PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 67-70 high mobility group box 1 Homo sapiens 35-40 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 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 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 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