Hmgb1 Antibody, Biotin conjugated

^{Rare Species}

說明書

中文名稱：

Hmgb1兔多克隆抗體, Biotin偶聯
貨號：

CSB-PA010553ND01RA
規格：

￥880
其他：

產品詳情
產品評價
相關產品
靶點詳情

產品詳情

產品名稱：

Rabbit anti-Rattus norvegicus (Rat) Hmgb1 Polyclonal antibody
Uniprot No.：

P63159
基因名：

Hmgb1
別名：

Hmgb1 antibody; Hmg-1 antibody; Hmg1 antibody; High mobility group protein B1 antibody; Amphoterin antibody; Heparin-binding protein p30 antibody; High mobility group protein 1 antibody; HMG-1 antibody
宿主：

Rabbit
反應種屬：

Rat
免疫原：

Peptide sequence from Rat Hmgb1 protein (2-18AA)
免疫原種屬：

Rattus norvegicus (Rat)
標記方式：

Biotin
克隆類型：

Polyclonal
抗體亞型：

IgG
純化方式：

>95%, Antigen Affinity purified & Affinity purified
濃度：

It differs from different batches. Please contact us to confirm it.
保存緩沖液：

Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, PH 7.4
產品提供形式：

Liquid
應用范圍：

ELISA
Protocols：

ELISA Protocol
儲存條件：

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
貨期：

Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
用途：

For Research Use Only. Not for use in diagnostic or therapeutic procedures.

產品評價

靶點詳情

功能：

Multifunctional redox sensitive protein with various roles in different cellular compartments. In the nucleus is one of the major chromatin-associated non-histone proteins and acts as a DNA chaperone involved in replication, transcription, chromatin remodeling, V(D)J recombination, DNA repair and genome stability. Proposed to be an universal biosensor for nucleic acids. Promotes host inflammatory response to sterile and infectious signals and is involved in the coordination and integration of innate and adaptive immune responses. In the cytoplasm functions as sensor and/or chaperone for immunogenic nucleic acids implicating the activation of TLR9-mediated immune responses, and mediates autophagy. Acts as danger associated molecular pattern (DAMP) molecule that amplifies immune responses during tissue injury. Released to the extracellular environment can bind DNA, nucleosomes, IL-1 beta, CXCL12, AGER isoform 2/sRAGE, lipopolysaccharide (LPS) and lipoteichoic acid (LTA), and activates cells through engagement of multiple surface receptors. In the extracellular compartment fully reduced HMGB1 (released by necrosis) acts as a chemokine, disulfide HMGB1 (actively secreted) as a cytokine, and sulfonyl HMGB1 (released from apoptotic cells) promotes immunological tolerance. Has proangiogenic activity. May be involved in platelet activation. Binds to phosphatidylserine and phosphatidylethanolamide. Bound to RAGE mediates signaling for neuronal outgrowth. May play a role in accumulation of expanded polyglutamine (polyQ) proteins.; Nuclear functions are attributed to fully reduced HGMB1. Associates with chromatin and binds DNA with a preference to non-canonical DNA structures such as single-stranded DNA, DNA-containing cruciforms or bent structures, supercoiled DNA and ZDNA. Can bent DNA and enhance DNA flexibility by looping thus providing a mechanism to promote activities on various gene promoters by enhancing transcription factor binding and/or bringing distant regulatory sequences into close proximity. May be involved in nucleotide excision repair (NER), mismatch repair (MMR) and base excision repair (BER) pathways, and double strand break repair such as non-homologous end joining (NHEJ). Involved in V(D)J recombination by acting as a cofactor of the RAG complex: acts by stimulating cleavage and RAG protein binding at the 23 bp spacer of conserved recombination signal sequences (RSS). In vitro can displace histone H1 from highly bent DNA. Can restructure the canonical nucleosome leading to relaxation of structural constraints for transcription factor-binding. Enhances binding of sterol regulatory element-binding proteins (SREBPs) such as SREBF1 to their cognate DNA sequences and increases their transcriptional activities. Facilitates binding of TP53 to DNA. May be involved in mitochondrial quality control and autophagy in a transcription-dependent fashion implicating HSPB1. Can modulate the activity of the telomerase complex and may be involved in telomere maintenance.; In the cytoplasm proposed to dissociate the BECN1:BCL2 complex via competitive interaction with BECN1 leading to autophagy activation. Can protect BECN1 and ATG5 from calpain-mediated cleavage and thus proposed to control their proautophagic and proapoptotic functions and to regulate the extent and severity of inflammation-associated cellular injury. In myeloid cells has a protective role against endotoxemia and bacterial infection by promoting autophagy. Involved in endosomal translocation and activation of TLR9 in response to CpG-DNA in macrophages.; In the extracellular compartment (following either active secretion or passive release) involved in regulation of the inflammatory response. Fully reduced HGMB1 (which subsequently gets oxidized after release) in association with CXCL12 mediates the recruitment of inflammatory cells during the initial phase of tissue injury; the CXCL12:HMGB1 complex triggers CXCR4 homodimerization. Induces the migration of monocyte-derived immature dendritic cells and seems to regulate adhesive and migratory functions of neutrophils implicating AGER/RAGE and ITGAM. Can bind to various types of DNA and RNA including microbial unmethylated CpG-DNA to enhance the innate immune response to nucleic acids. Proposed to act in promiscuous DNA/RNA sensing which cooperates with subsequent discriminative sensing by specific pattern recognition receptors. Promotes extracellular DNA-induced AIM2 inflammasome activation implicating AGER/RAGE. Disulfide HMGB1 binds to transmembrane receptors, such as AGER/RAGE, TLR2, TLR4 and probably TREM1, thus activating their signal transduction pathways. Mediates the release of cytokines/chemokines such as TNF, IL-1, IL-6, IL-8, CCL2, CCL3, CCL4 and CXCL10. Promotes secretion of interferon-gamma by macrophage-stimulated natural killer (NK) cells in concert with other cytokines like IL-2 or IL-12. TLR4 is proposed to be the primary receptor promoting macrophage activation and signaling through TLR4 seems to implicate LY96/MD-2. In bacterial LPS- or LTA-mediated inflammatory responses binds to the endotoxins and transfers them to CD14 for signaling to the respective TLR4:LY96 and TLR2 complexes. Contributes to tumor proliferation by association with ACER/RAGE. Can bind to IL1-beta and signals through the IL1R1:IL1RAP receptor complex. Binding to class A CpG activates cytokine production in plasmacytoid dendritic cells implicating TLR9, MYD88 and AGER/RAGE and can activate autoreactive B cells. Via HMGB1-containing chromatin immune complexes may also promote B cell responses to endogenous TLR9 ligands through a B-cell receptor (BCR)-dependent and ACER/RAGE-independent mechanism. Inhibits phagocytosis of apoptotic cells by macrophages; the function is dependent on poly-ADP-ribosylation and involves binding to phosphatidylserine on the cell surface of apoptotic cells. In adaptive immunity may be involved in enhancing immunity through activation of effector T-cells and suppression of regulatory T (TReg) cells. In contrast, without implicating effector or regulatory T-cells, required for tumor infiltration and activation of T-cells expressing the lymphotoxin LTA:LTB heterotrimer thus promoting tumor malignant progression. Also reported to limit proliferation of T-cells. Released HMGB1:nucleosome complexes formed during apoptosis can signal through TLR2 to induce cytokine production. Involved in induction of immunological tolerance by apoptotic cells; its pro-inflammatory activities when released by apoptotic cells are neutralized by reactive oxygen species (ROS)-dependent oxidation specifically on Cys-106. During macrophage activation by activated lymphocyte-derived self apoptotic DNA (ALD-DNA) promotes recruitment of ALD-DNA to endosomes.
基因功能參考文獻：
1. miR-381could inhibit neuropathic pain development through targeting HMGB1 and CXCR4. PMID: 30142543
2. Ketamine delays the progression of oxidative and damaged cataract by regulating HMGB-1/NF-kappaB expression, inhibiting TNF-alpha, IL-1beta, and apoptosis, and promoting cell proliferation. PMID: 30111205
3. High HMGB1 expression is associated with sepsis-induced kidney injury. PMID: 30130540
4. Chronic unpredictable stress (CUS) promotes significant morphological changes and causes robust upregulation of HMGB1 messenger RNA in enriched hippocampal microglia and robust and persistent upregulation of RAGE messenger RNA. CUS increased surface expression of RAGE protein on hippocampal microglia and anhedonic behavior. HMGB1 infusion into the hippocampus was sufficient to cause anhedonic behavior. PMID: 28882317
5. Autophagy was the leading cause of adriamycin-induced cardiotoxicity, and HMGB1 played a vital role in the process of up-regulating autophagy. PMID: 29715512
6. concluded that in mild oxidative stress, HMGB1 is cytoprotective, whereas in intense oxidative stress, HMGB1 actions promote cell death and liver damage PMID: 28695466
7. Findings suggested that overexpression of Pgp during seizures may be regulated by HMGB1 via the RAGE/NFkappaB signaling pathway. PMID: 28627626
8. Up-regulation of miR-129-5p might suppress the HMGB1-RAGE signaling pathway to restrain the revascularization of rats with ICH. PMID: 28645008
9. Investigation identified that HMGB1 promotes neurovascular recovery via Rage and may act in the oxidized state in the late stage of SAH. PMID: 28606778
10. our findings demonstrated an elevation of HMGB1 in pulmonary fibrosis; HMGB1 promoted the increment of proliferation, extracellular matrix production and aerobic glycolysis of embryonic lung fibroblast PMID: 28571757
11. the HMGB1-TLR9 signaling pathway may be involved in the pathogenesis of diabetic retinopathy. PMID: 28647749
12. 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. Also, targeting HMGB1 to modulate the microglia/macrophage polarization should be one potential therapeutic approach for TBI. PMID: 29448108
13. The neuroimmune activation induced by chronic alcohol may involve the danger signaling molecule high mobility group box 1 (HMGB1), which binds Toll-like receptors 4 (TLR4). PMID: 26857094
14. Glycyrrhizin may protect rats against sepsis by blocking the interaction of HMGB1 with cell surface receptors and HMGB1-mediated inflammatory responses PMID: 28484719
15. These results suggest that HMGB1-modulated TLR5 signaling is responsible for pain hypersensitivity. PMID: 27760316
16. HMGB1 modulation may lengthen the therapeutic window for stroke treatments. PMID: 27544687
17. this study provides the first evidence showing that HMGB1 plays a critical role in regulating VSMC phenotypic modulation, suggesting that HMGB1 may be a potential therapeutic target to prevent vascular occlusive diseases. PMID: 27579780
18. HMGB1 and its signaling transduction have critical roles in the pathogenesis of septic brain injury. PMID: 27889435
19. Anti-proliferative effect of terameprocol in pulmonary hypertension seems to be explained, at least in part, by the down-regulation of the transcription factor HMGB1. PMID: 28036116
20. 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. PMID: 28575153
21. Results suggest that electroacupuncture pretreatment could alleviate spinal cord ischemia-reperfusion injury. These protective effects of electroacupuncture pretreatment may relate to the block of pro-inflammatory cytokines release and attenuation of apoptosis via inhibition of HMGB1 release in a LXA4 receptor-dependent manner. PMID: 28089662
22. Further, HMGB1 antagonism prevented prolonged infection-induced neuroinflammatory and sickness responses in aged rats. Overall, blocking HMGB1 "desensitized" microglia in the aged brain, thereby preventing pathological infection-elicited neuroinflammatory responses. PMID: 27466339
23. HMGB1 plays a key pathophysiological role in the onset of epilepsy-related hyperexcitability. PMID: 28222432
24. Suggest that HMGB1 may not be a major player in cerebral vascular dilating dysfunction after subarachnoid hemorrhage. PMID: 27997923
25. study suggests that HMGB1 can positively influence the survival of spiral ganglion neurons following ototoxic exposure via both its extracellular and intranuclear functions PMID: 27704212
26. binding proteins of cytoplasmic HMGB1 during hepatic Ischemia/reperfusion injury were identified. PMID: 28275217
27. These findings suggested that the cytoplasmic translocation of HMGB1 may be caused by diabetes and high glucose in retinal pericytes, and that the pathogenic role of HMGB1 may be dependent on the expression of RAGE and activation of NFkappaB. PMID: 27599553
28. The present study confirmed that Cerebral ischemic postconditioning inhibited autophagy and HMGB1 secretion, autophagy inhibition induced a decrease in HMGB1 secretion, and HMGB1 secretion attenuation caused autophagy inhibition in return, as demonstrated by immunofluorescence and western blot analyses. PMID: 27666823
29. in an ANP model, HMGB1 was initially increased in the nuclei to initiate autophagy. Subsequently, it moved into the cytoplasm, where it interacted with Beclin 1 to enhance autophagy, and HMGB1 was released into the blood, leading to the deterioration of ANP. PMID: 27878276
30. Regnase-1 can be induced by HMGB1 in microglia and negatively regulates HMGB1-mediated neuroinflammation and neuronal toxicity PMID: 27044405
31. HMGB1 contributes significantly to cardiac arrest-induced brain dysfunction PMID: 27363991
32. the present study suggested that upregulation of miR451 could protect against A/Rinduced cardiomyocyte injury by inhibiting HMGB1 expression. PMID: 27121079
33. Hypoxia enhanced the expression of HMGB1 in bone marrow mesenchymal stem cells with influences on apoptosis and adhesion. PMID: 28050559
34. Bone marrow stromal cell-treated type 2 diabetic rats inhibited inflammation and improved functional outcome after stroke; data suggest that BMSCs-induced reduction of HMGB1 and RAGE in type 2 diabetic-middle cerebral artery occlusion rats contributed to attenuated inflammatory response in the ischemic brain, which may lead to the beneficial effects of bone marrow stromal cells treatment. PMID: 26946264
35. Hemorrhagic shock elicited significant increases in the mRNA and protein expressions of HMGB1 and RAGE in the kidney. PMID: 26513053
36. Results suggest that high mobility group box-1 mediates, in part, the neuroinflammatory effects of methamphetamine and thus may alert central nervous system innate immune cells to the toxic effects of methamphetamine. PMID: 26254235
37. ketamine protects rats against HMGB1-RAGE activation in a rat model of sepsis-induced acute lung injury PMID: 26945830
38. Extracellular high-mobility group box-1 (HMGB1) was identified as the likely endogenous regulator of IL1 expression after injury PMID: 26899371
39. Polygonum cuspidatum extract prevents diabetes-induced vascular permeability by inhibiting HMGB1/RAGE/NFkappaB activation in diabetic retinas. PMID: 26950148
40. bone marrow mesenchymal stem cell transplantation improves liver function/pathology in acute liver failure rats and decreases the serum/liver HMGB1. PMID: 26884873
41. HMGB1 is increasingly expressed in parallel to the development of cerebral vasospasm in this rat experimental model of subarachnoid hemorrhage PMID: 26765765
42. These findings indicate that administration of 1alpha,25(OH)2D3 might provide a favorable microenvironment for orthodontic tooth movement by downregulating expression of HMGB1 in periodontal ligament cells. PMID: 26956363
43. These results suggest that intravenous pre-treatment with HMGB1 may exert its cardioprotective effects via the upregulation of the myocardial expression of HIF-1alpha, which may be regulated by the PI3K/Akt signaling pathway, in rats following acute myocardial I/R. PMID: 26648172
44. Results indicate that HMGB1 is a critical regulator of autophagy and HMGB1-induced autophagy plays a protective role in spinal neurons against injuries PMID: 26705737
45. determined that the plasma levels and hepatic tissue levels of HMGB1 were significant increased in acute liver failure PMID: 26722388
46. Increased levels of PKR and HMGB1 in synovium or blood appear to be involved in the occurrence and development ofrheumatoid arthritis (RA )in a rat model. Selective inhibition of PKR improves the symptoms of RA perhaps by inhibiting the release of HMGB1 PMID: 26782432
47. HMGB1 or Beclin1 upregulate alpha-synuclein degradation, ameliorating alpha-synuclein-mediated autophagy reduction in PC12 cells. PMID: 26822891
48. The data indicate that HMGB1 accumulates in renal tissue and enters the urine, and the interaction between HMGB1 and TLR4 turns renal tubular epithelial cells into inflammatory promoters during sepsis. PMID: 26312770
49. Overexpression of miR141 alleviates neuropathic pain development via targeting and inhibiting HMGB1. PMID: 26398163
50. findings demonstrate an important role of HMGB1 in mediating inflammasome activation in the development of liver injury PMID: 25931416
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亞細胞定位：

Nucleus. Cytoplasm. Secreted. Chromosome. Cell membrane; Peripheral membrane protein; Extracellular side. Endosome. Endoplasmic reticulum-Golgi intermediate compartment.
蛋白家族：

HMGB family
數據庫鏈接：

KEGG: rno:25459

STRING: 10116.ENSRNOP00000040874

UniGene: Rn.144565

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