|strong|Mouse anti Human High Mobility Group Protein B2 antibody, clone 3E5|/strong| recognizes human high mobility group protein B2, also known as HMGPB2 or HMG-2. Human high mobility group protein B…

As a member of damage-associated molecular patterns (DAMPs), extracellular high-mobility group box 1 (HMGB1) plays a critical role in hepatocellular carcinoma (HCC) progression. Cluster differentiation 44 (CD44) has been demonstrated to participate in HCC progression. However, the relationship between extracellular HMGB1 and CD44 remains unclear. In this study, our results indicated that extracellular HMGB1 promoted the invasion, sphere formation and EMT process of HCC by increasing CD44 expression, which was dependent on miR-21. Moreover, miR-21 upregulated CD44 expression via activating OCT4/TGF-β1 signaling. Finally, we demonstrated the activation of Rage/JNK signaling caused by extracellular HMGB1 was responsible for miR-21 overexpression. Together, these findings reveal an important role of extracellular HMGB1 in HCC progression through upregulating miR-21/CD44.

Granulomatous nephritis can be triggered by diverse factors and results in kidney failure. However, despite accumulating data about granulomatous inflammation, pathogenetic mechanisms in nephritis remain unclear. The DNA-binding high-mobility group box-1 protein (HMGB1) initiates and propagates inflammation when released by activated macrophages, and functions as an alarm cytokine signaling tissue damage. In this study, we showed elevated HMGB1 expression in renal granulomas in rats with crystal-induced granulomatous nephritis caused by feeding an adenine-rich diet. HMGB1 levels were also raised in urine and serum, as well as in monocyte chemoattractant protein-1 (MCP-1), a mediator of granulomatous inflammation. Injection of HMGB1 worsened renal function and upregulated MCP-1 in rats with crystal-induced granulomatous nephritis. HMGB1 also induced MCP-1 secretion through mitogen-activated protein kinase (MAPK) and phosphoinositide-3-kinase (PI3K) pathways in rat renal tubular epithelial cells ...

Background: High-mobility group box 1 (HMGB1) is an endogenous molecule released during cell stress and death termed damage-associated molecular patterns (DAMPs). HMGB1 activates the pattern recognition receptor, toll-like receptor 4 (TLR4), and induces sterile inflammation. However, how HMGB1 and TLR4 affect restenosis, the major complication following balloon and stent intervention clinically, remains unknown. We tested the hypothesis that HMGB1 released following acute arterial injury promotes intimal hyperplasia (IH), a hallmark of restenosis, via TLR4 signaling pathway.. Methods and Results: Wire injury of the carotid artery in C57BL/6 wild-type (WT) mice significantly increased intima-to-media ratio in 4 weeks. Global deletion of HMGB1 using an inducible knockout mouse strain prevented IH and vessel remodeling. IH decreased by over 50% in WT mice treated with a HMGB1 neutralizing antibody. Of the mouse strains deficient in putative receptors and co-regulator for HMGB1 (TLR4-/-, TLR2-/-, ...

Ischemic strokes are caused by decreased blood flow into the brain, due to narrowed cerebral arteries. In the ischemic brain, high-mobility group box 1 (HMGB1) is released into extracellular spaces and induces inflammatory reactions. In this study, researchers from the Korea University delivered HMGB1 small interfering RNA (siRNA) into ischemic brains by intravenous administration using ...

TY - JOUR. T1 - Contributions of high mobility group box protein in experimental and clinical acute lung injury. AU - Ueno, Hiroshi. AU - Matsuda, Tomoyuki. AU - Hashimoto, Satoru. AU - Amaya, Fumimasa. AU - Kitamura, Yoshihiro. AU - Tanaka, Masaki. AU - Kobayash, Atsuko. AU - Maruyama, Ikuro. AU - Yamada, Shingo. AU - Hasegawa, Naoki. AU - Soejima, Junko. AU - Koh, Hidefumi. AU - Ishizaka, Akitoshi. PY - 2004/12/15. Y1 - 2004/12/15. N2 - This study was performed to examine the putative role of high mobility group box (HMGB) protein in the pathogenesis of acute lung injury (ALI). Observations were made (7) in 21 patients who were septic with ALI and 15 patients with normal lung function and (2) in a mouse model 24 hours after intratracheal instillation of lipopolysaccharide (LPS). The concentrations of HMGB1 were increased in plasma and lung epithelial lining fluid of patients with ALI and mice instilled with LPS. LPS-induced ALI was mitigated by anti-HMGB1 antibody. Although this protein was ...

The aim of present study was to evaluate the protective effects of dexmedetomidine (DEX) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and investigate its possible mechanisms mediated by HMGB1. In vivo, pulmonary pathology observation and myeloperoxidase (MPO) activity were also examined to evaluate the protective effect of DEX in the lungs. Tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in bronchoalveolar lavage fluid (BALF), serum and lung tissues LPS-induced rats were detected. The oxidative indices including superoxide dismutase (SOD), Malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) in serum were also determined. Additionally, nitric oxide (NO), TNF-α, IL-6 and IL-1β, MDA, SOD and GSH-Px in the supernatants of LPS-induced BEAS-2B cells were measured. Furthermore, we detected the protein expression of high mobility group box-1 protein (HMGB1), Toll-like receptor 4 (TLR4), myeloid differentiating factor 88 (MyD88), inhibitor of ...

Decades of research have uncovered a variety of molecular mechanisms by which High-mobility group box-1 (HMGB1), also known as HMG1 or Amphoterin, in both immune and non-immune cells, modulate the type and magnitude of immune responses. This ubiquitous, highly conserved protein, HMGB1, was originally discovered in 1973 as a nuclear non-histone protein. The pro-inflammatory activity of extracellular HMGB1 was first discovered as a late mediator of endotoxin lethality in 1999. These findings were explored in the early 2000s in a series of reports elucidating cellular signals activated through HMGB1 receptors including RAGE, toll-like receptor 2 (TLR2), TLR4 and C-X-C chemokine receptor 4 (CXCR4). Post-translational modifications of HMGB1 including oxidation, influence its secretion and function. A substantial number of studies have demonstrated that HMGB1 has a central role in the pathogenesis of many systemic inflammatory diseases such as sepsis, cancer, ischemic injury, neuroinflammation mediated

HMGB1 (high-mobility group box 1) protein, a pleiotropic cytokine released by several cell types under physiological and pathological conditions, has been identified as a signal molecule active on A431 cells. Although extracellular HMGB1 itself does not trigger any detectable signalling effect on these cells, it induces an increased susceptibility to EGF (epidermal growth factor) stimulation. Specifically, at concentrations of EGF which promote undetectable or limited cell responses, the addition of sub-nanomolar concentrations of HMGB1 potentiates the effect of EGF by specifically activating a downstream pathway that leads to enhanced cell motility through an increase in Ca2+ influx, activation of extracellular-signal-regulated kinase 1/2 and remodelling of the actin cytoskeleton. These results, which identify extracellular HMGB1 as an activator of human tumour cell migration operating in concert with EGF, have important implications in the search for novel strategies to control tumour ...

TY - JOUR. T1 - Interaction Analysis Between Polyglutamine-expanded TATA Box Binding Protein (TBP) and High Mobility Group Box 1 (HMGB1). AU - 楊, 淑婷(Shu-Ting Yang). AU - 陳, 襄銘(Hsiang-Ming Chen). AU - 李, 麗卿(Li-Ching Lee). AU - 黃, 詩涵(Shih-Han Huang). AU - 林, 志信(Chih-Hsin Lin). AU - 李, 冠群(Guan-Chiun Lee). AU - 李, 振綱(Cheng-Kang Lee). AU - 李, 桂楨(Guey-Jen Lee-Chen). PY - 2013. Y1 - 2013. N2 - 第十七型脊髓小腦共濟失調症（SCA17）與轉錄起始因子TATA binding protein （TBP）基因上的多麩醯胺擴增相關。TBP與包括high mobility group box 1 （HMGB1）在內的其他蛋白因子交互作用，來調節基因的表現。本研究藉重組的HMGB1 及TBP／Q20～61 N端蛋白，探討TBP Q長度是否影響其與HMGB1的結合。首先共表現HMGB1及TBP於 HEK-293細胞後，利用免疫共沉澱及GST pull-down試驗，確認HMGB1 與TBP在細胞內的結合。其次原核E. coli表現的重組HMGB1 ...

Human malignant gliomas, the most common primary brain tumors, are characterized by excessive proliferation and infiltrative growth. Although the molecular determinants of glioma properties are still unclear, a significant role for the altered regulation of modulators of glial growth and motility has been proposed. In the complex network of molecular signals involved in tumorigenesis, high mobility group box 1 protein (HMGB1) has recently emerged. This low molecular weight protein, previously considered solely as a chromatin-associated molecule, can be present extracellularly after passive release by necrotic cells or active secretion by some cell types. In the extracellular milieu, HMGB1 can act as a multifunctional paracrine/autocrine factor via its interaction with the receptor for advanced glycation end products (RAGE). Increasing evidence supports that HMGB1 plays an important role in tumors, promoting cancer cell growth, motility, and invasion. Although different human tumors overexpress ...

IV Vitamin C Stops Sepsis in Its Tracks. Reference: NPR, Chest, Managed Care, Barry Fowler, Biofactors,. The number three cause of death in America today is the overwhelming infection that causes blood pressure collapse, kidney shut down and death called sepsis. Three hundred thousand people in America die from it each year. As far is deaths in hospitals, its number one. Sepsis is dangerous.. The cause of sepsis is still not exactly known, but it acts like a runaway train. Cytokine storm is the term used to describe the same process in severe influenza, where all your hormones of inflammation fire off in a cycle of uncontrolled and dysfunctional activation. One thing in known, there is a leaking of capillaries all over the body while alarmins (danger-associated molecular patterns (DAMPs)) are released. These DAMPs are nuclear, cytoplasmic, or mitochondria structures that acquire new functions outside the cell. Examples of DAMPs have great names like high mobility group box-1 protein HMGB1, ...

Acetaminophen (APAP) overdose induces massive hepatocyte necrosis. Necrotic tissue releases high mobility group B1 (HMGB1), and HMGB1 contributes to liver injury. Even though blockade of HMGB1 does not protect against APAP-induced acute liver injury (ALI) at 9 h time point, the later time points are not studied and the role of HMGB1 in APAP overdose is unknown, it is possible that neutralization of HMGB1 might improve hepatocyte regeneration. This study aims to test whether blockade of HMGB1 improves hepatocyte regeneration after APAP overdose. Male C57BL/6 mice were treated with a single dose of APAP (350 mg/kg). 2 hrs after APAP administration, the APAP challenged mice were randomized to receive treatment with either anti-HMGB1 antibody (400 μg per dose) or non-immune (sham) IgG every 24 hours for a total of 2 doses. 24 hrs after APAP injection, anti-HMGB1 therapy instead of sham IgG therapy significantly improved hepatocyte regeneration microscopically; 48 hrs after APAP challenge, the sham IgG

Platelets are circulating cellular sensors that express and release the damage-associated molecular pattern molecule (DAMP) high-mobility group box 1 (HMGB1) at sites of disrupted vascular and tissue integrity. We have recently identified platelet-derived HMGB1 as a critical mediator of thrombosis. …

Background: High Mobility Group Box 1 (HMGB1) is as an abundant and ubiquitous nuclear DNA-binding protein that has multiple functions dependent on its cellular location. In the nucleus, HMGB1 binds to DNA and is critical for proper transcriptional regulation. However, little is known about the effects of HMGB1 on heart failure. The aim of this study was to examine the impact of HMGB1 on cardiac dysfunction induced by pressure overload.. Methods and Results: We generated transgenic mice with cardiac-specific overexpression of HMGB1 (HMGB1-TG) using α-myosin heavy chain promoter. There were no differences in cardiac morphology and function between wild-type (WT) and HMGB1-TG mice at basal condition. Thoracic transverse aortic constriction (TAC) was performed in transgenic mice with cardiac-specific overexpression of HMGB1 (HMGB1-TG) and wild-type (WT) mice. The survival rate after TAC was significantly higher in HMGB1-TG mice compared to WT mice. Increases in heart/body weight ratio after TAC ...

TY - JOUR. T1 - [High mobility group box 1 is increased in children with acute lymphocytic leukemia and stimulates the release of tumor necrosis factor-alpha in leukemic cell].. AU - Kang, Rui. AU - Tang, Dao lin. AU - Cao, Li zhi. AU - Yu, Yan. AU - Zhang, Guo yuan. AU - Xiao, Xian zhong. PY - 2007/5. Y1 - 2007/5. N2 - Cytokine mediated cell immunity is the main mode of anti-tumor immunity in organism, and the disequilibrium of cytokine network is the main cause of tumor cells escaping immunologic surveillance. High mobility group box 1 (HMGB1), a nuclear protein, has recently been identified as an important mediator of local and systemic inflammatory diseases when released into the extracellular milieu. In the present study, the investigators explored the clinical significance of alteration in the serum levels of HMGB1 in childhood acute lymphocytic leukemia (ALL) and the mechanism of HMGB1-induced tumor necrosis factor (TNF)-alpha secretion in leukemic cells. The serum levels of HMGB1 in ...

Background: Smokers show increased prevalence of insulin resistance for glucose and type 2 diabetes mellitus (T2DM). The underlying mechanisms, however, remain poorly understood. Tobacco smoke exposure increases tissue expression of high mobility group box 1 (HMGB1), a damage-associated molecular pattern (DAMP) that activates innate immunity. We recently reported that exposure of human macrophages to tobacco smoke extract (TSE) provokes the release of HMGB1 in two forms: as a soluble molecule and carried on membrane microvesicles (MV). Both soluble recombinant HMGB1 (rHMGB1) and MV-associated HMGB1 on TSE-induced MVs (TSE-MVs) mediate crucial crosstalk with adipocytes by impairing insulin signaling and by recruiting monocytes to the adipocytes -. GOAL- To identify the receptors on adipocytes that mediate the effects of HMGB1 on insulin signaling and monocyte recruitment.. Methods: Cultured 3T3-L1 adipocytes were incubated for 24h with rHMGB1 or TSE-MVs, in the absence or presence of neutralizing ...

This study aimed to investigate the association of serum high-mobility group box-1 (HMGB1) and toll-like receptor 4 (TLR4) expressions with the risk of epilepsy as well as their correlations with disease severity and resistance to anti-epilepsy drugs. One hundred and five epilepsy patients and 100 healthy controls (HCs) were enrolled in this case-control study, and serum samples were collected from all participants to assess the HMGB1 and TLR4 expressions by enzyme-linked immunosorbent assay (ELISA). Both serum HMGB1 (P,0.001) and TLR4 (P,0.001) expressions were higher in epilepsy patients than in HCs, and they displayed good predictive values for risk of epilepsy. Moreover, HMGB1 was positively correlated with TLR4 level (r=0.735, P,0.001). HMGB1 ...

Postoperative neurocognitive disorders are common complications in elderly patients following surgery or critical illness. High mobility group box 1 protein (HMGB1) is rapidly released after tissue trauma and critically involved in response to sterile injury. Herein we assessed the role of HMGB1 after liver surgery in aged rats and explored the therapeutic potential of a neutralizing anti-HMGB1 monoclonal antibody in a clinically relevant model of postoperative neurocognitive disorders. 19-22 months Sprague Dawley rats were randomly assigned as: (1) control with saline; (2) surgery, a partial hepatolobectomy under sevoflurane anesthesia and analgesia, + immunoglobulin G as control antibody; (3) surgery + anti-HMGB1. A separate cohort of animals was used to detect His-tagged HMGB1 in the brain. Systemic anti-HMGB1 antibody treatment exerted neuroprotective effects preventing postoperative memory deficits and anxiety in aged rats by preventing surgery-induced reduction of phosphorylated cyclic AMP

TY - JOUR. T1 - Exogenous high-mobility group box 1 improves myocardial recovery after acute global ischemia/reperfusion injury. AU - Abarbanell, Aaron M.. AU - Hartley, Jacob A.. AU - Herrmann, Jeremy L.. AU - Weil, Brent R.. AU - Wang, Yue. AU - Manukyan, Mariuxi C.. AU - Poynter, Jeffrey A.. AU - Meldrum, Daniel R.. PY - 2011/3/1. Y1 - 2011/3/1. N2 - Background: High-mobility group box 1 (HMGB1) is a mediator of inflammation with dose-dependent effects. In the setting of regional myocardial infarction, a high-dose HMGB1 treatment decreases myocardial function, whereas low-dose HMGB1 improves function; however, it is unknown what role HMGB1 has in the setting of global ischemia/reperfusion (I/R) injury. We hypothesized that a low-dose HMGB1 treatment would improve myocardial functional recovery and decrease infarct size after global I/R injury in association with increased levels of cardioprotective paracrine factors and decreased inflammation. Methods: Adult rat hearts were isolated and ...

Summary: Tissue damage occurs often in the life of mammals and is usually repaired. Dying cells are swiftly phagocytosed, but before disappearing, they alert surrounding cells to activate homeostatic programs. They release signals that recruit inflammatory cells to the site of injury, promote cell migration and cell division to replace dead cells, and activate the immune system in anticipation of microbial invasion. Many of these events involve high-mobility group box 1 protein (HMGB1), a nuclear protein that is released passively when necrotic cells lose the integrity of their membranes. HMGB1 behaves as a trigger of inflammation, attracting inflammatory cells, and of tissue repair, recruiting stem cells and promoting their proliferation. Moreover, HMGB1 activates dendritic cells (DCs) and promotes their functional maturation and their response to lymph node chemokines. Activated leukocytes actively secrete HMGB1 in the microenvironment. Thus, HMGB1 acts in an autocrine/paracrine fashion and ...

REPORT High Mobility Group Protein B1 (High Mobility Group Protein 1 or High Mobility Group Protein Box 1 or HMGB1) - High mobility group box 1 protein also known as high-mobility group protein 1 (HMG-1) is a protein encoded by ... > ...

The majority of glutathione, an important antioxidant, appears in the body in its reduced form (GSH), with 10% appearing in its oxidized form of glutathione disulfide (GSSG). A deficiency in glutathione results in oxidative stress and plays a major role in the pathogenesis of type 2 diabetes. Furthermore, oxidative stress is an important cause of intestinal epithelial cell death. High mobility group box 1 protein (HMGB1) has been shown to mitigate disease and inhibit apoptosis. This investigation sought to determine the effect of HMGB1 on oxidative stress in the gut to determine HMGB1s role in the pathogenesis of type 2 diabetes. The oxidative stress of HMGB1 f/f and HMGB1 f/f vil-CRE mice was measured using a GSH/GSSG ratio assay kit on ileal mucosal scrapings, cecal contents, stoop samples, and tissue taken from the liver. Future investigations could investigate the role of HMGB1 in conjunction with diet by also using mice that are fed either a high fat diet or a regular chow diet.

High-mobility group box-1 (HMGB1) protein acts as a transcription factor in the nucleus and also as a pro-inflammatory cytokine when released into extracellular fluids. The presence of higher levels of HMGB1 is reported in the gingival crevicular fluid from periodontal patients. Since the proliferat …

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Systemic lupus erythematosus (SLE) is a systemic inflammatory disease. Clinically, the distinction between ongoing inflammation attributed to SLE, and organ damage due to medication or co-morbidities remains challenging. In addition, SLE is a heterogeneous disease where the various disease phenotypes complicate the search for biomarkers that adequately reflect disease activity and/or signs of increasing organ damage. The aim of the thesis was to investigate and evaluate potential new biomarkers of disease activity and/or organ damage in SLE patients.. High mobility group box protein-1 (HMGB1) is a nuclear non-histone protein that can shuttle to the cytoplasm, become secreted extracellularly, and participate in systemic inflammation. Administration of monoclonal anti-HMGB1 antibodies has been reported both to attenuate and intensify disease in animal models of arthritis and lupus. In Paper I of the thesis, circulating anti-HMGB1 was found in 23% of the SLE patients and correlated with disease ...

Innate immune mechanisms represent bodys first line of defense against pathogens, capable of recognizing Pathogen-associated molecular patterns (PAMPs) and Damage-associated molecular pattern molecules (DAMPs). The PAMPs and DAMPs are recognized by pattern recognition receptors (PRRs), such as membrane bound Toll-like receptors (TLRs) or cytoplasmic NOD-like receptors (NLR) and RIG-I- like receptors (RLR). This page provides a broad review of the signaling pathways for these receptors leading to inflammation and immune activation. BioLegend develops and manufactures world-class, cutting-edge immunological reagents for biomedical research, offered at an outstanding value.

Patients surviving sepsis develop anemia but the molecular mechanism is unknown. Here we observed that mice surviving polymicrobial Gram-negative sepsis develop hypochromic, microcytic anemia with reticulocytosis. The bone marrow of sepsis survivors accumulates polychromatophilic and orthochromatic erythroblasts. Compensatory extramedullary erythropoiesis in the spleen is defective during terminal differentiation. Circulating TNF and IL-6 are elevated for five days after the onset of sepsis, and serum HMGB1 levels are increased from day seven until at least day 28. Administration of recombinant HMGB1 to healthy mice mediates anemia with extramedullary erythropoiesis and significantly elevated reticulocyte counts. Moreover, administration of anti-HMGB1 monoclonal antibodies after sepsis significantly ameliorates the development of anemia (hematocrit 48.5+/-9.0% versus 37.4+/-6.1%, p

Hypothermic preservation of solid allografts causes profound damage of vascular endothelial cells. This, in turn, might activate innate immunity. In the present study we employed an in vitro model to study to what extent supernatants of damaged endothelial cells are able to activate innate immunity and to study the nature of these signals. The expression of high mobility group box 1 (HMGB1) and adhesion molecules on human umbilical vein endothelial cell was studied by immunofluorescence, fluorescence activated cell sorter and Western blotting. Cytokine production was performed by enzyme-linked immunosorbent assay. HMGB1 expression was lost completely in endothelial cells after hypothermic preservation. This was associated with cell damage as it occurred only in untreated endothelial cell but not in cells rendered resistant to hypothermia-mediated damage by dopamine treatment. Only supernatants from hypothermia susceptible cells up-regulated the expression of interleukin (IL)-8 and adhesion molecules in

In study III, the association between plasma HMGB1 and objective cognitive function measured in four different cognitive domains (executive function, visual memory, sustained attention, working memory) was investigated. Interestingly, plasma levels of HMGB1 were significantly elevated in the ICU, at discharge, and at the three- and six-months follow-up visits as compared with reference popula- tions. Elevated plasma levels of HMGB1 were associated with reduced sustained attention at the three- and six-month follow-up visits. Based on these findings, further follow-up studies on HMGB1 biology in ICU survivors are warranted to investigate the potential for therapeutic targeting of HMGB1 function in preven- tion of cognitive impairment in ICU survivorsIn study IV we explore the association between plasma HMGB1 and physical performance at ICU follow-up. We observed no significant association between levels of plasma HMGB1 and the three physical tests performed (i.e., 6-min walk test, timed stands ...

High-mobility group box 1 (HMGB1) is an important molecule for several nuclear processes. Recently, HMGB1 has gained much attention as a damage-associated molecular pattern (DAMP) and has been...

High mobility group box B (HMGB) proteins are pivotal in the development of cancer. Although the proteomics of prostate cancer (PCa) cells has been reported, the involvement of HMGB proteins and their interactome in PCa is an unexplored field of considerable interest. We describe herein the results of the first HMGB1/HMGB2 interactome approach to PCa. Libraries constructed from the PCa cell line, PC-3, and from patients’ PCa primary tumor have been screened by the yeast 2-hybrid approach (Y2H) using HMGB1 and HMGB2 baits. Functional significance of this PCa HMGB interactome has been validated through expression and prognosis data available on public databases. Copy number alterations (CNA) affecting these newly described HMGB interactome components are more frequent in the most aggressive forms of PCa: those of neuroendocrine origin or castration-resistant PCa. Concordantly, adenocarcinoma PCa samples showing CNA in these genes are also associated with the worse prognosis. These findings open the

Cette publication a donnée lieu à un commentaire dans la revue Immunity, 2008, 29(1): 1-2. Kazama H, Ricci JE, Herndon JM, Hoppe G, Green DR and Ferguson TA. Induction of immunological tolerance by apoptotic cells requires caspase-dependent oxidation of high-mobility group box-1 protein. Immunity, 2008, 29(1): 21-32.. Mastino A, Basu S, Brunner T, Ricci JE and Diederich M. Long live the cell death! Cell Death Differ, 2008, 15(8): 1330-1332. 2007 Colell, A.,* Ricci, J. E.,* Tait, S., Milasta, S., Maurer, U., Bouchier-Hayes, L., Fitzgerald, P., Guio-Carrion, A., Waterhouse, N. J., Wei Li, C., Mari, B., Barbry, P., Newmeyer, D. D.,. Beere, H. and Green, D. R. (2007) GAPDH and autophagy preserve cellular survival during caspase-independent cell death Cell, 129(5):983-997. *co-first author.. Cette publication a donnée lieu à des commentaires dans les revues Cell et Nature Cell Biology (Cell. 2007 Jun 1;129(5):861-3 -- Nat Cell Biol. (2007) Aug;9(8):869-70). Ricci, JE, Munoz-Pinedo, C, Fitzgerald, ...

Aim: To determine whether high-mobility group box 1 (HMGB1) and Toll like receptor 4 (TLR4) drive the inflammatory cascade that promotes intimal hyperplasia (IH) following acute vascular injury. Methods and Results: Carotid artery wire injury in C57BL/6 mice induced a significant increase in intima to media (I/M) ratio at four weeks. Global deletion of HMGB1 using an inducible knockout mouse strain caused prevention of IH. IH was decreased by over 50% in WT mice treated with HMGB1 neutralizing antibody. Of knockout mouse strains deficient in putative receptors for HMGB1, TLR4-/- mice showed the greatest inhibition of IH. Both anti-HMGB1 treated mice and TLR4-/- mice exhibited a marked decrease in monocytic recruitment. Mice with selective depletion of TLR4 from macrophage exhibited a similar level of inhibition of IH to that seen in the global TLR4-/-. In vitro, dithiol HMGB1 dose-dependently promoted SMC migration and MCP-1/CCR2 expression, which was abolished by TLR4 inhibitory peptide. ...

Discussion The importance of inflammatory response in the pathophysiology of ischemic stroke is generally recognized. HMGB1 has been identified as an early mediator of hemorrhage after acute lung injury [33] and hepatic injury after liver ischemia/reperfusion [34]. Recent evidence suggests that the inflammatory cytokine HMGB1 is an active mediator of ischemic brain injury [29]. Moreover, elevated levels of HMGB1 in the serum of human patients with cerebral infarction have also been reported [35]. Therefore, HMGB1 has been attracting attention as a potential diagnostic marker [36,37]. HMGB1 was identified as a ubiquitously expressed, abundant nonhistone DNA-binding protein, which stabilizes the nucleosome formation and facilitates gene transcription. HMGB1 protein can be actively released into the extracellular space by macrophages and monocytes [16,20]. It is also passively released by necrotic cells, although not by apoptotic cells, and it triggers inflammation [38]. Extracellular HMGB1 ...

PREDICTED: similar to High mobility group protein 1 (HMG-1) (High mobility group protein B1) (Amphoterin) (Heparin-binding protein p30) isoform 1 [Canis familiaris ...

Macrophage polarization is critical to inflammation and resolution of inflammation. We previously showed that high-mobility group box 1 (HMGB1) can engage receptor for advanced glycation end product (RAGE) to direct monocytes to a proinflammatory phenotype characterized by production of type 1 IFN and proinflammatory cytokines. In contrast, HMGB1 plus C1q form a tetramolecular complex cross-linking RAGE and LAIR-1 and directing monocytes to an antiinflammatory phenotype. Lipid mediators, as well as cytokines, help establish a milieu favoring either inflammation or resolution of inflammation. This study focuses on the induction of lipid mediators by HMGB1 and HMGB1 plus C1q and their regulation of IRF5, a transcription factor critical for the induction and maintenance of proinflammatory macrophages. 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

Blood-brain barrier (BBB) breakdown and inflammatory responses are the major causes of tissue-type plasminogen activator (tPA)-induced hemorrhagic transformation (HT), while high-mobility group box 1 (HMGB1) exacerbates inflammatory damage to BBB during the process of brain ischemia/reperfusion. This study aimed to investigate the change of HMGB1 after thrombolytic therapy and whether blocking HMGB1 could ameliorate the neurovasculature complications secondary to tPA treatment in stroke rats. Sera from acute stroke patients and rats with thrombolytic therapy were collected to investigate HMGB1 secretion. Male Sprague-Dawley rats with 2 h or 4.5 h middle cerebral artery occlusion were continuously infused with tPA followed by administration of membrane permeable HMGB1-binding heptamer peptide (HBHP). The mortality rate, neurological score, HT, brain swelling, BBB permeability, and inflammatory factors were determined. The results revealed that HMGB1 levels were elevated in both stroke patients and rats

Declining renal function is commonly observed with age. Obesity induced by a high-fat diet (HFD) may reduce renal function. Korean red ginseng (KRG) has been reported to ameliorate oxidative tissue injury and have an anti-aging effect. This study was designed to investigate whether HFD would accelerate the D-galactose-induced aging process in the rat kidney and to examine the preventive effect of KRG on HFD and D-galactose-induced aging-related renal injury. When rats with D-galactose-induced aging were fed an HFD for 9 wk, enhanced oxidative DNA damage, renal cell apoptosis, protein glycation, and extracellular high mobility group box 1 protein (HMGB1), a signal of tissue damage, were observed in renal glomerular cells and tubular epithelial cells ...

HMGB1 is a ubiquitous, abundant nuclear protein highly conserved among all mammals (11, 45). Incubation of macrophages with LPS or TNF-α results in increased release of HMGB1, and HMGB1 itself can stimulate macrophages, monocytes, and neutrophils to release proinflammatory cytokines, including IL-1β, TNF-α, and IL-8 (2, 30, 44). Increased circulating levels of HMGB1, attributed to release from activated macrophages, have been measured in the serum of mice treated with endotoxin as well as from septic patients (44). Additionally, HMGB1 appears to function as a late mediator of endotoxin lethality, as demonstrated by improved survival after treatment with specific anti-HMGB1 antibodies (44). When added to target cell cultures, HMGB1 can potently induce multiple responses, including differentiation, cytoskeletal reorganization, migration, and release of proinflammatory cytokines (1, 2, 9, 32). Recent information also suggests that HMGB1 may be an indicator of cell death by necrosis because its ...

Results presented herein provide new insights into the release of HMGB1 by macrophages in cells stimulated by TLR ligands and suggest that the translocation of this protein and apoptosis are closely related processes that may reflect common mechanisms. Thus, as our findings show, stimulation of RAW 264.7 cells by either LPS or poly(I:C) leads to the translocation of HMGB1 from the nucleus into the extracellular milieu under conditions in which the frequency of apoptotic cells increases dramatically; similar results were obtained with primary macrophages cultured from mice. Although the presence of apoptotic cells in cultures of activated cells does not prove that they are the source of HMGB1, the failure of cells stimulated by CpG DNA to release HMGB1 suggests that activation by itself is not sufficient for this process. Thus, for macrophages, it appears that apoptosis is closely associated with events leading to HMGB1 release and, indeed, may be the origin of at least some of the HMGB1 released ...

HMGB3 silence inhibits breast cancer cell proliferation and tumor growth by interacting with hypoxia-inducible factor 1alpha Jun Gu, Tao Xu, Qin-Hua Huang, Chu-Miao Zhang, Hai-Yan ChenDepartment of Health Check-Up Center, Jinshan Hospital, Fudan University, Shanghai 201508, Peoples Republic of ChinaBackground: Breast cancer is the most common malignant tumor that affects women with higher incidence. High-mobility group box 3 (HMGB3) plays critical functions in DNA repair, recombination, transcription and replication. This study aimed to investigate the effects of HMGB3 silence on mammosphere formation and tumor growth of breast cancer.Methods: LV5-HMGB3 and LV3-siHMGB3 vectors were transfected into MCF10A, MDA-MB-231, HCC1937, ZR-75-1 and MCF7 cells. Cell counting kit-8 (CCK-8) assay was used to evaluate cell proliferation. Xenograft tumor mice model was established by injection of MDA-MB-231. qRT-PCR and western blot were used to examine the expression of Nanog, Sox2 and OCT-4. Mammosphere forming

Mouse monoclonal HMGB1 antibody [HAP46.5] validated for WB, ELISA and tested in Human, Mouse and Rat. Referenced in 11 publications. Immunogen corresponding to…

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Disease Markers is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies related to the identification of disease markers, the elucidation of their role and mechanism, as well as their application in the prognosis, diagnosis and treatment of diseases.

Infections induced by influenza viruses, as well as coronavirus disease 19 (COVID-19) pandemic induced by severe acute respiratory coronavirus 2 (SARS-CoV-2) led to acute lung injury (ALI) and multi organ failure, during which traditional Chinese medicine (TCM) played an important role in treatment of the pandemic. The study aimed to investigate the effect of Indigo Naturalis on ALI induced by influenza A virus (IAV) in mice. The anti-influenza and anti-inflammatory properties of aqueous extract of Indigo Naturalis (INAE) were evaluated in vitro. BALB/c mice inoculated intranasally with IAV (H1N1) were treated intragastrically with INAE (40, 80 and 160 mg/kg/day) 2 h later for 4 or 7 days. Animal lifespan and mortality were recorded. Expression of high mobility group box-1 protein (HMGB-1) and toll-like receptor 4 (TLR4) were evaluated through immunohistological staining. Inflammatory cytokines were also monitored by ELISA. INAE inhibited virus replication on Madin-Darby canine kidney (MDCK) cells and

Cisplatin is one of the most widely used chemical drugs for anticancer treatment. Recent studies have focused on the ability of cisplatin to retain the high mobility group box 1 (HMGB1) protein in cisplatin-DNA adducts, thereby preventing its release from the nucleus. Because HMGB1 is a powerful inflammatory mediator in many diseases, the aim of this study is to evaluate the therapeutic effect of cisplatin acute liver failure. In this study, low-dose cisplatin was administered to treat PMA-induced macrophage-like cells induced by PMA and rats with acute liver failure. We found that cell viability and liver injury were greatly improved by cisplatin treatment. The extracellular levels of HMGB1, TNF-α and IFN-γ were also significantly decreased by the administration of cisplatin. During inflammation, nuclear HMGB1 translocates from the nucleus to the cytoplasm. The administration of cisplatin reduced the cytoplasmic levels of HMGB1 and increased nuclear HMGB1 levels in vitro and in vivo. In conclusion,

Backgroundand objectives Idiopathic inflammatory myopathies (IIMs) are chronic inflammatory diseases characterised by muscle weakness and the mechanisms are still unclear. High mobility group box protein 1 (HMGB1) is often found together with aberrant expression of major histocompatibility complex (MHC) class I in muscle fibres of patients with IIMs but not in healthy individuals. Exogenous HMGB1 can accelerate development of muscle fatigue and increase MHC-class I expression in adult mice skeletal muscle fibres. In other tissues it has been shown that HMGB1 could mediate functions via different receptors including the receptor for advanced glycation end products (RAGE) and Toll-like receptor 4 (TLR4). In this study, the authors set out to investigate whether HMGB1 contribute to increased muscle fatigue and MHC-class I expression in muscle fibres via RAGE or TLR4 in adult skeletal muscle fibres.. ...

The nuclear protein high-mobility group box 1 (HMGB1) is a key trigger for the inflammatory reaction during liver ischemia reperfusion injury (IRI). Hydrogen treatment was recently associated with down-regulation of the expression of HMGB1 and pro-inflammatory cytokines during sepsis and myocardial IRI, but it is not known whether hydrogen has an effect on HMGB1 in liver IRI. A rat model of 60 minutes 70% partial liver ischemia reperfusion injury was used. Hydrogen enriched saline (2.5, 5 or 10 ml/kg) was injected intraperitoneally 10 minutes before hepatic reperfusion. Liver injury was assessed by serum alanine aminotransferase (ALT) enzyme levels and histological changes. We also measured malondialdehyde (MDA), hydroxynonenal (HNE) and 8-hydroxy-guanosine (8-OH-G) levels as markers of the peroxidation injury induced by reactive oxygen species (ROS). In addition, pro-inflammatory cytokines including TNF-α and IL-6, and high mobility group box B1 protein (HMGB1) were measured as markers of post

Human HMGB1 ELISA Kit from ELISA Genie is a pre-coated immunoassay with a sensitivity of 18.75 pg/ml and a range of 31.25-2000pg/ml and has been designed to measure Human HMGB1 ELISA Kit in serum, plasma & cell culture supernatant samples. The Human HMGB1 ELISA Kit accurately measures natural Human HMGB1 levels quantified versus standard curves obtained and is based on antibodies raised against a recombinant Human HMGB1 peptide.

The present study demonstrated that (1) methamphetamine increases the expression of HMGB1 and that (2) HMGB1 promotes the activation and migration of C6 astrocytes. Up-regulation of HMGB1 in reactive astrocytes may contribute to the activation and migration of astrocytes through an autocrine feedforward mechanism that increases HMGB1 expression, thus amplifying the neuroinflammatory cascade induced by methamphetamine. Although previous studies have demonstrated that HMGB1 functions as a damage-associated molecular pattern (DAMP) involved in inflammatory response, it is still remained unclear whether HMGB1 is involved in methamphetamine-induced neuroinflammation.. In the current study, we demonstrated that methamphetamine exposure increased HMGB1 expression in astrocytes via the methamphetamine cognate receptor, σ-1R, which interacted with Src and activated the downstream MAPK/ERK pathway and the NF-κB p65 transcription factor leading to HMGB1 expression with subsequent functional activation ...

Results CSF HMGB1 levels in NMO patients were higher than those in MS and ONNDs patients (p,0.001), and these levels in MS patients were higher than those in ONNDs patients (p,0.001). After treatment, the CSF HMGB1 levels in NMO patients decreased to normal. In addition, CSF HMGB1 levels correlated with CSF cell counts, CSF protein levels, CSF interleukin-6 levels, CSF glial fibrillary acidic protein levels, and CSF/serum albumin ratio (p≤0.001). Serum HMGB1 levels in MS patients were significantly higher than those in ONNDs patients (p=0.002).. ...

HMGB1, a non-histone nuclear factor, acts extracellularly as a mediator of delayed endotoxin lethality, which raises the question of how a nuclear protein can reach the extracellular space. We show that activation of monocytes results in the redistribution of HMGB1 from the nucleus to cytoplasmic organelles, which display ultrastructural features of endolysosomes. HMGB1 secretion is induced by stimuli triggering lysosome exocytosis. The early mediator of inflammation interleukin (IL)-1beta is also secreted by monocytes through a non-classical pathway involving exocytosis of secretory lysosomes. 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. Thus, in monocytes, non-classical

TY - JOUR. T1 - Thermodynamics of HMGB1 interaction with duplex DNA. AU - Müller, S.. AU - Bianchi, M. E.. AU - Knapp, S.. PY - 2001/8/28. Y1 - 2001/8/28. N2 - The high mobility group protein HMGB1 is a small, highly abundant protein that binds to DNA in a non-sequence-specific manner. 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. Isothermal titration calorimetry was used to characterize the binding of HMGB1 to the double-stranded model DNAs poly(dAdT)·(dTdA) and poly(dGdC)·(dCdG). To elucidate the contribution of the different structural motifs to DNA binding, calorimetric measurements were performed comparing the single boxes A and B, the two boxes plus or minus the basic sequence stretch (ABbt and AB), and the full-length HMGB1 protein. Thermodynamically, binding of HMGB1 and all truncated constructs to duplex DNA was characterized by a positive enthalpy change at 15 °C. From ...

HMG20B; high mobility group 20B; SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily E member 1-related; BRAF25; BRAF35; HMG box domain containing 2; HMGX2; HMGXB2; SMARCE1r; SOXL; SMARCE1-related protein; high-mobility grou; high-mobility group 20B; BRCA2-associated factor 35; HMG box-containing protein 20B; HMG domain-containing protein 2; Sox-like transcriptional factor; HMG domain-containing protein HMGX2; structural DNA-binding protein BRAF35; SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily E, member 1-related; PP7706; pp8857; FLJ26127; SOXL, HMGX2, BRAF25, BRAF35, HMGXB2, PP7706, pp8857, SMARCE1r; fc85b02; wu:fc85b02; zgc:110001; si:dkey-110c1.6; high mobility group box domain containing ...

Damage-associated molecular patterns (DAMPs), also known as danger-associated molecular patterns, danger signals, and alarmin, are host biomolecules that can initiate and perpetuate a noninfectious inflammatory response. In contrast, pathogen-associated molecular patterns (PAMPs) initiate and perpetuate the infectious pathogen-induced inflammatory response. A subset of DAMPs are nuclear or cytosolic proteins. When released outside the cell or exposed on the surface of the cell following tissue injury, they move from a reducing to an oxidizing milieu, which results in their denaturation. Also, following necrosis (a kind of cell death), tumor DNA is released outside the nucleus, and outside the cell, and becomes a DAMP. Two papers appearing in 1994 presaged the deeper understanding of innate immune reactivity, dictating the subsequent nature of the adaptive immune response. The first came from transplant surgeons who conducted a prospective randomized double-blind placebo-controlled trial. ...

To determine whether selected damage-associated molecular patterns (DAMPs) present in the osteoarthritic (OA) joints of mice excite nociceptors through Toll-like receptor 4 (TLR-4).The ability of S100A8 and ?2 -macroglobulin to excite nociceptors was determined by measuring the release of monocyte chemoattractant protein 1 (MCP-1) by cultured dorsal root ganglion (DRG) cells as well as by measuring the intracellular calcium concentration ([Ca(2+) ]i ) in cultured DRG neurons from naive mice or from mice that had undergone surgical destabilization of the medial meniscus (DMM) 8 weeks previously. The role of TLR-4 was assessed using TLR-4(-/-) cells or a TLR-4 inhibitor. The [Ca(2+) ]i in neurons within ex vivo intact DRGs was measured in samples from Pirt-GCaMP3 mice. Neuronal expression of the Tlr4 gene was determined by in situ hybridization. DMM surgery was performed in wild-type and TLR-4(-/-) mice; mechanical allodynia was monitored, and joint damage was assessed histologically after 16 weeks.DRG

Dr. Ofori-Acquah is an Associate Professor of Medicine and Human Genetics at the Universityof Pittsburgh. He is Director of the Center for Translational and International Hematology at the Universitys Vascular Medicine Institute. He is Director and Project Leader of a number of NIH and Wellcome Trust research and training programs. His research is focused on the role and mechanism of extracellular heme in the pathobiology of sickle cell disease (SCD). He has developed a mouse model of acute chest syndrome that recapitulates the clinical, biological and pathological features of the condition in humans. His group is using this model to unravel the mechanism of lung injury in acute chest syndrome, and to test candidate drugs for their potential to prevent and treat this lung condition. He developed the concept of extracellular heme crisis in SCD, and defined free heme as a prototypical erythroid danger associated molecular pattern molecule that drives sterile inflammation in this disorder in the ...

Dr. Ofori-Acquah is an Associate Professor of Medicine and Human Genetics at the Universityof Pittsburgh. He is Director of the Center for Translational and International Hematology at the Universitys Vascular Medicine Institute. He is Director and Project Leader of a number of NIH and Wellcome Trust research and training programs. His research is focused on the role and mechanism of extracellular heme in the pathobiology of sickle cell disease (SCD). He has developed a mouse model of acute chest syndrome that recapitulates the clinical, biological and pathological features of the condition in humans. His group is using this model to unravel the mechanism of lung injury in acute chest syndrome, and to test candidate drugs for their potential to prevent and treat this lung condition. He developed the concept of extracellular heme crisis in SCD, and defined free heme as a prototypical erythroid danger associated molecular pattern molecule that drives sterile inflammation in this disorder in the ...

Several plant pathogenic oomycetes have been under investigation using modern molecular approaches. Genome sequencing and annotations are underway or near to completion for some of the species. Pathogen-associated molecular pattern molecules (PAMPs) and effector molecules perform inter- and intracellular tasks as adaptation factors and manipulators of the defence network. Hundreds of secreted putative effectors have been discovered and conserved molecular patterns such as RXLR and EER motifs have been identified and used for classifications. PAMPs and effectors are recognized directly or indirectly by the pattern recognition receptors at the cell surface including receptor-like kinases and receptor-like proteins, and/or by nucleotide binding site-leucine rich repeat proteins within the cytoplasm. The current knowledge of effectors, immune receptors and the defence network, will help us understand the intricate genetic dance between the oomycete pathogens and their hosts. This review ...

Background The inflammatory response triggered by cardiac surgery with cardiopulmonary bypass (CPB) is a primary cause of postoperative atrial fibrillation (POAF). The objective of this study was to...

HMGB2 expression during chondrogenesis of human MSC. Immunohistochemistry shows that HMGB2 is expressed at days 1 and 3, but that expression is reduced at days 7, 14 upon induction of chondrogenesis. SO: safranin O staining. ...

The TLR family is a large family of receptors, with at least 11 members that have been identified thus far [24]. The TLRs play an important role in the host defense mechanism as part of the innate immune response. The different members of the TLR family have evolved to recognize pathogen-associated molecular patterns (PAMPs), including cell wall components of Gram-positive, Gram-negative bacteria, viruses and fungi [24]. TLRs are also stimulated by damage-associated molecular patterns (DAMPs). DAMPs are host-derived proteins including extracellular matrix components, and macromolecule fragments that are released due to tissue injury and cell death and can activate the TLRs [25]. Examples of DAMPs that were shown to activate TLRs, specifically TLR2 or TLR4, in the joint environment include biglycan, high mobility group box 1 protein (HMGB1), glycoprotein 96 (gp96), fibronectin, low molecular weight hyaluronan fragments, and an aggrecan fragment among others [26-32]. Binding of DAMPs to TLR2 or ...

Hori, O., Brett, J., Slattery, T., Cao, R., Zhang, J., Chen, J. X., Nagashima, M., Lundh, E. R., Vijay, S., Nitecki, D. et al., The receptor for advanced glycation end products (RAGE) is a cellular binding site for amphoterin. Mediation of neurite outgrowth and co-expression of RAGE and amphoterin in the developing nervous system. J. Biol. Chem. 1995. 270: 25752-25761 ...

Fingerprint Dive into the research topics of Stimulation of Transcription in Cultured Cells by High Mobility Group Protein 1: Essential Role of the Acidic Carboxyl-Terminal Region. Together they form a unique fingerprint. ...

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Recombinant Human HMGB1 / HMG1 Protein. Synthesized in e. coli. Protein Tag: GST. Purity: Greater than 90% as determined by SDS-PAGE. From $88

|div>A new study, published in the Journal of Allergy and Clinical Immunology, investigates a potential new approach to designing drugs for the treatment of asthma. Better interventions could be on the horizon.|/div> |div>Asthma causes an individuals airways to become inflamed and narrow, and additional mucus is produced. Breathing becomes difficult for this person, who may wheeze and cough as a result.|/div> |div>An estimated 1 in 12 people in the United States have asthma, which equates to

The protein encoded by this gene is a subunit of a heterodimer that, along with SUPT16H, forms chromatin transcriptional elongation factor FACT. FACT interacts specifically with histones H2A/H2B to effect nucleosome disassembly and transcription elongation. FACT and cisplatin-damaged DNA may be crucial to the anticancer mechanism of cisplatin. This encoded protein contains a high mobility group box which most likely constitutes the structure recognition element for cisplatin-modified DNA. This protein also functions as a co-activator of the transcriptional activator p63. An alternatively spliced transcript variant of this gene has been described, but its full-length nature is not known ...

Transcription factor high‐mobility group box‐containing protein 1 (HBP1) may function as a tumor suppressor in various types of cancer. In a previous study, we ...

Vertebrate brain is one of the most complex and mysterious objects for biological research. Embryonic brain development involves stereotypic brain structure formation, and a vast number of precise intercellular connections are established for the generation of the highly complex circuitry of the brain. This work aims at explaining HMGB1 and AMIGO1 function in modulating vertebrate brain development. Hmgb1 knockdown zebrafish morphants produced by injection of morpholino oligonucleotides display severe defects in the forebrain and gross deteriorated catecholaminergic system. The morphant is also deficient in survival and proliferation of neural progenitors. Similar central nervous system (CNS) developmental defects have been observed in HMGB1 knockout mouse embryo. The HMGB1 null mouse embryonic brain cells showed much lower proliferating and differentiating activities compared to wild type animals. HMGB1 knockdown and knockout model respectively from zebrafish and mouse have confirmed that AMIGO1

The present study contains novel findings to support the concept of immunogenic cell death induced by chemoradiotherapy in patients with ESCC. First, tumor antigen-specific T-cell responses were confirmed in 6 (38%) of 16 patients with ESCC following chemoradiotherapy. Second, the serum level of HMGB1 following chemoradiation in the patients with antigen-specific T-cell responses was significantly elevated in comparison to that in the patients without antigen-specific T-cell responses. Third, upregulation of HMGB1 within tumor microenvironments was significantly related to preoperative chemoradiotherapy and the degree of HMGB1 positively correlated with patients survival. Fourth, both irradiation and chemodrugs could induce upregulation of HMGB1 and calreticulin on ESCC cell lines in vitro. Finally, HMGB1 was able to induce maturation of DCs in an in vitro culture system.. In general, chemoradiotherapy is thought to induce an immunosuppressive state in both T-cell and natural killer-cell ...

Gene transfer of high-mobility group box 1 box-A domain in a rat acute liver failure model. Masayuki Tanaka; Masahiro Shinoda; Atsushi Takayanagi; Go Oshima; Ryo Nishiyama; Kazumasa Fukuda; Hiroshi Yagi; Tetsu Hayashida; Yohei Masugi; Koichi Suda; Shingo Yamada; Taku Miyasho; Taizo Hibi; Yuta Abe; Minoru Kitago; Hideaki Obara; Osamu Itano; Hiroya Takeuchi; Michiie Sakamoto; Minoru Tanabe; Ikuro Maruyama; Yuko Kitagawa. Journal of Surgical Research 194 （ 2 ） 571 - 580 2015.04. Research paper (scientific journal). ...

TY - JOUR. T1 - Ursolic Acid attenuates HMGB1-induced LOX-1 expression in vascular endothelial cells in vitro and inhibits atherogenesis in hypercholesterolemic mice in vivo. AU - Lee, Ai-Wei. AU - Huang, Chun-Yao. AU - Shih, Chun-Ming. AU - Lin, Yi Wen. AU - Tsao, Nai-Wen. AU - Chen, Yung Hsiang. AU - Chang, Yu-Jia. AU - Chang, Nen-Chung. AU - Li, Chi Yuan. AU - Fong, Tsorng-Harn. AU - Nien, Chih Hao. AU - Lin, Feng-Yen. PY - 2012. Y1 - 2012. N2 - Ursolic acid (UA), a triterpenoid compound found in plants, is used in both the human diet and in medicinal herbs and possesses a wide range of benefits, including antioxidative and anti-inflammatory effects. Additionally, UA may inhibit lipid absorption in pancreatic cells and enhance lipolysis in adipocytes. Oxidized LDL (oxLDL) acts as a major mediator of endothelium dysfunction, which mediates atherogenesis. Until now, we have not known what role UA plays in the absorption of oxidized LDL in vascular endothelial cells. Regardless of whether UA ...

These non-specific interactions are formed through basic residues in the histones making ionic bonds to the acidic sugar-phosphate backbone of the DNA, and are therefore largely independent of the base sequence. Chemical modifications of these basic amino acid residues include methylation, phosphorylation and acetylation. These chemical changes alter the strength of the interaction between the DNA and the histones, making the DNA more or less accessible to transcription factors and changing the rate of transcription. Other non-specific DNA-binding proteins in chromatin include the high-mobility group proteins, which bind to bent or distorted DNA. These proteins are important in bending arrays of nucleosomes and arranging them into the larger structures that make up chromosom ...

Interactions between stromal fibroblasts and cancer cells generate signals for cancer progression, therapy resistance, and inflammatory responses. Although endogenous RNAs acting as damage-associated molecular patterns (DAMPs) for pattern recognition receptors (PRRs) may represent one such signal, these RNAs must remain unrecognized under non-pathological conditions. We show that triggering of str ...

Results HMGB1 increased phosphorylation of ERK1/2 at 15 min and p38 at 30 min after stimulation HMGB1 increased IL-8 secretion (from 6.46 ng/ml to 8.75 ng/ml, p,0.01) and significant decrease in TIMP-1 secretion (from 19.79 ng/ml to 16.9 ng/ml, p,0.05) at 72 h. MAPK activation, IL-8 increase and TIMP-1 decrease was significantly reversed in the presence of sRAGE (p,0.05) (Abstract S52 Figure 1). Incubating cells with a RAGE blocking antibody inhibited MAPK phosphorylation by HMGB1. ...

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Hyperglycemia, which reduces the efficiency of remedies and worsens clinical results, is common in heart stroke. mind. Pregabalin-treated rats demonstrated considerably improved neurological function (31% reduction in rating), decreased infarct size (by 33%), fewer apoptotic cells (by 63%), and lower manifestation degrees of HMGB1, TLR4, p-NF-B, IL-1, and TNF- , weighed against control rats. Reduced p-iNOS and improved p-eNOS expressions had been also observed. Manifestation of Bax, Cytochrome C, and cleaved caspase-3/caspase3 was considerably downregulated, while Bcl-2 manifestation was improved by pregabalin treatment. Pregabalin administration upon reperfusion reduced neuronal loss of life and improved neurological function in hyperglycemic stroke rats. Cogent systems would consist of attenuation of HMGB1/TLR-4-mediated swelling and beneficial modulation from the NOS. Intro Irrespective of a brief history of diabetes, around 30C40% of individuals that present 175414-77-4 IC50 with severe ...

Hiramoto S, Tsubota M, Yamaguchi K, Okazaki K, Sakaegi A, Toriyama Y, Tanaka J, Sekiguchi F, Ishikura H, Wake H, Nishibori M, Du Nguyen H, Okada T, Toyooka N, Kawabata ...

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AMIGO (amphoterin-induced gene and orf) has been identified as an HMGB1-induced gene in hippocampal neurons using ordered differential display. AMIGO defines a novel gene family with three closely related members (AMIGO, AMIGO 2, and AMIGO 3) that belong to both LRR (leucine-rich repeat) and Ig (immunoglobulin) superfamilies of cell surface proteins. We have recently identified AMIGO as an auxiliary subunit of the Kv2.1 potassium channel. Furthermore, AMIGO affects the channel activity and thereby excitability of neurons.. ...

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Protein Related To Mammalian High Mobility Group (HMG) Proteins; Nuclear Protein; Essential For Function Of H/ACA-type SnoRNPs, Which Are Involved In 18S RRNA Processing

This includes boosted funding to support the NSW government with their transition to an electric bus fleet and to introduce a wide range of mobility …. To Read More, Please Visit Source. ...

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