sites within the terminal inverted repeats, a transpositional enhancer sequence, unequal affinity of the transposase to the binding sites and the activity of the cellular HMGB1 protein all contribute to a highly regulated assembly of SB synaptic complexes, which is likely a requirement for the subsequent catalytic steps.	Antimony	263-265	high mobility group box 1	Homo sapiens	200-205
14999020-0	2004	ATP-dependent chromatin structural modulation by multiprotein complex including HMGB1.	Adenosine Triphosphate	0-3	high mobility group box 1	Homo sapiens	80-85
14999020-5	2004	The multiprotein complex including HMGB1 showed ATP hydrolysis and ATP-dependent chromatin structural modulation activities that increased the susceptibility of chromatin to MNase digestion, while HMGB1 alone had no such activity.	Adenosine Triphosphate	48-51	high mobility group box 1	Homo sapiens	35-40
14534709-7	2003	The in vitro invasive capacity of PC-3, a prostatic cancer cell line that co-expressed amphoterin and RAGE, was suppressed by treatment with amphoterin antisense S-oligodeoxynucleotide (ODN).	Oligodeoxyribonucleotides	162-184	high mobility group box 1	Homo sapiens	87-97
14534709-7	2003	The in vitro invasive capacity of PC-3, a prostatic cancer cell line that co-expressed amphoterin and RAGE, was suppressed by treatment with amphoterin antisense S-oligodeoxynucleotide (ODN).	Oligodeoxyribonucleotides	162-184	high mobility group box 1	Homo sapiens	141-151
14534709-7	2003	The in vitro invasive capacity of PC-3, a prostatic cancer cell line that co-expressed amphoterin and RAGE, was suppressed by treatment with amphoterin antisense S-oligodeoxynucleotide (ODN).	Oligodeoxyribonucleotides	186-189	high mobility group box 1	Homo sapiens	87-97
14534709-7	2003	The in vitro invasive capacity of PC-3, a prostatic cancer cell line that co-expressed amphoterin and RAGE, was suppressed by treatment with amphoterin antisense S-oligodeoxynucleotide (ODN).	Oligodeoxyribonucleotides	186-189	high mobility group box 1	Homo sapiens	141-151
14534709-9	2003	The conditioned medium of human prostatic stromal cells deprived of androgen recovered the in vitro invasive capacity of PC-3 cells suppressed by amphoterin antisense S-ODN.	Oligodeoxyribonucleotides	167-172	high mobility group box 1	Homo sapiens	146-156
12646658-6	2003	AG490, a specific inhibitor for Janus kinase 2 of the IFN-gamma signaling pathway, dose-dependently attenuated IFN-gamma-induced HMGB1 release.	alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide	0-5	high mobility group box 1	Homo sapiens	129-134
12887690-0	2003	Regulation of expression of sulfoglucuronyl carbohydrate (HNK-1), Amphoterin and RAGE in retinoic acid-differentiated P19 embryonal carcinoma cells.	Tretinoin	89-102	high mobility group box 1	Homo sapiens	66-76
12887690-10	2003	RA also upregulated the synthesis of Amphoterin and RAGE in P19 cells.	Tretinoin	0-2	high mobility group box 1	Homo sapiens	37-47
12759333-4	2003	In a functional yeast survival screen designed to select new anti-apoptotic mammalian genes, we have identified the chromosomal high-mobility group box-1 protein (HMGB1) as an inhibitor of yeast cell death induced by the pro-apoptotic Bcl-2 family member Bak.	bakuchiol	255-258	high mobility group box 1	Homo sapiens	128-153
12759333-4	2003	In a functional yeast survival screen designed to select new anti-apoptotic mammalian genes, we have identified the chromosomal high-mobility group box-1 protein (HMGB1) as an inhibitor of yeast cell death induced by the pro-apoptotic Bcl-2 family member Bak.	bakuchiol	255-258	high mobility group box 1	Homo sapiens	163-168
12614161-0	2003	Nature of full-length HMGB1 binding to cisplatin-modified DNA.	Cisplatin	39-48	high mobility group box 1	Homo sapiens	22-27
12614161-1	2003	HMGB1, a highly conserved non-histone DNA-binding protein, interacts with specific DNA structural motifs such as those encountered at cisplatin damage, four-way junctions, and supercoils.	Cisplatin	134-143	high mobility group box 1	Homo sapiens	0-5
12614161-2	2003	The interaction of full-length HMGB1, containing two tandem HMG box domains and a C-terminal acidic tail, with cisplatin-modified DNA was investigated by hydroxyl radical footprinting and electrophoretic gel mobility shift assays.	Cisplatin	111-120	high mobility group box 1	Homo sapiens	31-36
12614161-4	2003	Site-directed mutagenesis of intercalating residues in both HMG domains A and B in full-length HMGB1 further supports the conclusion that only one HMG box domain is bound to the site of cisplatin damage.	Cisplatin	186-195	high mobility group box 1	Homo sapiens	95-100
12614161-7	2003	These results illuminate the respective roles of the tandem HMG boxes and the C-terminal acidic tail of HMGB1 in binding to DNA and to the major DNA adducts formed by the anticancer drug cisplatin.	Cisplatin	187-196	high mobility group box 1	Homo sapiens	104-109
12450412-7	2002	In the presence of protein HMGB1, shifted reassociation of the strands of DNA fragments containing a tract of the poly(CA).poly(TG) microsatellite leads to the formation of DNA loops maintained at their base by a hemicatenated junction located within the repetitive sequence.	poly(tg)	123-131	high mobility group box 1	Homo sapiens	27-32
12534292-10	2003	In addition, the monofunctional adducts of trans-[PtCl(2)(NH(3))(thiazole)] are recognized by HMGB1 domain proteins and removed by the nucleotide excision repair system similarly as the 1,2-GG intrastrand CL of cisplatin.	ptcl(2)(nh(3))	50-64	high mobility group box 1	Homo sapiens	94-99
12534292-10	2003	In addition, the monofunctional adducts of trans-[PtCl(2)(NH(3))(thiazole)] are recognized by HMGB1 domain proteins and removed by the nucleotide excision repair system similarly as the 1,2-GG intrastrand CL of cisplatin.	Thiazoles	65-73	high mobility group box 1	Homo sapiens	94-99
12534292-10	2003	In addition, the monofunctional adducts of trans-[PtCl(2)(NH(3))(thiazole)] are recognized by HMGB1 domain proteins and removed by the nucleotide excision repair system similarly as the 1,2-GG intrastrand CL of cisplatin.	1,2-gg	186-192	high mobility group box 1	Homo sapiens	94-99
12534292-10	2003	In addition, the monofunctional adducts of trans-[PtCl(2)(NH(3))(thiazole)] are recognized by HMGB1 domain proteins and removed by the nucleotide excision repair system similarly as the 1,2-GG intrastrand CL of cisplatin.	Cisplatin	211-220	high mobility group box 1	Homo sapiens	94-99
12517784-0	2003	A nuclear protein complex containing high mobility group proteins B1 and B2, heat shock cognate protein 70, ERp60, and glyceraldehyde-3-phosphate dehydrogenase is involved in the cytotoxic response to DNA modified by incorporation of anticancer nucleoside analogues.	Nucleosides	245-255	high mobility group box 1	Homo sapiens	37-106
12517784-6	2003	These findings indicate that the HMGB1-HMGB2-HSC70-ERp60-glyceraldehyde 3-phosphate dehydrogenase complex detects changes in DNA structure caused by incorporation of nonnatural nucleosides and is a determinant of cell sensitivity to such DNA modifying chemotherapy.	Nucleosides	177-188	high mobility group box 1	Homo sapiens	33-38
12468716-1	2002	Using a cloned single domain of the high mobility group protein 1 (HMGB1), we evaluated the effect of introducing metal binding site(s) on protein stability and function.	Metals	114-119	high mobility group box 1	Homo sapiens	67-72
12231511-5	2002	However, in keeping with their respective role of early and late inflammatory factors, IL-1beta and HMGB1 respond at different times to different stimuli: IL-1beta secretion is induced earlier by ATP, autocrinally released by monocytes soon after activation; HMGB1 secretion is triggered by lysophosphatidylcholine, generated later in the inflammation site.	Adenosine Triphosphate	196-199	high mobility group box 1	Homo sapiens	100-105
12231511-5	2002	However, in keeping with their respective role of early and late inflammatory factors, IL-1beta and HMGB1 respond at different times to different stimuli: IL-1beta secretion is induced earlier by ATP, autocrinally released by monocytes soon after activation; HMGB1 secretion is triggered by lysophosphatidylcholine, generated later in the inflammation site.	Lysophosphatidylcholines	291-314	high mobility group box 1	Homo sapiens	100-105
12006575-1	2002	Previously, we and others reported that the high mobility group proteins, HMGB-1/-2, enhance DNA binding in vitro and transactivation in situ by the steroid hormone subgroup of nuclear receptors but did not influence these functions of class II receptors.	Steroids	149-164	high mobility group box 1	Homo sapiens	74-83
12358771-1	2002	Sulfoglucuronyl carbohydrate (SGC), reactive with antibody against human natural killer cell antigen, is expressed in several glycolipids, glycoproteins and proteoglycans of the nervous system and has been implicated in cell-cell recognition, neurite outgrowth and neuronal migration during development, through its interaction with SGC-binding protein (SBP) 1.	sulfoglucuronyl carbohydrate	0-28	high mobility group box 1	Homo sapiens	333-360
12006575-2	2002	We show here that the DNA binding domain (DBD) is sufficient to account for the selective influence of HMGB-1/-2 on the steroid class of receptors.	Steroids	120-127	high mobility group box 1	Homo sapiens	103-112
12006575-4	2002	HMGB-1/-2 interact directly with the DBDs of steroid but not class II receptors, and this interaction requires the CTE.	4,4'-dibenzamido-2,2'-stilbenedisulfonic acid	37-41	high mobility group box 1	Homo sapiens	0-9
12006575-4	2002	HMGB-1/-2 interact directly with the DBDs of steroid but not class II receptors, and this interaction requires the CTE.	Steroids	45-52	high mobility group box 1	Homo sapiens	0-9
12006575-4	2002	HMGB-1/-2 interact directly with the DBDs of steroid but not class II receptors, and this interaction requires the CTE.	1,1,1-trifluoro-2-chloroethane	115-118	high mobility group box 1	Homo sapiens	0-9
12006575-5	2002	This in vitro interaction correlates with a requirement of the CTE for maximal HMGB-1/-2 enhancement of DNA binding in vitro and transcriptional activation in cells.	1,1,1-trifluoro-2-chloroethane	63-66	high mobility group box 1	Homo sapiens	79-88
12031669-2	2002	Electrophoretic mobility shift assays show that domains A and B of HMGB1 protein bind to (2R,3R)-diaminobutanedichloroplatinum(II)-generated crosslinks with a higher affinity than to those generated by (2S,3S)-diaminobutanedichloroplatinum(II).	(2r,3r)-diaminobutanedichloroplatinum	89-126	high mobility group box 1	Homo sapiens	67-72
12031669-2	2002	Electrophoretic mobility shift assays show that domains A and B of HMGB1 protein bind to (2R,3R)-diaminobutanedichloroplatinum(II)-generated crosslinks with a higher affinity than to those generated by (2S,3S)-diaminobutanedichloroplatinum(II).	(2s,3s)-diaminobutanedichloroplatinum	202-239	high mobility group box 1	Homo sapiens	67-72
10652254-4	2000	A role for amphoterin in extracellular matrix-dependent cell regulation is further suggested by the finding that specific decrease of amphoterin mRNA and protein, using antisense oligonucleotides transfected into cells, inhibits cell migration to laminin in a transfilter assay whereas the oligonucleotides in the culture medium have no effect.	Oligonucleotides	179-195	high mobility group box 1	Homo sapiens	134-144
11953450-0	2002	N -Glycans on the receptor for advanced glycation end products influence amphoterin binding and neurite outgrowth.	n -glycans	0-10	high mobility group box 1	Homo sapiens	73-83
11953450-1	2002	In this study we show that embryonic neurite growth-promoting protein amphoterin binds to carboxylated N -glycans previously identified on mammalian endothelial cells.	n -glycans	103-113	high mobility group box 1	Homo sapiens	70-80
11953450-2	2002	Since amphoterin is a ligand for the receptor for advanced glycation end products (RAGE), and the ligand-binding V-domain of the receptor contains two potential N -glycosylation sites, we hypothesized that N -glycans on RAGE may mediate its interactions with amphoterin.	Nitrogen	161-162	high mobility group box 1	Homo sapiens	6-16
11953450-2	2002	Since amphoterin is a ligand for the receptor for advanced glycation end products (RAGE), and the ligand-binding V-domain of the receptor contains two potential N -glycosylation sites, we hypothesized that N -glycans on RAGE may mediate its interactions with amphoterin.	n -glycans	206-216	high mobility group box 1	Homo sapiens	6-16
11953450-2	2002	Since amphoterin is a ligand for the receptor for advanced glycation end products (RAGE), and the ligand-binding V-domain of the receptor contains two potential N -glycosylation sites, we hypothesized that N -glycans on RAGE may mediate its interactions with amphoterin.	n -glycans	206-216	high mobility group box 1	Homo sapiens	259-269
11953450-4	2002	The binding potential of amphoterin to RAGE decreases significantly in presence of soluble carboxylated glycans or when the receptor is deglycosylated.	Polysaccharides	104-111	high mobility group box 1	Homo sapiens	25-35
11953450-9	2002	These results indicate that carboxylated N -glycans on RAGE play an important functional role in amphoterin-RAGE-mediated signalling.	n -glycans	41-51	high mobility group box 1	Homo sapiens	97-107
11514569-3	2001	Electrophoretic mobility shift assays show that both the A and B domains of HMGB1 as well as TBP discriminate between different platinum-DNA adducts.	Platinum	128-136	high mobility group box 1	Homo sapiens	76-81
11514569-4	2001	HMGB1 domain A is the most sensitive to the nature of the spectator ligands on platinum.	Platinum	79-87	high mobility group box 1	Homo sapiens	0-5
11514569-7	2001	The effects of HMGB1 overexpression in a BG-1 ovarian cancer cell line, induced by steroid hormones, on the sensitivity of cells treated with [Pt(1R,2R-diaminocyclohexane)Cl(2)] and cis-[Pt(NH(3))(cyclohexylamine)Cl(2)] were also examined.	Steroids	83-99	high mobility group box 1	Homo sapiens	15-20
11514569-7	2001	The effects of HMGB1 overexpression in a BG-1 ovarian cancer cell line, induced by steroid hormones, on the sensitivity of cells treated with [Pt(1R,2R-diaminocyclohexane)Cl(2)] and cis-[Pt(NH(3))(cyclohexylamine)Cl(2)] were also examined.	pt(1r,2r-diaminocyclohexane)cl(2)	143-176	high mobility group box 1	Homo sapiens	15-20
11514569-8	2001	The results suggest that HMGB1 protein levels influence the cellular processing of cis-[Pt(NH(3))- (cyclohexylamine)](2+), but not [Pt((1R,2R)-diaminocyclohexane)](2+), DNA lesions.	pt(nh(3))- (cyclohexylamine)	88-116	high mobility group box 1	Homo sapiens	25-30
11154118-9	2000	Resting platelets treated with PGI2 and forskolin bound to immobilised recombinant amphoterin independently of divalent cations.	Epoprostenol	31-35	high mobility group box 1	Homo sapiens	83-93
11154118-9	2000	Resting platelets treated with PGI2 and forskolin bound to immobilised recombinant amphoterin independently of divalent cations.	Colforsin	40-49	high mobility group box 1	Homo sapiens	83-93
11154118-11	2000	Amphoterin-binding protein components on the platelet surface were not identified, but amphoterin bound to phosphatidylserine and sulfatide in lipid binding assays.	Phosphatidylserines	107-125	high mobility group box 1	Homo sapiens	87-97
11154118-11	2000	Amphoterin-binding protein components on the platelet surface were not identified, but amphoterin bound to phosphatidylserine and sulfatide in lipid binding assays.	Sulfoglycosphingolipids	130-139	high mobility group box 1	Homo sapiens	87-97
11154118-13	2000	Interaction of amphoterin with the platelet surface may be mediated by sulfoglycolipids and phospholipids.	sulfoglycolipids	71-87	high mobility group box 1	Homo sapiens	15-25
11154118-13	2000	Interaction of amphoterin with the platelet surface may be mediated by sulfoglycolipids and phospholipids.	Phospholipids	92-105	high mobility group box 1	Homo sapiens	15-25
11739380-4	2002	In this study we have investigated a possible role of RAGE and amphoterin in the retinoic acid-induced differentiation of neuroblastoma cells.	Tretinoin	81-94	high mobility group box 1	Homo sapiens	63-73
11513603-2	2001	HMGB1 consists of 2 DNA binding domains, the HMG boxes A and B, followed by a short basic region and a continuous stretch of 30 glutamate or aspartate residues.	Glutamic Acid	128-137	high mobility group box 1	Homo sapiens	0-5
11513603-2	2001	HMGB1 consists of 2 DNA binding domains, the HMG boxes A and B, followed by a short basic region and a continuous stretch of 30 glutamate or aspartate residues.	Aspartic Acid	141-150	high mobility group box 1	Homo sapiens	0-5
10652254-4	2000	A role for amphoterin in extracellular matrix-dependent cell regulation is further suggested by the finding that specific decrease of amphoterin mRNA and protein, using antisense oligonucleotides transfected into cells, inhibits cell migration to laminin in a transfilter assay whereas the oligonucleotides in the culture medium have no effect.	Oligonucleotides	290-306	high mobility group box 1	Homo sapiens	134-144
9507007-6	1998	The chondroitin sulfate chains on neurocan and phosphacan account for at least 80% of their binding to amphoterin and HB-GAM.	Chondroitin Sulfates	4-23	high mobility group box 1	Homo sapiens	103-113
1909331-3	1991	Since the NH2-terminal part of amphoterin is exceptionally rich in lysine residues, we have studied its interactions with plasminogen and tissue plasminogen activator (t-PA).	Lysine	67-73	high mobility group box 1	Homo sapiens	31-41
9398056-6	1997	RA stimulated the association of t-PA with the external cell membrane surface, which could be inhibited by heparin sulphate but not by mannose sugars or chelators of divalent cations, consistent with a role for amphoterin.	Tretinoin	0-2	high mobility group box 1	Homo sapiens	211-221
9504913-0	1998	The identification of cDNAs that affect the mitosis-to-interphase transition in Schizosaccharomyces pombe, including sbp1, which encodes a spi1p-GTP-binding protein.	Guanosine Triphosphate	145-148	high mobility group box 1	Homo sapiens	117-121
1909331-5	1991	In purified systems, both t-PA and plasminogen bound to immobilized amphoterin, and their binding was inhibited by the lysine analogue epsilon-aminocaproic acid.	Lysine	119-125	high mobility group box 1	Homo sapiens	68-78
1909331-5	1991	In purified systems, both t-PA and plasminogen bound to immobilized amphoterin, and their binding was inhibited by the lysine analogue epsilon-aminocaproic acid.	Aminocaproic Acid	135-160	high mobility group box 1	Homo sapiens	68-78
1909331-9	1991	The results indicate that t-PA and plasminogen form through their lysine-binding sites a complex with amphoterin, which results in acceleration of plasminogen activation and effective degradation of amphoterin.	Lysine	66-72	high mobility group box 1	Homo sapiens	102-112
1909331-9	1991	The results indicate that t-PA and plasminogen form through their lysine-binding sites a complex with amphoterin, which results in acceleration of plasminogen activation and effective degradation of amphoterin.	Lysine	66-72	high mobility group box 1	Homo sapiens	199-209
33799527-4	2021	In our study, we found that the novel topoisomerase I inhibitor lipotecan (TLC388) can elicit immunogenic cell death (ICD) to release damage-associated molecular patterns (DAMPs), including HMGB1, ANXA1, and CRT exposure.	TLC 388	64-73	high mobility group box 1	Homo sapiens	190-195
33773396-2	2021	COVID-19 disease severity is correlated with heightened inflammatory responses, and HMGB1 is an important extracellular mediator in inflammation processes.In this study, we evaluated the effect of HMGB1 inhibitor Glycyrrhizin on the cellular perturbations in lung cells expressing SARS-CoV-2 viral proteins.	Glycyrrhizic Acid	213-225	high mobility group box 1	Homo sapiens	197-202
33777021-10	2021	Pretreatment with necrostatin-1 significantly reduced the expression of RIP1, RIP3 and MLKL as well as PGAM5, DRP1 and HMGB1, which subsequently led to obvious attenuation of hepatic inflammation and damage.	necrostatin-1	18-31	high mobility group box 1	Homo sapiens	119-124
33799527-4	2021	In our study, we found that the novel topoisomerase I inhibitor lipotecan (TLC388) can elicit immunogenic cell death (ICD) to release damage-associated molecular patterns (DAMPs), including HMGB1, ANXA1, and CRT exposure.	TLC 388	75-81	high mobility group box 1	Homo sapiens	190-195
34808298-12	2022	It was found that ZJP has a down-regulating effect on inflammatory reaction and could inhibit the relative mRNA and protein expression of JMJD2B/COX-2/VEGF axis and HMGB1/NF-kappaB signaling pathway in vivo and in vitro, including JMJD2B, COX-2, VEGF, VEGFR1, and VEGFR2, which in turn reduced the damage of gastric mucosal cells.	zjp	18-21	high mobility group box 1	Homo sapiens	165-170
33817244-6	2020	The binding relationship between miR-204-5p and LINC00704 or HMGB1 was predicted by LncBase Predicted v.2 or TargetScan, respectively, and then validated by dual luciferase reporter assay.	mir-204-5p	33-43	high mobility group box 1	Homo sapiens	61-66
33817244-10	2020	Meanwhile, miR-204-5p overexpression repressed proliferation, migration, and invasion by targeting HMGB1.	mir-204-5p	11-21	high mobility group box 1	Homo sapiens	99-104
33822516-8	2021	After cells were co-transfected with pcDNA-HMGB1 and pc-DNA-ctrl, we investigated apoptosis and autophagy in miR-451 overexpressed cells perturbed by exogenous HMGB1 through MTT, flow cytometry, and Western blot.	monooxyethylene trimethylolpropane tristearate	174-177	high mobility group box 1	Homo sapiens	160-165
25489880-12	2015	Immunofluorescence showed enhanced reactive astrocytes, microglial activation, and HMGB1 expression localized to the injured cortex of TBI/alcohol as compared to TBI/air animals.	Alcohols	139-146	high mobility group box 1	Homo sapiens	83-88
22895517-5	2012	Stimulation by hydrogen peroxide, or the TLR4 ligands recombinant human high-mobility group protein B1 or lipopolysaccharide, induced PTX3 expression in the Mile Sven 1 endothelial cell line and in primary renal endothelial cells, suggesting that endothelial PTX3 was induced by pathways involving TLR4 and reactive oxygen species.	Reactive Oxygen Species	307-330	high mobility group box 1	Homo sapiens	72-102
34808298-13	2022	CONCLUSIONS: The results suggested that ZJP exerts therapeutic effects on H. pylori-induced CAG by inhibiting the JMJD2B/COX-2/VEGF axis and HMGB1/NF-kappaB signaling pathway.	zjp	40-43	high mobility group box 1	Homo sapiens	141-146
34427852-5	2022	Our results showed that GA significantly attenuated LPS-induced ALI and decreased the production of inflammatory factors, including IL-1beta, MCP-1, COX2, HMGB1, and adhesion molecules, such as E-selectin, VCAM-1, and modulated expression of angiotensin-converting enzyme 2 (ACE2).	Glycyrrhizic Acid	24-26	high mobility group box 1	Homo sapiens	155-160
34973275-0	2022	miR-142-3p simultaneously targets HMGA1, HMGA2, HMGB1, and HMGB3 and inhibits tumorigenic properties and in-vivo metastatic potential of human cervical cancer cells.	mir-142-3p	0-10	high mobility group box 1	Homo sapiens	48-53
34363018-0	2022	Lactate promotes macrophage HMGB1 lactylation, acetylation, and exosomal release in polymicrobial sepsis.	Lactic Acid	0-7	high mobility group box 1	Homo sapiens	28-33
34971702-5	2022	Interestingly, inhibition of HMGB1 secretion by ethyl pyruvate (EP) enhanced viral propagation while silencing of HMGB1 resulted in abrogated viral replication in DENV-2 infected A549 cells.	ethyl pyruvate	48-62	high mobility group box 1	Homo sapiens	29-34
34971702-5	2022	Interestingly, inhibition of HMGB1 secretion by ethyl pyruvate (EP) enhanced viral propagation while silencing of HMGB1 resulted in abrogated viral replication in DENV-2 infected A549 cells.	ethyl pyruvate	64-66	high mobility group box 1	Homo sapiens	29-34
34363018-2	2022	However, it is unclear whether lactate could promote HMGB1 release during sepsis.	Lactic Acid	31-38	high mobility group box 1	Homo sapiens	53-58
34363018-3	2022	The present study demonstrated a novel role of lactate in HMGB1 lactylation and acetylation in macrophages during polymicrobial sepsis.	Lactic Acid	47-54	high mobility group box 1	Homo sapiens	58-63
34363018-4	2022	We found that macrophages can uptake extracellular lactate via monocarboxylate transporters (MCTs) to promote HMGB1 lactylation via a p300/CBP-dependent mechanism.	Lactic Acid	51-58	high mobility group box 1	Homo sapiens	110-115
34363018-5	2022	We also observed that lactate stimulates HMGB1 acetylation by Hippo/YAP-mediated suppression of deacetylase SIRT1 and beta-arrestin2-mediated recruitment of acetylases p300/CBP to the nucleus via G protein-coupled receptor 81 (GPR81).	Lactic Acid	22-29	high mobility group box 1	Homo sapiens	41-46
34363018-7	2022	In vivo reduction of lactate production and/or inhibition of GPR81-mediated signaling decreases circulating exosomal HMGB1 levels and improves survival outcome in polymicrobial sepsis.	Lactic Acid	21-28	high mobility group box 1	Homo sapiens	117-122
34696918-7	2022	Treatment with H2O2 + VD decreased gene/protein expression of NLRP1, NLRP3, caspase-1, HMGB1, IL-1beta, TNF-alpha and IL-18 in PE and NT explants with H2O2.	Hydrogen Peroxide	15-19	high mobility group box 1	Homo sapiens	87-92
34696918-7	2022	Treatment with H2O2 + VD decreased gene/protein expression of NLRP1, NLRP3, caspase-1, HMGB1, IL-1beta, TNF-alpha and IL-18 in PE and NT explants with H2O2.	Hydrogen Peroxide	151-155	high mobility group box 1	Homo sapiens	87-92
34696918-6	2022	Placental explants from NT cultured with H2O2 showed increased gene and protein expression of NLRP1, NLRP3, caspase-1, IL-1beta, TNF-alpha and HMGB1, while H2O2 was also able to increase TNF-alpha and caspase-1 gene expression in PE.	Hydrogen Peroxide	41-45	high mobility group box 1	Homo sapiens	143-148
34934826-2	2021	Glycyrrhizin (GL), a traditional Chinese medicine for liver disease, binds to HMGB1, thereby inhibits tissue injury.	Glycyrrhizic Acid	0-12	high mobility group box 1	Homo sapiens	78-83
34933679-3	2021	However, the mechanism how extracellular HMGB1 acts on AL cells and leads to chemoresistance remains elusive.	Aluminum	55-57	high mobility group box 1	Homo sapiens	41-46
34916485-0	2021	An RNA-RNA crosstalk network involving HMGB1 and RICTOR facilitates hepatocellular carcinoma tumorigenesis by promoting glutamine metabolism and impedes immunotherapy by PD-L1+ exosomes activity.	Glutamine	120-129	high mobility group box 1	Homo sapiens	39-44
34916485-8	2021	Mechanistically, the HMGB1-driven RNA-RNA crosstalk network facilitated HCC cell glutamine metabolism via dual mechanisms, activating a positive feedback loop involving mTORC2-AKT-C-MYC to upregulate glutamine synthetase (GS) expression, and inducing mTORC1 signaling to derepress SIRT4 on glutamate dehydrogenase (GDH).	Glutamine	81-90	high mobility group box 1	Homo sapiens	21-26
34906140-11	2021	CONCLUSION: Wogonin alleviated the inflammation and apoptosis in LPS-induced A549 cells by SIRT1-mediated HMGB1 deacetylation, which might represent the identification of a novel mechanism by which wogonin exerts protective effects on ALI and provide ideas for the application of wogonin to ALI treatment.	wogonin	12-19	high mobility group box 1	Homo sapiens	106-111
34906140-11	2021	CONCLUSION: Wogonin alleviated the inflammation and apoptosis in LPS-induced A549 cells by SIRT1-mediated HMGB1 deacetylation, which might represent the identification of a novel mechanism by which wogonin exerts protective effects on ALI and provide ideas for the application of wogonin to ALI treatment.	wogonin	198-205	high mobility group box 1	Homo sapiens	106-111
34966671-4	2021	The High-Mobility Group Box 1 (HMGB1) is a multifunctional protein involved in intrinsic resistance to cisplatin.	Cisplatin	103-112	high mobility group box 1	Homo sapiens	4-29
34966671-4	2021	The High-Mobility Group Box 1 (HMGB1) is a multifunctional protein involved in intrinsic resistance to cisplatin.	Cisplatin	103-112	high mobility group box 1	Homo sapiens	31-36
34966671-5	2021	HMGB1 is released when cytotoxic agents, such as cisplatin, induce cell death.	Cisplatin	49-58	high mobility group box 1	Homo sapiens	0-5
34966671-9	2021	Subcellular localization of HMGB1 was detected in the cell lines and in viable cells after a single exposure to cisplatin, which are designated as cisplatin-persistent cells.	Cisplatin	112-121	high mobility group box 1	Homo sapiens	28-33
34966671-9	2021	Subcellular localization of HMGB1 was detected in the cell lines and in viable cells after a single exposure to cisplatin, which are designated as cisplatin-persistent cells.	Cisplatin	147-156	high mobility group box 1	Homo sapiens	28-33
34966671-12	2021	Cisplatin-susceptible lung adenocarcinoma cell lines died by apoptosis or necrosis and released HMGB1.	Cisplatin	0-9	high mobility group box 1	Homo sapiens	96-101
34966671-13	2021	In cisplatin-persistent cells, nuclear relocalization of HMGB1 and overexpression of HMGB1 and RAGE, but not TLR-2 or TLR-4, were observed.	Cisplatin	3-12	high mobility group box 1	Homo sapiens	57-62
34966671-13	2021	In cisplatin-persistent cells, nuclear relocalization of HMGB1 and overexpression of HMGB1 and RAGE, but not TLR-2 or TLR-4, were observed.	Cisplatin	3-12	high mobility group box 1	Homo sapiens	85-90
34966671-14	2021	In tumor cells, this HMGB1-RAGE interaction may be associated with the development of cisplatin resistance.	Cisplatin	86-95	high mobility group box 1	Homo sapiens	21-26
34850958-0	2022	Corilagin induces apoptosis and inhibits autophagy of HL-60 cells by regulating miR-451/HMGB1 axis.	corilagin	0-9	high mobility group box 1	Homo sapiens	88-93
34850958-11	2022	In conclusion, these results indicated that corilagin induced apoptosis and inhibited autophagy in HL-60 cells by regulating the miR-451/HMGB1 axis, and corilagin may be a novel therapeutic drug for the treatment of AML.	corilagin	44-53	high mobility group box 1	Homo sapiens	137-142
34755645-0	2021	Indoprofen exerts a potent therapeutic effect against sepsis by alleviating high mobility group box 1-mediated inflammatory responses.	Indoprofen	0-10	high mobility group box 1	Homo sapiens	76-101
34755645-2	2021	This study was carried out to examine the inhibitory effect of indoprofen on high mobility group box 1 (HMGB1)-mediated inflammatory responses in vivo and in vitro.	Indoprofen	63-73	high mobility group box 1	Homo sapiens	77-102
34755645-2	2021	This study was carried out to examine the inhibitory effect of indoprofen on high mobility group box 1 (HMGB1)-mediated inflammatory responses in vivo and in vitro.	Indoprofen	63-73	high mobility group box 1	Homo sapiens	104-109
34755645-5	2021	Mechanistically, indoprofen potently inhibited the release of HMGB1 following stimulation by lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (poly I:C), and suppressed recombinant human HMGB1(rhHMGB1)-induced inflammatory responses.	Indoprofen	17-27	high mobility group box 1	Homo sapiens	62-67
34755645-5	2021	Mechanistically, indoprofen potently inhibited the release of HMGB1 following stimulation by lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (poly I:C), and suppressed recombinant human HMGB1(rhHMGB1)-induced inflammatory responses.	Indoprofen	17-27	high mobility group box 1	Homo sapiens	198-203
34755645-5	2021	Mechanistically, indoprofen potently inhibited the release of HMGB1 following stimulation by lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (poly I:C), and suppressed recombinant human HMGB1(rhHMGB1)-induced inflammatory responses.	polyinosinic	121-133	high mobility group box 1	Homo sapiens	62-67
34755645-5	2021	Mechanistically, indoprofen potently inhibited the release of HMGB1 following stimulation by lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (poly I:C), and suppressed recombinant human HMGB1(rhHMGB1)-induced inflammatory responses.	Poly C	134-152	high mobility group box 1	Homo sapiens	62-67
34755645-5	2021	Mechanistically, indoprofen potently inhibited the release of HMGB1 following stimulation by lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (poly I:C), and suppressed recombinant human HMGB1(rhHMGB1)-induced inflammatory responses.	Poly I-C	154-162	high mobility group box 1	Homo sapiens	62-67
34755645-6	2021	It was also found that indoprofen has both cyclooxygenase 2-dependent and -independent inhibitory effects on the proinflammatory effect of HMGB1 in THP-1 cells.	Indoprofen	23-33	high mobility group box 1	Homo sapiens	139-144
34755645-8	2021	Collectively, these data demonstrated that the anti-inflammatory effect of indoprofen in sepsis was associated with HMGB1-mediated inflammatory responses, thus offering a favorable mechanistic basis to support the therapeutic potential of indoprofen for the treatment of lethal sepsis or other inflammatory diseases.	Indoprofen	75-85	high mobility group box 1	Homo sapiens	116-121
34755645-8	2021	Collectively, these data demonstrated that the anti-inflammatory effect of indoprofen in sepsis was associated with HMGB1-mediated inflammatory responses, thus offering a favorable mechanistic basis to support the therapeutic potential of indoprofen for the treatment of lethal sepsis or other inflammatory diseases.	Indoprofen	239-249	high mobility group box 1	Homo sapiens	116-121
34917229-0	2021	Folic Acid Protects Melanocytes from Oxidative Stress via Activation of Nrf2 and Inhibition of HMGB1.	Folic Acid	0-10	high mobility group box 1	Homo sapiens	95-100
34934826-2	2021	Glycyrrhizin (GL), a traditional Chinese medicine for liver disease, binds to HMGB1, thereby inhibits tissue injury.	Glycyrrhizic Acid	14-16	high mobility group box 1	Homo sapiens	78-83
34101714-13	2021	Furthermore, dexmedetomidine induced a significant reduction in peri-operative serum HMGB1 level from the baseline (222.5 +- 408.3 pg ml-1) to the first postoperative day (152.2 +- 280.0 pg ml-1) P = 0.0033.	Dexmedetomidine	13-28	high mobility group box 1	Homo sapiens	85-90
34477479-7	2021	By analyzing the expression of High-Mobility Group Box 1 (HMGB1) and RAGE in HSC-4 cells, the result showed that EVO slightly reduced HMBG1 levels and dramatically decreased RAGE levels, while RAGE overexpression did have no marked influences on HMBG1 levels.	evodiamine	113-116	high mobility group box 1	Homo sapiens	31-56
34477479-7	2021	By analyzing the expression of High-Mobility Group Box 1 (HMGB1) and RAGE in HSC-4 cells, the result showed that EVO slightly reduced HMBG1 levels and dramatically decreased RAGE levels, while RAGE overexpression did have no marked influences on HMBG1 levels.	evodiamine	113-116	high mobility group box 1	Homo sapiens	58-63
34943830-0	2021	Post-Translational Modification of HMGB1 Disulfide Bonds in Stimulating and Inhibiting Inflammation.	Disulfides	41-50	high mobility group box 1	Homo sapiens	35-40
34737812-11	2021	Mechanistically, the upregulation of HMGB1/RAGE expression induced by LPS was markedly blocked by anagliptin.	anagliptin	98-108	high mobility group box 1	Homo sapiens	37-42
34737812-12	2021	In conclusion, anagliptin alleviated inflammation, apoptosis and endothelial dysfunction in LPS-induced HPMVECs via modulating HMGB1/RAGE expression.	anagliptin	15-25	high mobility group box 1	Homo sapiens	127-132
34338955-9	2021	MIR3142HG impaired miR-450b-5p-mediated inhibition of HMGB1.	mir-450b	19-27	high mobility group box 1	Homo sapiens	54-59
34338955-9	2021	MIR3142HG impaired miR-450b-5p-mediated inhibition of HMGB1.	CHEMBL3740941	28-30	high mobility group box 1	Homo sapiens	54-59
34815344-0	2021	BAP1 forms a trimer with HMGB1 and HDAC1 that modulates gene x environment interaction with asbestos.	Asbestos	92-100	high mobility group box 1	Homo sapiens	25-30
34943830-2	2021	As reviewed here, HMGB1 is an oxidation-reduction sensitive DAMP bearing three cysteines, and the post-translational modification of these residues establishes its proinflammatory and anti-inflammatory activities by binding to different extracellular cell surface receptors.	Cysteine	79-88	high mobility group box 1	Homo sapiens	18-23
34867338-7	2021	Then, we used the HMGB1 inhibitor glycyrrhizin to reverse the effects of HMGB1 on C2C12 myotubes.	Glycyrrhizic Acid	34-46	high mobility group box 1	Homo sapiens	18-23
34916197-0	2021	(Aloin inhibits lactate-induced proliferation and migration of gastric cancer cells by downregulating HMGB1 expression).	alloin	1-6	high mobility group box 1	Homo sapiens	102-107
34916197-0	2021	(Aloin inhibits lactate-induced proliferation and migration of gastric cancer cells by downregulating HMGB1 expression).	Lactic Acid	16-23	high mobility group box 1	Homo sapiens	102-107
34916197-5	2021	HMGB1 expression was knocked down in BGC-823 cells using RNA interference technique, and the effects of HMGB1 knockdown on proliferation and migration of the cells stimulated with lactate for 24 h were examined using EdU and wound healing assays.	Lactic Acid	180-187	high mobility group box 1	Homo sapiens	104-109
34916197-7	2021	Treatment with lactate obviously up-regulated the expressions of cyclin D1, cyclin E1, PCNA, N-cadherin, MMP-2, MMP-9 and HMGB1, which were significantly inhibited by aloin; aloin significantly reversed inhibition of E-cadherin and blocked the release of HMGB1 in lactate-treated cells.	Lactic Acid	15-22	high mobility group box 1	Homo sapiens	122-127
34916197-7	2021	Treatment with lactate obviously up-regulated the expressions of cyclin D1, cyclin E1, PCNA, N-cadherin, MMP-2, MMP-9 and HMGB1, which were significantly inhibited by aloin; aloin significantly reversed inhibition of E-cadherin and blocked the release of HMGB1 in lactate-treated cells.	Lactic Acid	15-22	high mobility group box 1	Homo sapiens	255-260
34916197-7	2021	Treatment with lactate obviously up-regulated the expressions of cyclin D1, cyclin E1, PCNA, N-cadherin, MMP-2, MMP-9 and HMGB1, which were significantly inhibited by aloin; aloin significantly reversed inhibition of E-cadherin and blocked the release of HMGB1 in lactate-treated cells.	alloin	167-172	high mobility group box 1	Homo sapiens	122-127
34916197-7	2021	Treatment with lactate obviously up-regulated the expressions of cyclin D1, cyclin E1, PCNA, N-cadherin, MMP-2, MMP-9 and HMGB1, which were significantly inhibited by aloin; aloin significantly reversed inhibition of E-cadherin and blocked the release of HMGB1 in lactate-treated cells.	alloin	167-172	high mobility group box 1	Homo sapiens	255-260
34916197-7	2021	Treatment with lactate obviously up-regulated the expressions of cyclin D1, cyclin E1, PCNA, N-cadherin, MMP-2, MMP-9 and HMGB1, which were significantly inhibited by aloin; aloin significantly reversed inhibition of E-cadherin and blocked the release of HMGB1 in lactate-treated cells.	alloin	174-179	high mobility group box 1	Homo sapiens	122-127
34916197-7	2021	Treatment with lactate obviously up-regulated the expressions of cyclin D1, cyclin E1, PCNA, N-cadherin, MMP-2, MMP-9 and HMGB1, which were significantly inhibited by aloin; aloin significantly reversed inhibition of E-cadherin and blocked the release of HMGB1 in lactate-treated cells.	alloin	174-179	high mobility group box 1	Homo sapiens	255-260
34916197-7	2021	Treatment with lactate obviously up-regulated the expressions of cyclin D1, cyclin E1, PCNA, N-cadherin, MMP-2, MMP-9 and HMGB1, which were significantly inhibited by aloin; aloin significantly reversed inhibition of E-cadherin and blocked the release of HMGB1 in lactate-treated cells.	Lactic Acid	264-271	high mobility group box 1	Homo sapiens	255-260
34916197-8	2021	BGC-823 cells with HMGB1 knockdown, as compared with the cells transfected with the negative control plasmid, showed significantly lowered proliferation and migration abilities following lactate treatment.	Lactic Acid	187-194	high mobility group box 1	Homo sapiens	19-24
34916197-9	2021	CONCLUSION: Aloin inhibits lactate-induced proliferation and migration of gastric cancer cells by down-regulating the expression and release of HMGB1 and the expressions of proliferation- and migration-related proteins.	alloin	12-17	high mobility group box 1	Homo sapiens	144-149
34916197-9	2021	CONCLUSION: Aloin inhibits lactate-induced proliferation and migration of gastric cancer cells by down-regulating the expression and release of HMGB1 and the expressions of proliferation- and migration-related proteins.	Lactic Acid	27-34	high mobility group box 1	Homo sapiens	144-149
34867338-7	2021	Then, we used the HMGB1 inhibitor glycyrrhizin to reverse the effects of HMGB1 on C2C12 myotubes.	Glycyrrhizic Acid	34-46	high mobility group box 1	Homo sapiens	73-78
34727314-7	2021	Both age (r = 0.210, p = 0.001), serum creatinine (r = 0.509, p < 0.001), eGFR (r =  - 0.459, p < 0.001) and Hcy (r = 0.531, p < 0.001) were significantly correlated with HMGB1.	Creatinine	39-49	high mobility group box 1	Homo sapiens	171-176
34403663-3	2021	This study aimed to address the effect of miR-141-3p on astrocyte activation and inflammatory response in BM through HMGB1.	mir-141-3p	42-52	high mobility group box 1	Homo sapiens	117-122
34939761-9	2021	Sequential exposure of the cells to 5-aza and Alimta enhanced miR-34a expression and significantly downregulated HMGB1, HMGA2 and BCL-2 expressions.	Azacitidine	36-41	high mobility group box 1	Homo sapiens	113-118
34939761-9	2021	Sequential exposure of the cells to 5-aza and Alimta enhanced miR-34a expression and significantly downregulated HMGB1, HMGA2 and BCL-2 expressions.	Pemetrexed	46-52	high mobility group box 1	Homo sapiens	113-118
34939761-11	2021	Caspase-3 activation, HMGB1 release into extracellular space and staining of the cells with annexine V/PI suggested that 5-aza reduced late apoptotic/necrotic cell death induced by Alimta.	Pemetrexed	181-187	high mobility group box 1	Homo sapiens	22-27
34543830-8	2021	The CSF HMGB1 concentrations were significantly higher in the DRE and NDE groups compared with the ONNDs group (p < 0.001).	NDE	70-73	high mobility group box 1	Homo sapiens	8-13
34657898-7	2022	Correlation analysis indicated that the levels of HMGB1 and TLR4 were positively correlated with triglyceride (TG), fasting plasma glucose (FPG) levels and BMI, whereas a negative correlation between HMGB1 and high density lipoprotein (HDL) was noted.	Triglycerides	111-113	high mobility group box 1	Homo sapiens	50-55
34164831-3	2021	The activation of HMGB1 secretion involves viral induction of reactive oxygen species and is mediated by the p38/STAT1 axis.	Oxygen	71-77	high mobility group box 1	Homo sapiens	18-23
34619434-2	2021	Dociparstat sodium (DSTAT, CX-01) is a low anticoagulant heparin with multiple mechanisms of action, including inhibition of the CXCR4/CXCL12 axis, blocking HMGB1, and binding platelet factor 4 (PF-4).	GM 1892	0-18	high mobility group box 1	Homo sapiens	157-162
34619434-2	2021	Dociparstat sodium (DSTAT, CX-01) is a low anticoagulant heparin with multiple mechanisms of action, including inhibition of the CXCR4/CXCL12 axis, blocking HMGB1, and binding platelet factor 4 (PF-4).	GM 1892	20-25	high mobility group box 1	Homo sapiens	157-162
34351732-7	2021	We discovered that HSoligo 7 (HS oligosaccharide 7), a 3-O-sulfated octasaccharide, binds to high mobility group box 1 protein (HMGB1) and tau protein, both believed to be involved in the process of inflammation.	Oligosaccharides	33-48	high mobility group box 1	Homo sapiens	93-126
34351732-7	2021	We discovered that HSoligo 7 (HS oligosaccharide 7), a 3-O-sulfated octasaccharide, binds to high mobility group box 1 protein (HMGB1) and tau protein, both believed to be involved in the process of inflammation.	Oligosaccharides	33-48	high mobility group box 1	Homo sapiens	128-133
34351732-7	2021	We discovered that HSoligo 7 (HS oligosaccharide 7), a 3-O-sulfated octasaccharide, binds to high mobility group box 1 protein (HMGB1) and tau protein, both believed to be involved in the process of inflammation.	Octasaccharide	68-82	high mobility group box 1	Homo sapiens	93-126
34351732-7	2021	We discovered that HSoligo 7 (HS oligosaccharide 7), a 3-O-sulfated octasaccharide, binds to high mobility group box 1 protein (HMGB1) and tau protein, both believed to be involved in the process of inflammation.	Octasaccharide	68-82	high mobility group box 1	Homo sapiens	128-133
34778055-0	2021	HMGB1 Promotes Resistance to Doxorubicin in Human Hepatocellular Carcinoma Cells by Inducing Autophagy via the AMPK/mTOR Signaling Pathway.	Doxorubicin	29-40	high mobility group box 1	Homo sapiens	0-5
34778055-4	2021	In the present study, we found that administration of doxorubicin (DOX) significantly promoted HMGB1 expression and induced HMGB1 cytoplasmic translocation in human HCC cell lines BEL7402 and SMMC7721, which enhanced autophagy that contributes to protecting HCC cells from apoptosis and increasing drug resistance.	Doxorubicin	54-65	high mobility group box 1	Homo sapiens	95-100
34778055-4	2021	In the present study, we found that administration of doxorubicin (DOX) significantly promoted HMGB1 expression and induced HMGB1 cytoplasmic translocation in human HCC cell lines BEL7402 and SMMC7721, which enhanced autophagy that contributes to protecting HCC cells from apoptosis and increasing drug resistance.	Doxorubicin	54-65	high mobility group box 1	Homo sapiens	124-129
34778055-4	2021	In the present study, we found that administration of doxorubicin (DOX) significantly promoted HMGB1 expression and induced HMGB1 cytoplasmic translocation in human HCC cell lines BEL7402 and SMMC7721, which enhanced autophagy that contributes to protecting HCC cells from apoptosis and increasing drug resistance.	Doxorubicin	67-70	high mobility group box 1	Homo sapiens	95-100
34778055-4	2021	In the present study, we found that administration of doxorubicin (DOX) significantly promoted HMGB1 expression and induced HMGB1 cytoplasmic translocation in human HCC cell lines BEL7402 and SMMC7721, which enhanced autophagy that contributes to protecting HCC cells from apoptosis and increasing drug resistance.	Doxorubicin	67-70	high mobility group box 1	Homo sapiens	124-129
34778055-5	2021	Moreover, we observed HMGB1 translocation and elevation of autophagy in DOX-resistant BEL7402 and SMMC7721 cells.	Doxorubicin	72-75	high mobility group box 1	Homo sapiens	22-27
34778055-6	2021	Additionally, inhibition of HMGB1 and autophagy increased the sensitivities of BEL-7402 and SMMC-7721 cells to DOX and re-sensitized their DOX-resistant cells.	Doxorubicin	111-114	high mobility group box 1	Homo sapiens	28-33
34778055-8	2021	In summary, our results indicate that HMGB1 promotes acquired DOX resistance in DOX-treated BEL7402 and SMMC7721 cells by enhancing autophagy through the AMPK/mTOR signaling pathway.	Doxorubicin	62-65	high mobility group box 1	Homo sapiens	38-43
34778055-8	2021	In summary, our results indicate that HMGB1 promotes acquired DOX resistance in DOX-treated BEL7402 and SMMC7721 cells by enhancing autophagy through the AMPK/mTOR signaling pathway.	Doxorubicin	80-83	high mobility group box 1	Homo sapiens	38-43
34914264-1	2021	Objective: To investigate the effect of silencing the high-mobility group box-1 protein (HMGB1) combined with docetaxel (DTX) on the proliferation and apoptosis of PCa cells and its possible action mechanism.	Docetaxel	121-124	high mobility group box 1	Homo sapiens	54-79
34914264-10	2021	The expression of the HMGB1 protein was markedly lower in the si-HMGB1+DTX than in the DTX group (P < 0.05).	Docetaxel	87-90	high mobility group box 1	Homo sapiens	22-27
34914264-11	2021	CONCLUSIONS: Silencing HMGB1 combined with DTX chemotherapy can inhibit the proliferation and promote the apoptosis of PCa cells, which may be attributed to its regulatory effect on the expressions of the Bcl-2 family-related proteins.	Docetaxel	43-46	high mobility group box 1	Homo sapiens	23-28
34657898-7	2022	Correlation analysis indicated that the levels of HMGB1 and TLR4 were positively correlated with triglyceride (TG), fasting plasma glucose (FPG) levels and BMI, whereas a negative correlation between HMGB1 and high density lipoprotein (HDL) was noted.	Triglycerides	97-109	high mobility group box 1	Homo sapiens	50-55
34657898-7	2022	Correlation analysis indicated that the levels of HMGB1 and TLR4 were positively correlated with triglyceride (TG), fasting plasma glucose (FPG) levels and BMI, whereas a negative correlation between HMGB1 and high density lipoprotein (HDL) was noted.	Glucose	131-138	high mobility group box 1	Homo sapiens	50-55
34627452-2	2021	METHODS: Different concentrations of recombinant human HMGB1 protein (100, 200, 400, 800 and 1000 ng/ml) were incubated with MSC for 24, 48, 72 h and the proliferation of MSC were detected respectively by using the CCK-8 method and flow cytometry.	Sincalide	215-220	high mobility group box 1	Homo sapiens	55-60
34546745-4	2021	Using synthetic protein chemistry, we generated site-specifically O-GlcNAc-modified HMGB1 at S100 and characterized biochemically the effect of the sugar modification on its DNA binding activity.	Sugars	148-153	high mobility group box 1	Homo sapiens	84-89
34671276-2	2021	Salicylic acid can bind to human high mobility group box 1 (HMGB1) and interrupt its role in mediating immune responses.	Salicylic Acid	0-14	high mobility group box 1	Homo sapiens	33-58
34671276-2	2021	Salicylic acid can bind to human high mobility group box 1 (HMGB1) and interrupt its role in mediating immune responses.	Salicylic Acid	0-14	high mobility group box 1	Homo sapiens	60-65
34639171-8	2021	Cardiomyocytes exposed to 25mM glucose resulted in the downregulation of HSP60 and SIRT1 after 48 h. We further examined that hyperglycemia mediated the decrease in the gap junction protein CX43, as well as CXC chemokine receptor CXCR4 which may affect the physiological functions of the cardiomyocytes when exposed to high glucose for 24 and 48 h. Upregulated expression of DNA-binding nuclear protein HMGB1, along with changes in histone methylation marker H3K9me1 have demonstrated hyperglycemia-induced damage to cardiomyocyte at 24 h of exposure.	Glucose	31-38	high mobility group box 1	Homo sapiens	403-408
34639171-8	2021	Cardiomyocytes exposed to 25mM glucose resulted in the downregulation of HSP60 and SIRT1 after 48 h. We further examined that hyperglycemia mediated the decrease in the gap junction protein CX43, as well as CXC chemokine receptor CXCR4 which may affect the physiological functions of the cardiomyocytes when exposed to high glucose for 24 and 48 h. Upregulated expression of DNA-binding nuclear protein HMGB1, along with changes in histone methylation marker H3K9me1 have demonstrated hyperglycemia-induced damage to cardiomyocyte at 24 h of exposure.	Glucose	324-331	high mobility group box 1	Homo sapiens	403-408
34617194-11	2022	HMGB1 inhibitor, glycyrrhizin, abolishes all the observed proangiogenic phenotypes.	Glycyrrhizic Acid	17-29	high mobility group box 1	Homo sapiens	0-5
34739475-0	2021	HMGB1-antagonism exerted by glycyrrhizin could be fruitful against COVID-19.	Glycyrrhizic Acid	28-40	high mobility group box 1	Homo sapiens	0-5
34739475-5	2021	As HMGB1 is antagonized by glycyrrhizin, this substance could be potentially useful as ancillary treatment in COVID-19.	Glycyrrhizic Acid	27-39	high mobility group box 1	Homo sapiens	3-8
34573077-0	2021	Verbascoside Protects Gingival Cells against High Glucose-Induced Oxidative Stress via PKC/HMGB1/RAGE/NFkappaB Pathway.	acteoside	0-12	high mobility group box 1	Homo sapiens	91-96
34583662-0	2021	Overweight with HBV infection limited the efficacy of TACE in hepatocellular carcinoma by inhibiting the upregulated HMGB1.	Chlorotrianisene	54-58	high mobility group box 1	Homo sapiens	117-122
34583662-10	2021	Irrespective of TACE, the average expression of HMGB1 in hepatitis or obesity patients was higher than that in normal individuals and did not show upregulation after TACE.	Chlorotrianisene	16-20	high mobility group box 1	Homo sapiens	48-53
34583662-11	2021	Patients without overweight or HBV infection had a low expression of serum HMGB1 that was substantially upregulated after TACE.	Chlorotrianisene	122-126	high mobility group box 1	Homo sapiens	75-80
34583662-13	2021	Thus, HBV and BMI maybe two factors affecting the efficacy of TACE via upregulated HMGB1.	Chlorotrianisene	62-66	high mobility group box 1	Homo sapiens	83-88
34638242-4	2021	Anthracycline and taxane treatments cause ICD and immunogenic modulations, resulting in the activation of antitumor immunity through damage-associated molecular patterns (DAMPs), such as adenosine triphosphate, calreticulin, high mobility group box 1, heat shock proteins 70/90, and annexin A1.	Anthracyclines	0-13	high mobility group box 1	Homo sapiens	225-250
34638242-4	2021	Anthracycline and taxane treatments cause ICD and immunogenic modulations, resulting in the activation of antitumor immunity through damage-associated molecular patterns (DAMPs), such as adenosine triphosphate, calreticulin, high mobility group box 1, heat shock proteins 70/90, and annexin A1.	taxane	18-24	high mobility group box 1	Homo sapiens	225-250
34624942-0	2021	(Effect of PPAR-gamma agonist pioglitazone on the prolifeiration of malignant nesothelionma cells induced by HMGB1).	Pioglitazone	30-42	high mobility group box 1	Homo sapiens	109-114
34624942-8	2021	There was a significant decrease in the mRNA expression level of HMGB1 in the PGZ-treated group (100 mumol/L) as compared to the control group in MSTO-211H (P<0.05) ; however, the expression level of HMGB1 in NCI-H2452 was an increase or no significant differences (P>0.05) .	Pioglitazone	78-81	high mobility group box 1	Homo sapiens	65-70
34624942-9	2021	Western blotting and immunofluorescence results showed that the protein expression of HMGB1 was reduced in the PGZ-treated group compared with the control group in MSTO-211H (P<0.05) , but the protein expression of that in NCI-H2452 was no significant differences (P>0.05) .	Pioglitazone	111-114	high mobility group box 1	Homo sapiens	86-91
34624942-11	2021	Conclusion: Pioglitazone suppresses the proliferation of MM cells through inhibition of HMGB1 by the activation of PPAR-gamma.	Pioglitazone	12-24	high mobility group box 1	Homo sapiens	88-93
34538217-5	2022	In 2.5D culture, treatment with HMGB1 induced permeability of FITC-dextran into the lumen formed by human lung, nasal and intestinal epithelial cells.	fluorescein isothiocyanate dextran	62-74	high mobility group box 1	Homo sapiens	32-37
34684184-6	2021	Success has also been obtained after other means to inhinit HMGB1 and include: use of HMGB1 Box A (one of three HMGB1 domains), anti-HMGB1 antibody blockage of HMGB1 and/or its receptors, Toll like receptor (TLR) 4, treatment with thrombomodulin (TM) or vasoactive intestinal peptide (VIP) and glycyrrhizin (GLY, a triterpenoid saponin) that directly binds to HMGB1.	Glycyrrhizic Acid	294-306	high mobility group box 1	Homo sapiens	360-365
34684184-6	2021	Success has also been obtained after other means to inhinit HMGB1 and include: use of HMGB1 Box A (one of three HMGB1 domains), anti-HMGB1 antibody blockage of HMGB1 and/or its receptors, Toll like receptor (TLR) 4, treatment with thrombomodulin (TM) or vasoactive intestinal peptide (VIP) and glycyrrhizin (GLY, a triterpenoid saponin) that directly binds to HMGB1.	Glycyrrhizic Acid	308-311	high mobility group box 1	Homo sapiens	360-365
34684184-6	2021	Success has also been obtained after other means to inhinit HMGB1 and include: use of HMGB1 Box A (one of three HMGB1 domains), anti-HMGB1 antibody blockage of HMGB1 and/or its receptors, Toll like receptor (TLR) 4, treatment with thrombomodulin (TM) or vasoactive intestinal peptide (VIP) and glycyrrhizin (GLY, a triterpenoid saponin) that directly binds to HMGB1.	triterpenoid saponin	315-335	high mobility group box 1	Homo sapiens	360-365
34621188-7	2021	Immunohistochemical analysis of vagal sensory neurons collected from mice after intranasal infection with murine pneumovirus or influenza A virus (IAV), or after intratracheal administration with the viral mimetic PolyI:C, revealed a significant increase in nuclear-to-cytoplasm translocation of HMGB1 compared to mock-inoculated mice.	Poly I-C	214-221	high mobility group box 1	Homo sapiens	296-301
34573077-7	2021	Likewise, we showed the inhibitory effect of verbascoside on oxidative stress was via repression of PKC/HMGB1/RAGE/NFkappaB activation.	acteoside	45-57	high mobility group box 1	Homo sapiens	104-109
34573077-6	2021	Moreover, verbascoside upregulated the PGC1-alpha and NRF1 expression and promoted mitochondrial biogenesis, which was mediated by suppression of PKC/HMGB1/RAGE/NFkappaB signaling.	acteoside	10-22	high mobility group box 1	Homo sapiens	150-155
34568076-0	2021	CD68+ Macrophage Infiltration Associates With Poor Outcome of HPV Negative Oral Squamous Carcinoma Patients Receiving Radiation: Poly(I:C) Enhances Radiosensitivity of CAL-27 Cells but Promotes Macrophage Recruitment Through HMGB1.	Poly I-C	129-138	high mobility group box 1	Homo sapiens	225-230
34566641-6	2021	Acute liver injury triggered by carbon tetrachloride (CCl4) injection resulted in significant upregulation of the plasma kallikrein gene (Klkb1) and was highly associated with the high mobility group box 1 gene, the marker of cell death (r = 0.75, p < 0.0005, n = 7).	Carbon Tetrachloride	32-52	high mobility group box 1	Homo sapiens	180-205
34375967-5	2021	In the presented study, model drug OP loaded poly(lactic-co-glycolic acid) (PLGA) nanoparticles (NPs) targeted with spike-binding peptide 1 (SBP1) of SARS-CoV-2 were designed to be used as an efficient and prolonged released antiviral drug delivery systems.	Polylactic Acid-Polyglycolic Acid Copolymer	45-74	high mobility group box 1	Homo sapiens	141-145
34566641-6	2021	Acute liver injury triggered by carbon tetrachloride (CCl4) injection resulted in significant upregulation of the plasma kallikrein gene (Klkb1) and was highly associated with the high mobility group box 1 gene, the marker of cell death (r = 0.75, p < 0.0005, n = 7).	Carbon Tetrachloride	54-58	high mobility group box 1	Homo sapiens	180-205
34287039-7	2021	These findings indicate that PCV2-induced activation of the PERK-ERO1alpha axis would lead to enhanced generation of ROS sufficient to decrease HMGB1 retention in the nuclei, thus derepressing viral DNA from HMGB1 sequestration.	ros	117-120	high mobility group box 1	Homo sapiens	144-149
34287039-7	2021	These findings indicate that PCV2-induced activation of the PERK-ERO1alpha axis would lead to enhanced generation of ROS sufficient to decrease HMGB1 retention in the nuclei, thus derepressing viral DNA from HMGB1 sequestration.	ros	117-120	high mobility group box 1	Homo sapiens	208-213
34287039-9	2021	Cysteine residues 107 and 305 of Rep or 108 of Cap played important roles in PCV2-induced PERK activation and distribution of HMGB1.	Cysteine	0-8	high mobility group box 1	Homo sapiens	126-131
34287039-11	2021	Collectively, this study offers novel insight into the mechanism of enhanced viral replication in which PCV2 manipulates ER to perturb its redox homeostasis via the PERK-ERO1alpha axis and the ER-sourced ROS from oxidative folding is sufficient to reduce HMGB1 retention in the nuclei, hence the release of HMGB1-bound viral DNA for replication.	ros	204-207	high mobility group box 1	Homo sapiens	255-260
34287039-11	2021	Collectively, this study offers novel insight into the mechanism of enhanced viral replication in which PCV2 manipulates ER to perturb its redox homeostasis via the PERK-ERO1alpha axis and the ER-sourced ROS from oxidative folding is sufficient to reduce HMGB1 retention in the nuclei, hence the release of HMGB1-bound viral DNA for replication.	ros	204-207	high mobility group box 1	Homo sapiens	307-312
34287039-12	2021	IMPORTANCE Considering the fact that clinical PCVAD mostly results from activation of latent PCV2 infection by confounding factors such as co-infection or environmental stresses, we propose that such confounding factors might impose oxidative stress to the animals where PCV2 in infected cells might utilize the elevated ROS to promote HMGB1 migration out of nuclei in favor of its replication.	pcvad	46-51	high mobility group box 1	Homo sapiens	336-341
34287039-12	2021	IMPORTANCE Considering the fact that clinical PCVAD mostly results from activation of latent PCV2 infection by confounding factors such as co-infection or environmental stresses, we propose that such confounding factors might impose oxidative stress to the animals where PCV2 in infected cells might utilize the elevated ROS to promote HMGB1 migration out of nuclei in favor of its replication.	ros	321-324	high mobility group box 1	Homo sapiens	336-341
34479472-0	2021	Correction to: 2-O, 3-O desulfated heparin (ODSH) increases bacterial clearance and attenuates lung injury in cystic fibrosis by restoring HMGB1-compromised macrophage function.	2-o	15-18	high mobility group box 1	Homo sapiens	139-144
34488792-5	2021	RESULTS: Nano-DOX were first shown to stimulate the tumor cells and the TAMs to release the cytokine HMGB1 which, regardless of its source, acted through the RAGE/NF-kappaB pathway to induce PD-L1 in the tumor cells and PD-L1/PD-1 in the TAMs.	Doxorubicin	14-17	high mobility group box 1	Homo sapiens	101-106
34488792-6	2021	Interestingly, Nano-DOX also induced NF-kappaB-dependent RAGE expression in the tumor cells and thus reinforced HMGB1"s action thereon.	Doxorubicin	20-23	high mobility group box 1	Homo sapiens	112-117
34488792-11	2021	CONCLUSIONS: PD-L1/PD-1 upregulation mediated by autocrine and paracrine activation of the HMGB1/RAGE/NF-kappaB signaling is a key response of lung cancer cells and their TAMs to stress, which can be induced by Nano-DOX.	Doxorubicin	216-219	high mobility group box 1	Homo sapiens	91-96
34181980-3	2021	Using nuclear magnetic resonance (NMR), fluorescence, and computational approaches, we investigated how the D/E repeats causes the autoinhibition of HMGB1 against its specific binding to cisplatin-modified DNA.	Cisplatin	187-196	high mobility group box 1	Homo sapiens	149-154
34479472-0	2021	Correction to: 2-O, 3-O desulfated heparin (ODSH) increases bacterial clearance and attenuates lung injury in cystic fibrosis by restoring HMGB1-compromised macrophage function.	3-o	20-23	high mobility group box 1	Homo sapiens	139-144
34479472-0	2021	Correction to: 2-O, 3-O desulfated heparin (ODSH) increases bacterial clearance and attenuates lung injury in cystic fibrosis by restoring HMGB1-compromised macrophage function.	Heparin	35-42	high mobility group box 1	Homo sapiens	139-144
34415075-11	2021	The induction of HMGB1-TLR-MyD88-NFkappaB proinflammatory signaling pathways correlates with neurodegeneration (i.e., Fluoro-Jade B), lifetime alcohol consumption, and age of drinking onset.	Alcohols	143-150	high mobility group box 1	Homo sapiens	17-22
34118353-0	2021	Serum HMGB1 Associates with Liver Disease and Predicts Readmission and Mortality in Patients with Alcohol Use Disorder.	Alcohols	98-105	high mobility group box 1	Homo sapiens	6-11
34237593-5	2021	Similarly, compound 48/80 increased levels of cardiac troponin I (cTnI) and tryptase, cardiomyocytes apoptosis, and expression of high-mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), and nuclear factor-kappa B p65 (NF-kappaB p65) in cardiac tissues induced by I/R injury, but it can be partially decreased by dexmedetomidine pretreatment.	Dexmedetomidine	320-335	high mobility group box 1	Homo sapiens	130-155
34237593-5	2021	Similarly, compound 48/80 increased levels of cardiac troponin I (cTnI) and tryptase, cardiomyocytes apoptosis, and expression of high-mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), and nuclear factor-kappa B p65 (NF-kappaB p65) in cardiac tissues induced by I/R injury, but it can be partially decreased by dexmedetomidine pretreatment.	Dexmedetomidine	320-335	high mobility group box 1	Homo sapiens	157-162
34237593-7	2021	Our data suggest that dexmedetomidine preconditioning alleviates the degranulation of mast cells and the apoptosis of cardiomyocytes caused by I/R injury, and inhibits the activation of inflammatory related factors HMGB1, TLR4, and NF-kappaB p65.	Dexmedetomidine	22-37	high mobility group box 1	Homo sapiens	215-220
34384355-10	2021	Serum NLRP3 levels were correlated with headache duration and hospital stay, while headache response to paracetamol was negatively correlated with HMGB1 and positively associated with IL-10 levels.	Acetaminophen	104-115	high mobility group box 1	Homo sapiens	147-152
34816916-8	2021	The correlation analysis showed that, in acute aortic dissection patients, the high-mobility group box 1 and receptor for advanced glycation end products levels were negatively correlated with partial pressure of oxygen/fraction of inspired oxygen, respectively (p<0.05).	Oxygen	213-219	high mobility group box 1	Homo sapiens	79-117
34816916-8	2021	The correlation analysis showed that, in acute aortic dissection patients, the high-mobility group box 1 and receptor for advanced glycation end products levels were negatively correlated with partial pressure of oxygen/fraction of inspired oxygen, respectively (p<0.05).	Oxygen	241-247	high mobility group box 1	Homo sapiens	79-117
34370950-0	2021	Molecular-Level Understanding of the Influence of Ions and Water on HMGB1 Adsorption Induced by Surface Hydroxylation of Titanium Implants.	Water	59-64	high mobility group box 1	Homo sapiens	68-73
34370950-0	2021	Molecular-Level Understanding of the Influence of Ions and Water on HMGB1 Adsorption Induced by Surface Hydroxylation of Titanium Implants.	Titanium	121-129	high mobility group box 1	Homo sapiens	68-73
34370950-4	2021	To develop different surface strategies that improve the clinical outcome of titanium-based implants by controlling their biological activity, a molecular-scale understanding of HMGB1-surface interactions is desired.	Titanium	77-85	high mobility group box 1	Homo sapiens	178-183
34370950-5	2021	Here, we use molecular dynamics (MD) computer simulations to provide direct insight into the HMGB1 interactions and the possible molecular arrangements of HMGB1 on fully hydroxylated and nonhydroxylated rutile (110) TiO2 surfaces.	titanium dioxide	216-220	high mobility group box 1	Homo sapiens	155-160
34370950-7	2021	The hydroxylated TiO2 surface shows a greater affinity for HMGB1 than the nonhydroxylated surface.	titanium dioxide	17-21	high mobility group box 1	Homo sapiens	59-64
34457261-4	2021	Here we review the pathophysiological underpinnings of lidocaine"s role as an anti-nociceptive, anti-inflammatory mediated by toll-like receptor (TLR) and nuclear factor kappa-beta (NF-kbeta) signalling pathways and downstream cytokine effectors high mobility group box 1 (HMGB1) and tumour necrosis factor-alpha (TNF-alpha).	Lidocaine	55-64	high mobility group box 1	Homo sapiens	246-271
34457261-4	2021	Here we review the pathophysiological underpinnings of lidocaine"s role as an anti-nociceptive, anti-inflammatory mediated by toll-like receptor (TLR) and nuclear factor kappa-beta (NF-kbeta) signalling pathways and downstream cytokine effectors high mobility group box 1 (HMGB1) and tumour necrosis factor-alpha (TNF-alpha).	Lidocaine	55-64	high mobility group box 1	Homo sapiens	273-278
34153664-7	2021	Inhibition of HMGB1 decreased Nrf2 expression and ROS release, improved MMP level and reduced NLRP3 inflammasome activation.	ros	50-53	high mobility group box 1	Homo sapiens	14-19
34294368-0	2021	Calunduloside E inhibits HepG2 cell proliferation and migration via p38/JNK-HMGB1 signalling axis.	calunduloside e	0-15	high mobility group box 1	Homo sapiens	76-81
34374662-0	2021	lncRNA ANRIL aggravates the chemoresistance of pancreatic cancer cells to gemcitabine by targeting inhibition of miR-181a and targeting HMGB1-induced autophagy.	gemcitabine	74-85	high mobility group box 1	Homo sapiens	136-141
34445093-9	2021	In 2.5D Matrigel culture, treatment with HMGB1 induced permeability of FITC-dextran (FD-4) into the lumen.	fluorescein isothiocyanate dextran	71-83	high mobility group box 1	Homo sapiens	41-46
34445093-10	2021	Pretreatment with EW-7197 prevented the effects of HMGB1.	vactosertib	18-25	high mobility group box 1	Homo sapiens	51-56
34128295-10	2021	The target gene of miR-141-5p was predicted with the TargetScan database, and the interaction between miR-141-5p and HMGB1/nuclear factor-kappaB (NF-kappaB) was further validated by dual-luciferase reporter assay, qRT-PCR, and Western blot analysis.	mir-141-5p	19-29	high mobility group box 1	Homo sapiens	117-122
34128295-10	2021	The target gene of miR-141-5p was predicted with the TargetScan database, and the interaction between miR-141-5p and HMGB1/nuclear factor-kappaB (NF-kappaB) was further validated by dual-luciferase reporter assay, qRT-PCR, and Western blot analysis.	mir-141-5p	102-112	high mobility group box 1	Homo sapiens	117-122
34366853-9	2021	As a result, LPS evidently promoted the expression of pro-inflammatory cytokines and HMGB1, the MyD88-NF-kappaB activation, and the NLRP3 inflammasome profile in THP-1 cells, while MAG obviously inhibited the "M1"" polarization of THP-1 cells.	magnoflorine	181-184	high mobility group box 1	Homo sapiens	85-90
34366853-0	2021	Magnoflorine Alleviates "M1" Polarized Macrophage-Induced Intervertebral Disc Degeneration Through Repressing the HMGB1/Myd88/NF-kappaB Pathway and NLRP3 Inflammasome.	magnoflorine	0-12	high mobility group box 1	Homo sapiens	114-119
34366853-12	2021	Furthermore, MAG dampened the HMGB1 expression and inactivated the MyD88/NF-kappaB pathway and NLRP3 inflammasome in NP cells.	magnoflorine	13-16	high mobility group box 1	Homo sapiens	30-35
34366853-13	2021	In conclusion, this study confirmed that MAG alleviates "M1" polarized macrophage-mediated NP cell damage by inactivating the HMGB1-MyD88-NF-kappaB pathway and NLRP3 inflammasome, which provides a new reference for IDD treatment.	magnoflorine	41-44	high mobility group box 1	Homo sapiens	126-131
34214538-8	2021	We hypothesized that mutating the hydrophobic residues (F28, F32, and F40) of SBP1 which do not directly interact with the spike protein to alanine would reduce peptide oligomerization without affecting its spike binding affinity.	Alanine	140-147	high mobility group box 1	Homo sapiens	78-82
34350063-4	2021	Alternol triggered ICD in prostate cancer cells, as evidenced by the release of damage-associated molecular patterns (DAMPs) (i.e., calreticulin, CALR; high mobility group protein B1, HMGB1; and adenosine triphosphate, ATP) and pro-inflammatory cytokine (i.e., interleukin (IL)-1alpha, IL-1beta, IL-6, and IL-8) expression.	Alternol	0-8	high mobility group box 1	Homo sapiens	152-182
34350063-4	2021	Alternol triggered ICD in prostate cancer cells, as evidenced by the release of damage-associated molecular patterns (DAMPs) (i.e., calreticulin, CALR; high mobility group protein B1, HMGB1; and adenosine triphosphate, ATP) and pro-inflammatory cytokine (i.e., interleukin (IL)-1alpha, IL-1beta, IL-6, and IL-8) expression.	Alternol	0-8	high mobility group box 1	Homo sapiens	184-189
34289368-4	2021	TauO exposure triggers astrocyte senescence through high mobility group box 1 (HMGB1) release and inflammatory senescence-associated secretory phenotype (SASP), which mediates paracrine senescence in adjacent cells.	tauo	0-4	high mobility group box 1	Homo sapiens	52-77
34289368-4	2021	TauO exposure triggers astrocyte senescence through high mobility group box 1 (HMGB1) release and inflammatory senescence-associated secretory phenotype (SASP), which mediates paracrine senescence in adjacent cells.	tauo	0-4	high mobility group box 1	Homo sapiens	79-84
34289368-5	2021	HMGB1 release inhibition using ethyl pyruvate (EP) and glycyrrhizic acid (GA) prevents TauO-induced senescence through inhibition of p38-mitogen-activated protein kinase (MAPK) and nuclear factor kappaB (NF-kappaB)-the essential signaling pathways for SASP development.	ethyl pyruvate	31-45	high mobility group box 1	Homo sapiens	0-5
34289368-5	2021	HMGB1 release inhibition using ethyl pyruvate (EP) and glycyrrhizic acid (GA) prevents TauO-induced senescence through inhibition of p38-mitogen-activated protein kinase (MAPK) and nuclear factor kappaB (NF-kappaB)-the essential signaling pathways for SASP development.	ethyl pyruvate	47-49	high mobility group box 1	Homo sapiens	0-5
34289368-5	2021	HMGB1 release inhibition using ethyl pyruvate (EP) and glycyrrhizic acid (GA) prevents TauO-induced senescence through inhibition of p38-mitogen-activated protein kinase (MAPK) and nuclear factor kappaB (NF-kappaB)-the essential signaling pathways for SASP development.	Glycyrrhizic Acid	55-72	high mobility group box 1	Homo sapiens	0-5
34289368-5	2021	HMGB1 release inhibition using ethyl pyruvate (EP) and glycyrrhizic acid (GA) prevents TauO-induced senescence through inhibition of p38-mitogen-activated protein kinase (MAPK) and nuclear factor kappaB (NF-kappaB)-the essential signaling pathways for SASP development.	Glycyrrhizic Acid	74-76	high mobility group box 1	Homo sapiens	0-5
34289368-5	2021	HMGB1 release inhibition using ethyl pyruvate (EP) and glycyrrhizic acid (GA) prevents TauO-induced senescence through inhibition of p38-mitogen-activated protein kinase (MAPK) and nuclear factor kappaB (NF-kappaB)-the essential signaling pathways for SASP development.	tauo	87-91	high mobility group box 1	Homo sapiens	0-5
34289368-7	2021	Collectively, TauO-induced HMGB1 release promotes cellular senescence and neuropathology, which could represent an important common pathomechanism in tauopathies including AD and FTD.	tauo	14-18	high mobility group box 1	Homo sapiens	27-32
34412765-5	2021	This study focuses on the HMGB1 release progress, which connected with Janus kinases/signal transducer and activator of transcription (JAK/STAT), nuclear factor-kappaB (NF-kappaB), Notch, inflammasome, tumor necrosis factor (TNF), mitogen-activated protein kinase (MAPK), reactive oxygen species (ROS), peroxisome proliferator-activated receptor (PPAR) and other signaling or dependent pathways in ARDS.	Reactive Oxygen Species	272-295	high mobility group box 1	Homo sapiens	26-31
33318439-0	2021	Role of N4-acetylcytidine for continuously activating NLRP3 inflammosome by HMGB1 pathway in microglia.	N-acetylcytidine	8-25	high mobility group box 1	Homo sapiens	76-81
34412765-5	2021	This study focuses on the HMGB1 release progress, which connected with Janus kinases/signal transducer and activator of transcription (JAK/STAT), nuclear factor-kappaB (NF-kappaB), Notch, inflammasome, tumor necrosis factor (TNF), mitogen-activated protein kinase (MAPK), reactive oxygen species (ROS), peroxisome proliferator-activated receptor (PPAR) and other signaling or dependent pathways in ARDS.	Reactive Oxygen Species	297-300	high mobility group box 1	Homo sapiens	26-31
34187428-11	2021	Moreover, the regression of tumors in mice that received PV-10 in combination with gemcitabine was associated with the depletion of splenic CD11b+Gr-1+ cells and increases in damage associated molecular patterns HMGB1, S100A8, and IL-1alpha.	pv-10	57-62	high mobility group box 1	Homo sapiens	212-217
34187428-11	2021	Moreover, the regression of tumors in mice that received PV-10 in combination with gemcitabine was associated with the depletion of splenic CD11b+Gr-1+ cells and increases in damage associated molecular patterns HMGB1, S100A8, and IL-1alpha.	gemcitabine	83-94	high mobility group box 1	Homo sapiens	212-217
34182538-0	2021	GPR30-mediated HMGB1 upregulation in CAFs induces autophagy and tamoxifen resistance in ERalpha-positive breast cancer cells.	Tamoxifen	64-73	high mobility group box 1	Homo sapiens	15-20
34182538-3	2021	Herein, considering that GPR30 mediates transcriptional regulation in different cell backgrounds, a microarray strategy was applied in immortalized CAFs derived from primary breast cancer samples, resulting in the identification of 165 GPR30 target genes, among which HMGB1 was confirmed to be upregulated by 17-beta estradiol(E2)- and TAM-triggered GPR30 activation in CAFs.	Estradiol	309-326	high mobility group box 1	Homo sapiens	268-273
34182538-5	2021	GPR30-induced HMGB1 upregulation triggered MEK/ERK signaling, leading to increased autophagic behavior to protect cancer cells from TAM-induced apoptosis, mimicking the recombinant HMGB1-mediated increase in cancer cell resistance potential to TAM.	Tamoxifen	244-247	high mobility group box 1	Homo sapiens	181-186
34182538-7	2021	CAF-expressed GPR30 induced TAM resistance via HMGB1 in vivo.	Tamoxifen	28-31	high mobility group box 1	Homo sapiens	47-52
34182538-3	2021	Herein, considering that GPR30 mediates transcriptional regulation in different cell backgrounds, a microarray strategy was applied in immortalized CAFs derived from primary breast cancer samples, resulting in the identification of 165 GPR30 target genes, among which HMGB1 was confirmed to be upregulated by 17-beta estradiol(E2)- and TAM-triggered GPR30 activation in CAFs.	Estradiol	327-329	high mobility group box 1	Homo sapiens	268-273
34182538-8	2021	Overall, TAM upregulated HMGB1 expression and secretion in CAFs via GPR30/PI3K/AKT signaling, and the secreted HMGB1 induced autophagy to enhance TAM resistance in MCF-7 cells in an ERK-dependent manner.	Tamoxifen	9-12	high mobility group box 1	Homo sapiens	25-30
34182538-8	2021	Overall, TAM upregulated HMGB1 expression and secretion in CAFs via GPR30/PI3K/AKT signaling, and the secreted HMGB1 induced autophagy to enhance TAM resistance in MCF-7 cells in an ERK-dependent manner.	Tamoxifen	9-12	high mobility group box 1	Homo sapiens	111-116
34182538-8	2021	Overall, TAM upregulated HMGB1 expression and secretion in CAFs via GPR30/PI3K/AKT signaling, and the secreted HMGB1 induced autophagy to enhance TAM resistance in MCF-7 cells in an ERK-dependent manner.	Tamoxifen	146-149	high mobility group box 1	Homo sapiens	111-116
34182538-3	2021	Herein, considering that GPR30 mediates transcriptional regulation in different cell backgrounds, a microarray strategy was applied in immortalized CAFs derived from primary breast cancer samples, resulting in the identification of 165 GPR30 target genes, among which HMGB1 was confirmed to be upregulated by 17-beta estradiol(E2)- and TAM-triggered GPR30 activation in CAFs.	Tamoxifen	336-339	high mobility group box 1	Homo sapiens	268-273
34182538-4	2021	Activated GPR30 increased extracellular HMGB1 secretion by CAFs, which was reduced by blocking PI3K/AKT signaling using G15 or LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	127-135	high mobility group box 1	Homo sapiens	40-45
34182538-5	2021	GPR30-induced HMGB1 upregulation triggered MEK/ERK signaling, leading to increased autophagic behavior to protect cancer cells from TAM-induced apoptosis, mimicking the recombinant HMGB1-mediated increase in cancer cell resistance potential to TAM.	Tamoxifen	132-135	high mobility group box 1	Homo sapiens	14-19
34163481-3	2021	The mechanisms by which metformin regulates the function of macrophages include AMPK, AMPK independent targets, NF-kappaB, ABCG5/8, Sirt1, FOXO1/FABP4 and HMGB1.	Metformin	24-33	high mobility group box 1	Homo sapiens	155-160
34164408-6	2021	In contrast, the HMGB1-mediated expression of HLA-DR, CD40, and CD86 on dendritic cells and production of IL-1beta, IL-6, and TNF-alpha were reduced by rapamycin.	Sirolimus	152-161	high mobility group box 1	Homo sapiens	17-22
34164408-7	2021	Rapamycin can inhibit HMGB1-induced activation of mDCs and secretion of pro-inflammatory cytokines.	Sirolimus	0-9	high mobility group box 1	Homo sapiens	22-27
34214372-0	2021	Analysis of HMGB-1 level before and after providing atorvastatin standard therapy in coronary artery disease patients with type-2 diabetes mellitus compared to without type-2 diabetes mellitus.	Atorvastatin	52-64	high mobility group box 1	Homo sapiens	12-18
34214372-2	2021	Atorvastatin has a pleiotropic effect as anti-inflammatory through one of the target levels of High Mobility Group Box-1 (HMGB-1).	Atorvastatin	0-12	high mobility group box 1	Homo sapiens	95-120
34214372-2	2021	Atorvastatin has a pleiotropic effect as anti-inflammatory through one of the target levels of High Mobility Group Box-1 (HMGB-1).	Atorvastatin	0-12	high mobility group box 1	Homo sapiens	122-128
34214372-3	2021	This prospective observational study aimed to analyze the effect of atorvastatin on serum HMGB-1 levels in CAD.	Atorvastatin	68-80	high mobility group box 1	Homo sapiens	90-96
34214372-5	2021	Serum HMGB-1 levels were measured in patients with CAD who were given atorvastatin for CAD with type-2 diabetes mellitus compared without type-2 diabetes mellitus in a patient ward.	Atorvastatin	70-82	high mobility group box 1	Homo sapiens	6-12
34214372-13	2021	CONCLUSIONS: HMGB-1 levels after providing atorvastatin in CAD with type-2 diabetes mellitus increased significantly, meanwhile, in CAD without type-2 diabetes mellitus did not decrease significantly.	Atorvastatin	43-55	high mobility group box 1	Homo sapiens	13-19
34295655-7	2021	Among the various treatment modalities administered, platinum-based combination or single-agent chemotherapy tended to elicit robust increases in the concentrations of HMGB1 and CRT.	Platinum	53-61	high mobility group box 1	Homo sapiens	168-173
34198762-7	2021	The Spearman"s rho revealed that HMGB1 SCs were positively correlated with the AQ attention to detail subscale (rs = 0.46, p = 0.045) and with the SQ total score (rs = 0.42, p = 0.04) in the ASD group.	aq	79-81	high mobility group box 1	Homo sapiens	33-38
34127858-6	2021	Mechanistically, exercise-induced HMGB1 release enhances itaconate metabolism in the tricarboxylic acid cycle that impacts Kupffer cells in an NRF2-dependent manner.	itaconic acid	57-66	high mobility group box 1	Homo sapiens	34-39
34127858-6	2021	Mechanistically, exercise-induced HMGB1 release enhances itaconate metabolism in the tricarboxylic acid cycle that impacts Kupffer cells in an NRF2-dependent manner.	Tricarboxylic Acids	85-103	high mobility group box 1	Homo sapiens	34-39
34079539-0	2021	Prednisolone Suppresses the Extracellular Release of HMGB-1 and Associated Inflammatory Pathways in Kawasaki Disease.	Prednisolone	0-12	high mobility group box 1	Homo sapiens	53-59
34094941-0	2021	lncRNA MIAT/HMGB1 Axis Is Involved in Cisplatin Resistance via Regulating IL6-Mediated Activation of the JAK2/STAT3 Pathway in Nasopharyngeal Carcinoma.	Cisplatin	38-47	high mobility group box 1	Homo sapiens	12-17
34094941-7	2021	Furthermore, we determine that elevated lncRNA MIAT level upregulates HMGB1 expression, contributing to cisplatin resistance in NPC cells.	Cisplatin	104-113	high mobility group box 1	Homo sapiens	70-75
34094941-8	2021	We find that the deficiency of the lncRNA MIAT/HMGB1 axis, inhibition of JAK2/STAT3, or neutralization of IL6 by antibodies significantly re-sensitizes resistant NPC cells to cisplatin in resistant NPC cells.	Cisplatin	175-184	high mobility group box 1	Homo sapiens	47-52
34094941-9	2021	Moreover, we provide the in vivo evidence that the deficiency of HMGB1 reduces cisplatin-resistant tumor growth.	Cisplatin	79-88	high mobility group box 1	Homo sapiens	65-70
34079539-10	2021	Our findings suggest that extracellular HMGB-1 plays an important role in mediating KD pathogenesis and that PSL treatment during the acute phase of KD may ameliorate HMGB-1-mediated inflammatory responses in KD vasculitis.	Prednisolone	109-112	high mobility group box 1	Homo sapiens	40-46
34079539-10	2021	Our findings suggest that extracellular HMGB-1 plays an important role in mediating KD pathogenesis and that PSL treatment during the acute phase of KD may ameliorate HMGB-1-mediated inflammatory responses in KD vasculitis.	Prednisolone	109-112	high mobility group box 1	Homo sapiens	167-173
34567165-0	2021	Inhibition of HMGB1 Might Enhance the Protective Effect of Taxifolin in Cardiomyocytes via PI3K/AKT Signaling Pathway.	taxifolin	59-68	high mobility group box 1	Homo sapiens	14-19
34068442-8	2021	Treatment of gastric cancer cells with CML-HMGB1 enhanced cell proliferation and invasion, sphere formation, and protection from thapsigargin-induced apoptosis, and decreased 5-FU sensitivity in comparison to HMGB1.	Thapsigargin	129-141	high mobility group box 1	Homo sapiens	43-48
34068442-8	2021	Treatment of gastric cancer cells with CML-HMGB1 enhanced cell proliferation and invasion, sphere formation, and protection from thapsigargin-induced apoptosis, and decreased 5-FU sensitivity in comparison to HMGB1.	Fluorouracil	175-179	high mobility group box 1	Homo sapiens	43-48
34066647-0	2021	Ethyl Pyruvate Attenuates Microglial NLRP3 Inflammasome Activation via Inhibition of HMGB1/NF-kappaB/miR-223 Signaling.	ethyl pyruvate	0-14	high mobility group box 1	Homo sapiens	85-90
34066647-6	2021	Furthermore, ethyl pyruvate reduced the formation of total and mitochondrial ROS and suppressed inflammasome-induced HMGB1 upregulation and nuclear NF-kappaB translocation and reversed the inflammasome activation-induced miRNA expression profile for miR-223 in N9 cells.	ethyl pyruvate	13-27	high mobility group box 1	Homo sapiens	117-122
34066647-7	2021	Our study suggests that ethyl pyruvate effectively suppresses the NLRP3 inflammasome activation in microglial cells regulation by miR-223 and NF-kappaB/HMGB1 axis.	ethyl pyruvate	24-38	high mobility group box 1	Homo sapiens	152-157
35471628-9	2022	Therefore, targeting of the HMGB1 pathway by anti-HMGB1 agents, such as heparin, resveratrol and metformin, may decrease COVID-19 severity.	Heparin	72-79	high mobility group box 1	Homo sapiens	28-33
34163767-3	2021	Herein, we developed a dual-modal microscopy imaging strategy to investigate, in situ, the formation of ternary binding complexes of the transcription cofactor HMGB1 and transcription factor Smad3 with cisplatin crosslinked DNA in single cells.	Cisplatin	202-211	high mobility group box 1	Homo sapiens	160-165
35617997-0	2022	Decreased HMGB1 expression contributed to cutaneous toxicity caused by lapatinib.	Lapatinib	71-80	high mobility group box 1	Homo sapiens	10-15
35617997-7	2022	Therefore, restoring HMGB1 expression might be an effective remedy against lapatinib-induced cutaneous toxicity.	Lapatinib	75-84	high mobility group box 1	Homo sapiens	21-26
35471628-9	2022	Therefore, targeting of the HMGB1 pathway by anti-HMGB1 agents, such as heparin, resveratrol and metformin, may decrease COVID-19 severity.	Heparin	72-79	high mobility group box 1	Homo sapiens	50-55
35471628-9	2022	Therefore, targeting of the HMGB1 pathway by anti-HMGB1 agents, such as heparin, resveratrol and metformin, may decrease COVID-19 severity.	Resveratrol	81-92	high mobility group box 1	Homo sapiens	28-33
35471628-9	2022	Therefore, targeting of the HMGB1 pathway by anti-HMGB1 agents, such as heparin, resveratrol and metformin, may decrease COVID-19 severity.	Resveratrol	81-92	high mobility group box 1	Homo sapiens	50-55
35471628-9	2022	Therefore, targeting of the HMGB1 pathway by anti-HMGB1 agents, such as heparin, resveratrol and metformin, may decrease COVID-19 severity.	Metformin	97-106	high mobility group box 1	Homo sapiens	28-33
35471628-9	2022	Therefore, targeting of the HMGB1 pathway by anti-HMGB1 agents, such as heparin, resveratrol and metformin, may decrease COVID-19 severity.	Metformin	97-106	high mobility group box 1	Homo sapiens	50-55
35596723-0	2022	The HN1/HMGB1 axis promotes the proliferation and metastasis of hepatocellular carcinoma and attenuates the chemosensitivity to oxaliplatin.	Oxaliplatin	128-139	high mobility group box 1	Homo sapiens	8-13
35605331-9	2022	Therefore, we further studied how hippocampal neurons affected microglia under PM2.5 exposure, Further investigation indicated that silencing HMGB1 could affect the activation of P2X7R and reduce the release of ATP from hippocampal neurons, thus protecting the interaction between microglia and hippocampal neurons.	Adenosine Triphosphate	211-214	high mobility group box 1	Homo sapiens	142-147
35596723-8	2022	In the nucleus, downregulation of HMGB1 followed by HN1 knockdown resulted in increased DNA damage and cell death in the oxaliplatin-treated HCC cells.	Oxaliplatin	121-132	high mobility group box 1	Homo sapiens	34-39
35596723-10	2022	Furthermore, HN1 knockdown in combination with HMGB1 overexpression restored the aggressive phenotypes of HCC cells and sensitivity of these cells to oxaliplatin.	Oxaliplatin	150-161	high mobility group box 1	Homo sapiens	47-52
35543500-5	2022	Total internal reflection microscopy (TIRFM) and molecular dynamic (MD) simulation show that although HMGB1 is adsorbed more on plates with lower SAA, the exposure ratio of cysteine (CYS) residue in HMGB1 is significantly decreased in lower SAA group.	saa	146-149	high mobility group box 1	Homo sapiens	102-107
35582883-11	2022	These results suggest that ketamine may reduce HMGB1 and RAGE accumulation in patients with depression, thereby providing a new therapeutic target for preventing and treating this disease.	Ketamine	27-35	high mobility group box 1	Homo sapiens	47-52
35577872-0	2022	Doxorubicin impacts chromatin binding of HMGB1, Histone H1 and retinoic acid receptor.	Doxorubicin	0-11	high mobility group box 1	Homo sapiens	41-46
35577872-2	2022	Here, we studied the effects of Dox on the chromatin binding of the architectural proteins high mobility group B1 (HMGB1) and the linker histone H1, and the transcription factor retinoic acid receptor (RARalpha) by fluorescence recovery after photobleaching (FRAP) and fluorescence correlation spectroscopy (FCS) in live cells.	Doxorubicin	32-35	high mobility group box 1	Homo sapiens	91-113
35577872-2	2022	Here, we studied the effects of Dox on the chromatin binding of the architectural proteins high mobility group B1 (HMGB1) and the linker histone H1, and the transcription factor retinoic acid receptor (RARalpha) by fluorescence recovery after photobleaching (FRAP) and fluorescence correlation spectroscopy (FCS) in live cells.	Doxorubicin	32-35	high mobility group box 1	Homo sapiens	115-120
35577872-3	2022	At lower doses, Dox increased the binding of HMGB1 to DNA while decreasing the binding of the linker histone H1.	Doxorubicin	16-19	high mobility group box 1	Homo sapiens	45-50
35577872-4	2022	At higher doses that correspond to the peak plasma concentrations achieved during chemotherapy, Dox reduced the binding of HMGB1 as well.	Doxorubicin	96-99	high mobility group box 1	Homo sapiens	123-128
35551614-15	2022	The suppression of ezrin by siRNA or the blockade of ROCK activation with Y-27632 reduced the production of TNF-alpha, IL-1beta, and HMGB1 in response to LPS.	Y 27632	74-81	high mobility group box 1	Homo sapiens	133-138
35543500-5	2022	Total internal reflection microscopy (TIRFM) and molecular dynamic (MD) simulation show that although HMGB1 is adsorbed more on plates with lower SAA, the exposure ratio of cysteine (CYS) residue in HMGB1 is significantly decreased in lower SAA group.	Cysteine	173-181	high mobility group box 1	Homo sapiens	199-204
35543500-5	2022	Total internal reflection microscopy (TIRFM) and molecular dynamic (MD) simulation show that although HMGB1 is adsorbed more on plates with lower SAA, the exposure ratio of cysteine (CYS) residue in HMGB1 is significantly decreased in lower SAA group.	Cysteine	183-186	high mobility group box 1	Homo sapiens	199-204
35632744-0	2022	PRRSV Induces HMGB1 Phosphorylation at Threonine-51 Residue to Enhance Its Secretion.	Threonine	39-48	high mobility group box 1	Homo sapiens	14-19
35526247-4	2022	This study was conducted to determine whether HMGB1 polymorphisms (rs1360485, rs2249825 and rs1060348) are associated with the incidence of differentiation syndrome in acute promyelocytic leukemia patients treated with all-trans retinoic acid and arsenic trioxide.	Tretinoin	219-242	high mobility group box 1	Homo sapiens	46-51
35625834-5	2022	Among these peptides, Nal-P-113 demonstrated the best anticancer activity and caused cancer cells to release potent danger-associated molecular patterns (DAMPs), such as reactive oxygen species (ROS), cytochrome c, ATP, and high-mobility group box 1 (HMGB1).	nal-p-113	22-31	high mobility group box 1	Homo sapiens	224-249
35625834-5	2022	Among these peptides, Nal-P-113 demonstrated the best anticancer activity and caused cancer cells to release potent danger-associated molecular patterns (DAMPs), such as reactive oxygen species (ROS), cytochrome c, ATP, and high-mobility group box 1 (HMGB1).	nal-p-113	22-31	high mobility group box 1	Homo sapiens	251-256
35526247-4	2022	This study was conducted to determine whether HMGB1 polymorphisms (rs1360485, rs2249825 and rs1060348) are associated with the incidence of differentiation syndrome in acute promyelocytic leukemia patients treated with all-trans retinoic acid and arsenic trioxide.	Arsenic Trioxide	247-263	high mobility group box 1	Homo sapiens	46-51
35632744-4	2022	Here, we discovered that the phosphorylation level of HMGB1 in threonine residues increased in PRRSV-infected cells.	Threonine	63-72	high mobility group box 1	Homo sapiens	54-59
35632744-5	2022	A site-directed mutagenesis study showed that HMGB1 phosphorylation at threonine-51 was associated with HMGB1 secretion induced by PRRSV infection.	Threonine	71-80	high mobility group box 1	Homo sapiens	46-51
35632744-5	2022	A site-directed mutagenesis study showed that HMGB1 phosphorylation at threonine-51 was associated with HMGB1 secretion induced by PRRSV infection.	Threonine	71-80	high mobility group box 1	Homo sapiens	104-109
35632744-8	2022	Moreover, the phosphorylation of HMGB1 at threonine-51 was correlated with the interaction between HMGB1 and RPS3.	Threonine	42-51	high mobility group box 1	Homo sapiens	33-38
35632744-8	2022	Moreover, the phosphorylation of HMGB1 at threonine-51 was correlated with the interaction between HMGB1 and RPS3.	Threonine	42-51	high mobility group box 1	Homo sapiens	99-104
35632744-10	2022	These results demonstrate that PRRSV may induce HMGB1 phosphorylation at threonine-51 and increase its interaction with RPS3 to enhance HMGB1 secretion.	Threonine	73-82	high mobility group box 1	Homo sapiens	48-53
35632744-10	2022	These results demonstrate that PRRSV may induce HMGB1 phosphorylation at threonine-51 and increase its interaction with RPS3 to enhance HMGB1 secretion.	Threonine	73-82	high mobility group box 1	Homo sapiens	136-141
35490244-0	2022	Correction to: miR-495-3p depresses cell proliferation and migration by downregulating HMGB1 in colorectal cancer.	mir-495-3p	15-25	high mobility group box 1	Homo sapiens	87-92
35255342-6	2022	Additionally, 7 at 0.1 and 1.0 microM synergistically enhanced the cytotoxicity of etoposide against SBC-3 cells; compound 7 induced the release of DAMPs; the release of HMGB1, the secretion of ATP, and the exposure of CALR in the SBC-3 cells.	Etoposide	83-92	high mobility group box 1	Homo sapiens	170-175
34990082-0	2022	Perfluorooctane sulfonate aggravates CCl4-induced hepatic fibrosis via HMGB1/TLR4/Smad signaling.	perfluorooctane sulfonic acid	0-25	high mobility group box 1	Homo sapiens	71-76
34990082-5	2022	Furthermore, PFOS exposure may promote the activation of high-mobility group box 1 (HMGB1)/toll-like receptor 4 (TLR4) signaling pathway through inducing the secretion of HMGB1 from hepatocytes.	perfluorooctane sulfonic acid	13-17	high mobility group box 1	Homo sapiens	57-82
34990082-5	2022	Furthermore, PFOS exposure may promote the activation of high-mobility group box 1 (HMGB1)/toll-like receptor 4 (TLR4) signaling pathway through inducing the secretion of HMGB1 from hepatocytes.	perfluorooctane sulfonic acid	13-17	high mobility group box 1	Homo sapiens	84-89
34990082-5	2022	Furthermore, PFOS exposure may promote the activation of high-mobility group box 1 (HMGB1)/toll-like receptor 4 (TLR4) signaling pathway through inducing the secretion of HMGB1 from hepatocytes.	perfluorooctane sulfonic acid	13-17	high mobility group box 1	Homo sapiens	171-176
35147911-0	2022	All-Trans Retinoic Acid-Preconditioned Mesenchymal Stem Cells Improve Motor Function and Alleviate Tissue Damage After Spinal Cord Injury by Inhibition of HMGB1/NF-kappaB/NLRP3 Pathway Through Autophagy Activation.	Tretinoin	0-23	high mobility group box 1	Homo sapiens	155-160
35477503-4	2022	METHODS: In this study, we developed oncolytic herpes simplex virus type 1 expressing HMGB1 protein (HSV-HMGB1) and investigated the cytotoxic effect of HSV-HMGB1 and its parental virus (HSV-ble) on three colorectal cancer cells (HCT116, SW480, and HT29) under normoxic (20% oxygen) and hypoxic (1% oxygen) conditions.	Oxygen	299-305	high mobility group box 1	Homo sapiens	86-91
35366433-0	2022	HMGB1 is increased in patients with immune thrombocytopenia and negatively associates with Tregs.	tregs	91-96	high mobility group box 1	Homo sapiens	0-5
35477503-4	2022	METHODS: In this study, we developed oncolytic herpes simplex virus type 1 expressing HMGB1 protein (HSV-HMGB1) and investigated the cytotoxic effect of HSV-HMGB1 and its parental virus (HSV-ble) on three colorectal cancer cells (HCT116, SW480, and HT29) under normoxic (20% oxygen) and hypoxic (1% oxygen) conditions.	Oxygen	275-281	high mobility group box 1	Homo sapiens	86-91
35624958-9	2022	The knockout of MMP-9 rescues cognitive impairment and cisplatin-induced upregulation of HMGB1 in SHSY5Y cells.	Cisplatin	55-64	high mobility group box 1	Homo sapiens	89-94
35573828-5	2022	Herein, we report that administration of recombinant HMGB1 into the spinal cord at the time of lysolecithin administration resulted in arrest of OPC differentiation in vivo, and a profound impairment of remyelination.	Lysophosphatidylcholines	95-107	high mobility group box 1	Homo sapiens	53-58
35477503-4	2022	METHODS: In this study, we developed oncolytic herpes simplex virus type 1 expressing HMGB1 protein (HSV-HMGB1) and investigated the cytotoxic effect of HSV-HMGB1 and its parental virus (HSV-ble) on three colorectal cancer cells (HCT116, SW480, and HT29) under normoxic (20% oxygen) and hypoxic (1% oxygen) conditions.	Oxygen	299-305	high mobility group box 1	Homo sapiens	105-110
35477503-4	2022	METHODS: In this study, we developed oncolytic herpes simplex virus type 1 expressing HMGB1 protein (HSV-HMGB1) and investigated the cytotoxic effect of HSV-HMGB1 and its parental virus (HSV-ble) on three colorectal cancer cells (HCT116, SW480, and HT29) under normoxic (20% oxygen) and hypoxic (1% oxygen) conditions.	Oxygen	275-281	high mobility group box 1	Homo sapiens	105-110
35440409-6	2022	MEASUREMENTS AND MAIN RESULTS: Significant reductions in high mobility group box-1 protein (HMGB-1), calprotectin, serum amyloid A, and granulocyte colony-stimulating factor (G-CSF), and an increase in insulin-like growth factor (IGF-1) occurred 1 month after ivacaftor.	ivacaftor	260-269	high mobility group box 1	Homo sapiens	92-98
35510176-9	2023	Additionally, photothermal therapy and CDT-mediated immunogenic cell death of tumor cells can further enhance anti-tumor immunity via exposure of CRT, HMGB1 and ATP.	1,5,9-cyclododecatriene	39-42	high mobility group box 1	Homo sapiens	151-156
35496500-4	2022	In tumor cell line models, AmB induced ICD with its typical hallmarks of calreticulin (CALR) expression and release of high mobility group box 1 (HMGB1) as well as Adenosine 5"-triphosphate (ATP).	Amphotericin B	27-30	high mobility group box 1	Homo sapiens	119-144
35496500-4	2022	In tumor cell line models, AmB induced ICD with its typical hallmarks of calreticulin (CALR) expression and release of high mobility group box 1 (HMGB1) as well as Adenosine 5"-triphosphate (ATP).	Amphotericin B	27-30	high mobility group box 1	Homo sapiens	146-151
35432719-5	2022	Herein, glycyrrhizin (GL), an HMGB1 inhibitor, was used to investigate the relationship between ferroptosis and HMGB1.	Glycyrrhizic Acid	8-20	high mobility group box 1	Homo sapiens	30-35
35432719-5	2022	Herein, glycyrrhizin (GL), an HMGB1 inhibitor, was used to investigate the relationship between ferroptosis and HMGB1.	Glycyrrhizic Acid	22-24	high mobility group box 1	Homo sapiens	30-35
35432719-7	2022	Western blot analysis revealed that GL markedly suppressed the expression of HMGB1 and increased the level of GPX4 in the context of HIBD.	Glycyrrhizic Acid	36-38	high mobility group box 1	Homo sapiens	77-82
35432719-12	2022	More importantly, GL may improve oxidative stress imbalance and mitochondrial damage, alleviate the downstream production of inflammatory factors, and ultimately reduce ferroptosis and damage to cortical neurons following HIBD via the HMGB1/GPX4 pathway.	Glycyrrhizic Acid	18-20	high mobility group box 1	Homo sapiens	235-240
35432719-13	2022	In conclusion, we showed for the first time that GL could suppress the occurrence of neuronal ferroptosis and reduce neuronal loss in HIBD via the HMGB1/GPX4 pathway.	Glycyrrhizic Acid	49-51	high mobility group box 1	Homo sapiens	147-152
35432719-14	2022	These findings highlight the potential of HMGB1 signaling antagonists to treat neuronal damage by suppressing ferroptosis, provide new and unique insights into GL as a neuroprotective agent, and suggest new prevention and treatment strategies for HIBD.	Glycyrrhizic Acid	160-162	high mobility group box 1	Homo sapiens	42-47
35278873-6	2022	Both HMGB1 neutralizing antibody and sRAGE inhibited Ang II-induced calcium deposition.	Calcium	68-75	high mobility group box 1	Homo sapiens	5-10
35316522-5	2022	However, whether PQ exposure affects HMGB1, alpha-synuclein, and autophagy function have rarely been reported.	pq	17-19	high mobility group box 1	Homo sapiens	37-42
35534452-0	2022	Erratum: Vitexin Inhibits Gastric Cancer Growth and Metastasis through HMGB1-mediated Inactivation of the PI3K/AKT/mTOR/HIF-1alpha Signaling Pathway.	vitexin	9-16	high mobility group box 1	Homo sapiens	71-76
35392631-13	2022	Expression levels of other complement pathway-related proteins (HMGB1, S100A8, S100A9, CRP, C4) were decreased by DTMP, although not significantly affected by SNI.	2',3'-dideoxy-2',3'-didehydrothymidine monophosphate	114-118	high mobility group box 1	Homo sapiens	64-69
35415314-0	2023	ROS-responsive 18beta-glycyrrhetic acid-conjugated polymeric nanoparticles mediate neuroprotection in ischemic stroke through HMGB1 inhibition and microglia polarization regulation.	Reactive Oxygen Species	0-3	high mobility group box 1	Homo sapiens	126-131
35415314-0	2023	ROS-responsive 18beta-glycyrrhetic acid-conjugated polymeric nanoparticles mediate neuroprotection in ischemic stroke through HMGB1 inhibition and microglia polarization regulation.	Glycyrrhetinic Acid	15-39	high mobility group box 1	Homo sapiens	126-131
35415314-4	2023	18beta-glycyrrhetinic acid (GA) is an effective intracellular inhibitor of HMGB1, but of poor water solubility and dose-dependent toxicity.	18alpha-glycyrrhetinic acid	0-26	high mobility group box 1	Homo sapiens	75-80
35415314-4	2023	18beta-glycyrrhetinic acid (GA) is an effective intracellular inhibitor of HMGB1, but of poor water solubility and dose-dependent toxicity.	18alpha-glycyrrhetinic acid	28-30	high mobility group box 1	Homo sapiens	75-80
35415314-5	2023	To overcome the shortcomings of GA delivery and to improve the efficacy of cerebral ischemia therapy, herein, we designed reactive oxygen species (ROS) responsive polymer-drug conjugate nanoparticles (DGA) to manipulate microglia polarization by suppressing the translocation of nuclear HMGB1.	Reactive Oxygen Species	122-145	high mobility group box 1	Homo sapiens	287-292
35415314-5	2023	To overcome the shortcomings of GA delivery and to improve the efficacy of cerebral ischemia therapy, herein, we designed reactive oxygen species (ROS) responsive polymer-drug conjugate nanoparticles (DGA) to manipulate microglia polarization by suppressing the translocation of nuclear HMGB1.	Reactive Oxygen Species	147-150	high mobility group box 1	Homo sapiens	287-292
35316522-0	2022	Paraquat Inhibits Autophagy Via Intensifying the Interaction Between HMGB1 and alpha-Synuclein.	Paraquat	0-8	high mobility group box 1	Homo sapiens	69-74
35316522-6	2022	In this study, we found that PQ exposure impaired autophagy function via disturbing the complex formation of HMGB1 and Beclin1.	pq	29-31	high mobility group box 1	Homo sapiens	109-114
35316522-7	2022	Moreover, the expression of alpha-synuclein is modulated by HMGB1 and the interaction between HMGB1 and alpha-synuclein was intensified by PQ exposure.	pq	139-141	high mobility group box 1	Homo sapiens	94-99
35354479-0	2022	miR-495-3p depresses cell proliferation and migration by downregulating HMGB1 in colorectal cancer.	mir-495-3p	0-10	high mobility group box 1	Homo sapiens	72-77
35224793-0	2022	Lucidone inhibits autophagy and MDR1 via HMGB1/RAGE/PI3K/Akt signaling pathway in pancreatic cancer cells.	lucidone	0-8	high mobility group box 1	Homo sapiens	41-46
35224793-7	2022	The data showed that lucidone significantly promoted apoptotic cell death and inhibited the expression of autophagic proteins (Atg5, Beclin-1, LC3-II, and Vps34) and MDR1 by inhibiting the HMGB1/RAGE/PI3K/Akt axis in both MIA Paca-2 cells and MIA Paca-2GEMR cells (GEM-resistant cells).	lucidone	21-29	high mobility group box 1	Homo sapiens	189-194
35224793-10	2022	Collectively, this study provided the underlying mechanism by which lucidone treatment inhibited HMGB1/RAGE-initiated PI3K/Akt/MDR1 signaling and consequently enhanced chemosensitivity in PDAC.	lucidone	68-76	high mobility group box 1	Homo sapiens	97-102
35354479-9	2022	We finally demonstrated that miR-495-3p inhibited CRC cell proliferation by targeting HMGB1 in vitro and in vivo.	mir-495-3p	29-39	high mobility group box 1	Homo sapiens	86-91
35340325-0	2022	Doxorubicin induced immune abnormalities and inflammatory responses via HMGB1, HIF1-alpha and VEGF pathway in progressive of cardiovascular damage.	Doxorubicin	0-11	high mobility group box 1	Homo sapiens	72-77
35462475-0	2022	HMGB1-mediated autophagy promotes gefitinib resistance in human non-small cell lung cancer.	Gefitinib	34-43	high mobility group box 1	Homo sapiens	0-5
35462475-4	2022	In this study, we found that HMGB1 is highly expressed in drug-resistant cells and confers to gefitinib resistance in NSCLC cells via activating autophagy process.	Gefitinib	94-103	high mobility group box 1	Homo sapiens	29-34
35462475-5	2022	Gefitinib upregulates HMGB1 expression in time-dependent and dose-dependent manners in human NSCLC cells.	Gefitinib	0-9	high mobility group box 1	Homo sapiens	22-27
35462475-6	2022	RNA interference-mediated knockdown of HMGB1 reduces PC9GR cell viability, induces apoptosis, and partially restores gefitinib sensitivity.	Gefitinib	117-126	high mobility group box 1	Homo sapiens	39-44
35462475-7	2022	Mechanistic analyses indicate that elevated HMGB1 expression contributes to gefitinib resistance by inducing autophagy.	Gefitinib	76-85	high mobility group box 1	Homo sapiens	44-49
35462475-8	2022	Thus, our results suggest that HMGB1 is an autophagy regulator and plays a key role in gefitinib resistance of NSCLC.	Gefitinib	87-96	high mobility group box 1	Homo sapiens	31-36
35408786-0	2022	A Dual Anti-Inflammatory and Anti-Proliferative 3-Styrylchromone Derivative Synergistically Enhances the Anti-Cancer Effects of DNA-Damaging Agents on Colon Cancer Cells by Targeting HMGB1-RAGE-ERK1/2 Signaling.	3-styrylchromone	48-64	high mobility group box 1	Homo sapiens	183-188
35340325-7	2022	Results: Several articles were revealed that molecular mechanisms of the DOX in cardiomyocyte damage and related to HMGB1, HIF-1alpha and VEGF and may potential treatment and prevention to cardiovascular disease in DOX intervention.	Doxorubicin	73-76	high mobility group box 1	Homo sapiens	116-121
35340325-8	2022	Conclusion: HMGB1, HIF-1alpha and VEGF has a pivotal regulator in DOX-induce cardiomyocyte damage and predominantly acts through different pathways.	Doxorubicin	66-69	high mobility group box 1	Homo sapiens	12-17
35340325-9	2022	The role of HMGB1 in DOX-induced myocardial damage suggests that HMGB1 is a mediator of DOX-induced damage.	Doxorubicin	21-24	high mobility group box 1	Homo sapiens	12-17
35340325-9	2022	The role of HMGB1 in DOX-induced myocardial damage suggests that HMGB1 is a mediator of DOX-induced damage.	Doxorubicin	21-24	high mobility group box 1	Homo sapiens	65-70
35340325-9	2022	The role of HMGB1 in DOX-induced myocardial damage suggests that HMGB1 is a mediator of DOX-induced damage.	Doxorubicin	88-91	high mobility group box 1	Homo sapiens	65-70
35154909-6	2022	Indeed, in vitro experiments performed with a cell-permeable small molecule KSPi closely related to the active payload released from the TWEAKR-KSPi-ADCs revealed that KSPi was capable of stimulating several hallmarks of immunogenic cell death (ICD) on three different human cancer cell lines: cellular release of adenosine triphosphate (ATP) and high mobility group B1 protein (HMGB1), exposure of calreticulin on the cell surface as well as a transcriptional type-I interferon response.	kspi	76-80	high mobility group box 1	Homo sapiens	347-377
35315432-3	2022	Mechanistically, Panx1 on endothelial cells acts as a conduit for ATP release that stimulates macrophage activation via P2X7 receptors and mitochondrial DNA release to increase IL-1beta and HMGB1 secretion.	Adenosine Triphosphate	66-69	high mobility group box 1	Homo sapiens	190-195
35328729-6	2022	AGDP not only inhibited the expression of TNF-alpha and IL-8 but also appeared to suppress the extracellular release of high-mobility group box 1 (HMGB1) by inhibiting the output of nuclear HMGB1 in cells.	agdp	0-4	high mobility group box 1	Homo sapiens	120-145
35328729-6	2022	AGDP not only inhibited the expression of TNF-alpha and IL-8 but also appeared to suppress the extracellular release of high-mobility group box 1 (HMGB1) by inhibiting the output of nuclear HMGB1 in cells.	agdp	0-4	high mobility group box 1	Homo sapiens	147-152
35328729-6	2022	AGDP not only inhibited the expression of TNF-alpha and IL-8 but also appeared to suppress the extracellular release of high-mobility group box 1 (HMGB1) by inhibiting the output of nuclear HMGB1 in cells.	agdp	0-4	high mobility group box 1	Homo sapiens	190-195
35045357-6	2022	After treatment with anagliptin, the state of oxidative stress in macrophages was alleviated, with the downregulation of TLR4, HMGB-1, iNOS, and the declined release of NO.	anagliptin	21-31	high mobility group box 1	Homo sapiens	127-133
35246019-9	2022	However, miR-142-3p inhibitor reverses the effect of circHECTD1 on all the above-mentioned aspects, including HMGB1 expression.	mir-142-3p	9-19	high mobility group box 1	Homo sapiens	110-115
35193644-0	2022	Autophagy-based unconventional secretion of HMGB1 in glioblastoma promotes chemosensitivity to temozolomide through macrophage M1-like polarization.	Temozolomide	95-107	high mobility group box 1	Homo sapiens	44-49
35193644-5	2022	METHODS: Cancer genome databases and paired-GB patient samples with or without TMZ treatment were used to assess the relationship between HMGB1 mRNA levels and overall patient survival.	Temozolomide	79-82	high mobility group box 1	Homo sapiens	138-143
35193644-6	2022	The relationship between HMGB1 protein level and TMZ sensitivity was measured by immunohistochemistry, ELISA, Western blot and qRT-PCR.	Temozolomide	49-52	high mobility group box 1	Homo sapiens	25-30
35193644-13	2022	Clinically, the elevated level of HMGB1 in sera may serve as a beneficial therapeutic-predictor for GB patients under TMZ treatment.	Temozolomide	118-121	high mobility group box 1	Homo sapiens	34-39
35193644-15	2022	HMGB1 acts as a key regulator in the crosstalk between GB cells and tumor-suppressive M1-like TAMs in GB microenvironment and may be considered as an adjuvant for the chemotherapeutic agent TMZ.	tams	94-98	high mobility group box 1	Homo sapiens	0-5
35193644-15	2022	HMGB1 acts as a key regulator in the crosstalk between GB cells and tumor-suppressive M1-like TAMs in GB microenvironment and may be considered as an adjuvant for the chemotherapeutic agent TMZ.	Temozolomide	190-193	high mobility group box 1	Homo sapiens	0-5
35080850-3	2022	Au10SG10 caused the loss of mitochondrial metabolic activity, increased lipid peroxidation and translocation of an alarmin molecule, high mobility group box 1 (HMGB1), from the nucleus to the cytosol.	au10sg10	0-8	high mobility group box 1	Homo sapiens	133-158
35080850-3	2022	Au10SG10 caused the loss of mitochondrial metabolic activity, increased lipid peroxidation and translocation of an alarmin molecule, high mobility group box 1 (HMGB1), from the nucleus to the cytosol.	au10sg10	0-8	high mobility group box 1	Homo sapiens	160-165
35080850-5	2022	We show that Au10SG10 can bind directly to the defined sites of reduced, oxidized, and acetylated HMGB1.	au10sg10	13-21	high mobility group box 1	Homo sapiens	98-103
35154909-6	2022	Indeed, in vitro experiments performed with a cell-permeable small molecule KSPi closely related to the active payload released from the TWEAKR-KSPi-ADCs revealed that KSPi was capable of stimulating several hallmarks of immunogenic cell death (ICD) on three different human cancer cell lines: cellular release of adenosine triphosphate (ATP) and high mobility group B1 protein (HMGB1), exposure of calreticulin on the cell surface as well as a transcriptional type-I interferon response.	kspi	76-80	high mobility group box 1	Homo sapiens	379-384
35154909-6	2022	Indeed, in vitro experiments performed with a cell-permeable small molecule KSPi closely related to the active payload released from the TWEAKR-KSPi-ADCs revealed that KSPi was capable of stimulating several hallmarks of immunogenic cell death (ICD) on three different human cancer cell lines: cellular release of adenosine triphosphate (ATP) and high mobility group B1 protein (HMGB1), exposure of calreticulin on the cell surface as well as a transcriptional type-I interferon response.	kspi	168-172	high mobility group box 1	Homo sapiens	347-377
35154909-6	2022	Indeed, in vitro experiments performed with a cell-permeable small molecule KSPi closely related to the active payload released from the TWEAKR-KSPi-ADCs revealed that KSPi was capable of stimulating several hallmarks of immunogenic cell death (ICD) on three different human cancer cell lines: cellular release of adenosine triphosphate (ATP) and high mobility group B1 protein (HMGB1), exposure of calreticulin on the cell surface as well as a transcriptional type-I interferon response.	kspi	168-172	high mobility group box 1	Homo sapiens	379-384
35096875-14	2021	Taken together, our data here suggest that upregulation of DUOX2 plays a crucial role in ROS production, thereafter, induce HMGB1 release and cell death, which triggers ocular surface inflammation in DED.	Reactive Oxygen Species	89-92	high mobility group box 1	Homo sapiens	124-129
34997217-0	2022	Deubiquitylase USP12 induces pro-survival autophagy and bortezomib resistance in multiple myeloma by stabilizing HMGB1.	Bortezomib	56-66	high mobility group box 1	Homo sapiens	113-118
34997217-8	2022	Furthermore, basal autophagy activity associated with USP12/HMGB1 was elevated in bortezomib (BTZ)-resistant MM cell lines.	Bortezomib	82-92	high mobility group box 1	Homo sapiens	60-65
34997217-9	2022	USP12 depletion, concomitant with a reduced expression of HMGB1, suppressed autophagy and increased the sensitivity of resistant cells to BTZ.	Bortezomib	138-141	high mobility group box 1	Homo sapiens	58-63
34997217-10	2022	Collectively, our findings have identified an important role of the deubiquitylase USP12 in pro-survival autophagy and resultant BTZ resistance in MM by stabilizing HMGB1, suggesting that the USP12/HMGB1 axis might be pursued as a potential diagnostic and therapeutic target in human MM.	Bortezomib	129-132	high mobility group box 1	Homo sapiens	165-170
34997217-10	2022	Collectively, our findings have identified an important role of the deubiquitylase USP12 in pro-survival autophagy and resultant BTZ resistance in MM by stabilizing HMGB1, suggesting that the USP12/HMGB1 axis might be pursued as a potential diagnostic and therapeutic target in human MM.	Bortezomib	129-132	high mobility group box 1	Homo sapiens	198-203
35058496-9	2022	Treatment of the ZIKV-infected cells with dexamethasone (150 microM) reduced HMGB1 extracellular release in a dose-dependent manner, with a maximum reduction of 71 +- 5.84% (P < 0.01).	Dexamethasone	42-55	high mobility group box 1	Homo sapiens	77-82
35058496-12	2022	These results suggest that translocation of HMGB1 occurred during ZIKV infection and inhibition of the translocation by dexamethasone coincided with a reduction in ZIKV replication.	Dexamethasone	120-133	high mobility group box 1	Homo sapiens	44-49
35145563-12	2022	Further studies showed that circ0036602 could bind to miR-34-5p and miR-431-5p to regulate the expression of the target gene HMGB1.	circ0036602	28-39	high mobility group box 1	Homo sapiens	125-130
35006556-14	2022	Finally, miR-142-3p interacted with HMGB1 directly and inhibition of HMGB1 protein expression mediated by MALAT1 knockdown was reversed by miR-142-3p inhibitor.	mir-142-3p	9-19	high mobility group box 1	Homo sapiens	36-41
35006556-14	2022	Finally, miR-142-3p interacted with HMGB1 directly and inhibition of HMGB1 protein expression mediated by MALAT1 knockdown was reversed by miR-142-3p inhibitor.	mir-142-3p	9-19	high mobility group box 1	Homo sapiens	69-74
35006556-14	2022	Finally, miR-142-3p interacted with HMGB1 directly and inhibition of HMGB1 protein expression mediated by MALAT1 knockdown was reversed by miR-142-3p inhibitor.	mir-142-3p	139-149	high mobility group box 1	Homo sapiens	36-41
35006556-14	2022	Finally, miR-142-3p interacted with HMGB1 directly and inhibition of HMGB1 protein expression mediated by MALAT1 knockdown was reversed by miR-142-3p inhibitor.	mir-142-3p	139-149	high mobility group box 1	Homo sapiens	69-74
35006556-17	2022	MALAT1 exerted its effects on IH-treated HUVECs via miR-142-3p/HMGB1.	mir-142	52-59	high mobility group box 1	Homo sapiens	63-68
35442113-11	2022	RESULTS: miR-200b-3p directly target HMGB1.	mir-200b	9-17	high mobility group box 1	Homo sapiens	37-42
35442113-16	2022	CONCLUSION: Decreased miR-200b-3p may function as a biomarker for the diagnosis and survival prognosis of MODS patients, and miR-200b-3p may be involved in the progression of acute paraquat-induced MODS via regulating inflammatory responses by targeting HMGB1.	Paraquat	181-189	high mobility group box 1	Homo sapiens	254-259