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Validated All-in-One™ qPCR Primer for HMGB1(NM_001313893.1) Search again
Product ID:
HQP088570
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HMG-1, HMG1, HMG3, SBP-1
Gene Description:
high mobility group box 1
Target Gene Accession:
NM_001313893.1(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- ubiquitously expressed HMGB1 and HMGB2 have potential to cell- and promoter-specifically down- or up-regulate in vivo transcriptional activity of different members of the p53 family
- Release of chromatin protein HMGB1 by necrotic cells triggers inflammation; hmgb1(-/-) necrotic cells have a greatly reduced ability to promote inflammation, which proves that the release of HMGB1 can signal the demise of a cell to its neighbours
- HMGB1 is produced and stored intracellularly in the adenoid gland and contributes to the local antibacterial barrier defense system in the upper respiratory tract.
- HMGB1 secretion from monocytes is induced by stimuli triggering lysosome exocytosis
- pathogenetic role for HMGB-1 in synovitis
- effects on human microvascular endothelial cells
- REVIEW: role of extracellular and nuclear HMGB1 as an inflammation mediator
- HMG1 may regulate the homeostasis of extracellular amyloid-beta peptides in Alzheimer's disease.
- HMGB1 leads to a different profile of gene expression, pattern of cytokine expression, and kinetics of p38 activation compared with LPS.
- Stable antisense-HMG1 expression in melanoma cells led to the reduction of MIA promoter activity and protein expression.
- Overexpression of HMGB1 is common in gastrointestinal stromal tumors and is related to the KIT mutation.
- HMGB1 is abundantly expressed in human breast carcinoma.
- Lipopolysaccharides (endotoxins) stimulate expression of this protein in skeletal muscle.
- The acidic C-terminal domain and A-box of HMGB-1 regulates p53-mediated transcription.
- Intracellular expression repressed HIV-1 gene expression in Hela cells and monocytic cells by repression of terminal repeat (LTR)-mediated transcription, but did not affect HIV replication in unstimulated Jurkat cells.
- molecular characterization of the mechanism of HMGB1 transfer from the nucleus to secretory lysosomes
- Amphoterin induction in prostatic stromal cells by androgen deprivation is associated with metastatic prostate cancer
- interaction of estrogen receptor alpha and beta with HMGB requires the C-terminal extension (CTE) of the estrogen receptor alpha and beta DNA binding domain
- Results suggest that HMGB1 is involved in chromatin structural modulation in global nuclear events through its interaction with a multiprotein complex in HeLa cells.
- HMGB1 physically interacts with MutSalpha and is required at a step prior to the excision of mispaired nucleotide in mismatch repair.
- results suggest that amphoterin is an autocrine/paracrine regulator of monocyte invasion through the endothelium.
- The cytoplasmic and extracellular distribution of HMGB-1 in muscle tissue may indicate an important role of this proinflammatory molecule in the pathogenesis of polymyositis and dermatomyositis
- HMGB1 is a proinflammatory mediator (review).
- HMGB-1 with estrogen accelerates the cell cycle progression in tumor cell lines
- The HMGB1 B box induces dendritic cell maturation and Th1 cell polarization.
- in chlaymdia infected cells, HMGB1 is released by necrotic or permeabilized viable cells, but not apoptotic cells
- HMGB1 in neutrophils is conformationally changed in the epitope or the peripheral structure of the epitope from the protein in lymphocytes
- Amphoterin mRNA was expressed in three prostate cancer cell lines.
- results identify extracellular HMGB1 as an activator of human tumour cell migration operating in concert with EGF
- HMGB1/amphoterin induces growth inhibition and apoptosis in macrophages through RAGE intracellular signaling pathway
- HMGB1 has the ability to recognize DNA interstrand cross-links (ICLs), can cooperate with replication protein A in doing so, and likely modulates ICL repair by the base excision repair machinery.
- HMGB1 induced endothelial cell migration and sprouting
- activated NK cells release HMGB1, which promotes inflammation and induces dendritic cell maturation, thus favoring the onset of the adaptive immune response
- HMGB1 and RAGE are the first known autocrine loop proteins modulating the maturation of human plasmacytoid dendritic cells
- A potential protein-folding pathway is proposed for the HMG box 1 domain of upstream binding factor based on the early stages of its pH 2.1 unfolded state characterized by multidimensional heteronuclear magnetic resonance spectroscopy.
- HMGB1 secreted by maturing dendritic cells orchestrates the priming, activation, and Th1 polarization of T cells and upregulates dendritic cell surface markers and IL-12 production.
- Data show that HMGB1 promotes RAG-mediated cleavage largely through the activity of box B, but optimal stimulation requires a functional A box tethered in the correct orientation.
- HMGB1 is potentially involved in the regulation of lipogenic and cholesterogenic gene transcription
- Data support the view that HMGB1 is secreted by immunostimulated enterocytes, which may exacerbate inflammation-induced epithelial hyperpermeability via an autocrine feedback loop.
- Our data indicate a correlation between HMG-1 expression and the invasiveness of uveal malanoma cells.
- extracellular HMGB1 has a dichotomic effect on the HIV-1 infection in monocytes but not in lymphocytes
- In contrast to the proinflammatory role of HMGB1 in hepatic ischemia/reperfusion (I/R), pretreatment of mice with recombinant human HMGB1 significantly decreases liver damage after I/R.
- The increased amount of extracellular HMGB-1 observed in salivary glands of patients with Sjogren's syndrome (SS) indicates that HMGB-1 is involved in the inflammatory process of the disease.
- Induction of the three known receptors of HMGB1, namely RAGE, TLR-2, and TLR-4, by IL-1beta suggests that proinflammatory cytokines sensitize VSMCs to HMGB1
- Results indicate that high mobility group box 1 protein (HMGB1) release can occur during the course of apoptosis as well as necrosis and suggest that the release process may vary with cell type.
- The HMG1 was observed of the DNA repair pathways for understanding the cellular DNA damage/repair system in human colorectal cancer tissues.
- Data suggest that cysteines 23 and 45 induce conformational changes in response to oxidative stress, whereas Cys106 appears to be critical for the nucleocytoplasmic shuttling of high mobility group protein B1 (Hmgb1).
- Based on its dual DC-attracting and -activating activities as well as its reported capacity to promote an antigen-specific immune response, we consider HMGB1 to have the properties of an immune alarmin.
- Specifically, HMGB1 may promote healing or immune reactivity, depending on the nature of the local inflammatory response and the presence (or absence) of immune effectors.
- Together, our data indicate that NK cells comprise functionally different subsets, endowed with different capacities to secrete HMGB1 and to induce maturation of autologous iDC. Nonetheless, maturation properties can be modulated by different stimuli.
- RT-PCR and in situ hybridization revealed high-level testicular expression of HMGB1 mRNA and localization of this expression to the Sertoli cells and germ cells of the human and rat testis.
- data suggest that the autocrine/paracrine release of HMGB1 and the integrity of the HMGB1/RAGE pathway are required for the migratory function of dendritic cells
- This study demonstrated that human atherosclerotic plaques, but not normal arteries, produce extracellular HMGB1.
- HMGB1 suppresses PDC cytokine secretion and maturation in response to TLR9 agonists including the hypomethylated oligodeoxynucleotide CpG- and DNA-containing viruses
- The role for this protein in arthritis was established by observations of the expression of HMG1 in synovial tissue of patients with rheumatoid arthritis as well as in the joints of animals used to model arthritis
- HMGB1 induces adhesion of endothelial progenitor cells (EPC) to human vascular endothelium and stimulates EPC homing to ischemic tissues. HMGB1 rapidly increases integrin affinity and induces integrin polarization.
- In a cohort of patients with suspected community-acquired infections and sepsis, HMGB1 levels were statistically significantly higher in patients compared to the healthy controls.
- HMGB1 release from macrophages is correlated with the occurrence of apoptosis.
- High-mobility group box 1 produced by activated vascular smooth muscle cells may contribute to the progression and vulnerability of human atherosclerotic lesions toward rupture.
- This review focuses on current knowledge and speculation on the role of HMGB1 in the development of cancer, metastasis.
- Study results are consistent with the hypothesis that decreased cholinergic anti-inflammatory pathway activity is associated with increased HMGB1 blood levels in patients with rheumatoid arthritis.
- Several polymorphisms and mutations in the HMGB1 gene could play a potential role in regulating its expression, and provide the basis for molecular investigations of the HMGB1 gene in different disease settings.
- study presents the novel finding of both nuclear and cytoplasmic expression as well as new synthesis of the HMGB1 in term placenta
- this provides an appraisal of the emerging roles of HMGB1 in neuropathology and the neuroinflammatory response--REVIEW
- HMGB1 can induce expression of TNF-alpha and IL-1beta, and formation of a pro-inflammatory loop between HMGB1, TNF-alpha, and IL-1beta may be responsible for the prolonged and sustained inflammation in CLE.
- HMGB-1 levels were elevated in patients with bacterial pneumonia coinfected with influenza virus compared to those with mild bacterial pneumonia; data suggest HMGB-1 is involved in pathogenesis of severe bacterial pneumonia coinfected with influenza viru
- Results show that HMGB1 is present in HUVEC mitochondria and that it may play a part in mitochondrial DNA events related to fission and fusion processes during HUVEC-T. gondii infection.
- terrestrial adaptation triggers the induction of the endogenous "danger signal" high mobility group box chromosomal protein 1 in the skin of the newborn infant, perhaps in response to the first commensal bacteria colonization
- HMGB1 may play an important role in the relationship between necrosis and malignancy in glioma tumours
- Interactions between porcine aortic endothelail cells and human T cells may trigger HMGB1 release, which may be associated with graft rejection.
- We observed HMGB1 secretion by Dengue Virus-2 infected epithelial cells. This supports the hypothesis that HMGB1 is an important factor that enhances inflammation and cell death.
- High-mobility group box 1 protein in human and murine skin may have roles in wound healing
- HMGB1 induces only minimal cytokine production by macrophges and murine neutrophils unless bound to proinflammatory mediators, such as interleukin(IL)-1beta.
- Serum concentrations of HMGB-1 in asphyxiated neonates were significantly higher than those in normally delivered neonates without asphyxia.
- High mobility group box 1 protein is induced by Mycobacterium bovis BCG
- high mobility group box chromosomal protein 1 may be a useful marker for evaluating the tumour stage and predicting prognosis in hepatocellular carcinoma.
- Data show that High Mobility Group Box Protein-1 (HMGB-1) is elevated significantly in chronic kidney disease patients and correlates with glomerular filtration rate as well as with markers of inflammation and malnutrition.
- HMGB1 may represent a TNF-independent molecule that could be considered as a possible target for future therapeutic intervention in RA.
- HMGB1 plays an important role in Gram-negative sepsis by catalyzing movement of LPS monomers from LPS aggregates to CD14 to initiate a TLR4-mediated proinflammatory response
- high mobility group box protein 1 release is inhibited by sodium salicylate in A549 lung adenocarcinoma cells
- HMGB1 can be released in the vitreous of eyes with endophthalmitis depending on inflammation and tissue damage.
- HMGB1 significantly induced proliferation, but not apoptosis or collagen synthesis on cultured fibroblasts. HMGB1 may be a promising target against pulmonary fibrosis as well as acute lung injury.
- High levels of HMGB1 is associated with Non-Hodgkin lymphoma
- The present article is the first report of clinical implications of variation in the human HMGB1 gene and two polymorphisms were determined as significant risk factors associated mortality of systemic inflammatory response syndrome.
- HMGB1 degradation products were detected in the serum septic patients with disseminated intravascular coagulation, indicating that HMGB1 could be degraded under conditions in which proteases were activated in the systemic circulation.
- caspase activation targeted the mitochondria to produce reactive oxygen species (ROS), which oxidized the potential danger signal high-mobility group box-1 protein (HMGB1) released from dying cells
- Expression of HMGB1 and its receptors on accumulating activated macrophages and resident microglia may provide a positive feedback loop that amplifies the inflammatory response during multiple sclerosis.
- Patients with higher levels of HMGB1 expression had poorer overall survival and disease-free survival, whereas patients with lower levels of HMGB1 expression had better survival.
- DNA aptamers provide a valuable tool to further investigate the extracellular functions of HMGB1 and its involvement in inflammatory pathologies.
- These results suggest Rta autostimulation may be mediated by a transient complex involving Oct1 and HMGB1.
- HMGB1-treated MSCs displayed unchanged suppressive activity on in vitro lymphocyte cell proliferation elicited by ConA. Collectively, the data suggest that MSCs are a target of HMGB1.
- Serum levels of HMGB1 in Kawasaki disease patients were the highest in the early acute phase and gradually decreased after defervescence.
- HMGB1 may inhibit recognition of apoptotic cells by phagocytes through covering phosphatidylserine on the apoptotic cell's surface.
- In liver transplantation, HMGB1 originates from the graft and is a marker of hepatocellular injury.
- Dying cells in which autophagy is induced selectively release the immune modulator high-mobility group B1 (HMGB1) without causing lysis of the cell membrane and classical necrosis.
- HMGB1 induced the activation of p38MAPK, ERK1/2 and Akt.
- The results demonstrated that HMGB1 may play an important role as a modulator in apoptotic changes in polymorphonuclear granulocytes during lipopolysaccharide-induced acute lung injury.
- Inhibition of HMGB1 activity by glycyrrhizin, known to bind specifically to HMGB1, or blocking anti-HMGB1 antibodies, abrogated NK-dependent HIV-1 replication in dendritic cells.
- Role of high-mobility group box 1 protein in post-infarction healing process and left ventricular remodelling.
- These data suggest that the oxidized HMGB1 may accumulate even in cells under oxidative stress.
- Thus, HMGB1-RAGE signaling links necrosis with macrophage activation and may provide a target for anti-inflammatory therapy in stroke.
- Data show that translocation and secretion of HMGB-1 mediated by toxic shock syndrome toxin-1 is dependent on the presence of both activated T cells and monocytes, and that nuclear HMGB-1 is released from TSST-1 stimulated T cells.
- Periodontal ligament cells produce IL-6 and IL-11 in response to HMGB1 via RAGE, TLR2 and TLR4.
- findings suggest HMGB1 is a crucial nuclear protein & is released as a danger signal of retinal tissue damage; extracellular HMGB1 may be an important mediator in retinal detachment, potentially acting as a chemotactic factor for RPE cell migration
- Proinflammatory HMGB1 and structural nucleosome linker H1 couple as a component of the epigenetic complex that silences acute proinflammatory TNF-alpha during the assembly of heterochromatin in the severe systemic inflammation phenotype.