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Human Polyclonal HMOX1 Primary Antibody pour IHC (p), WB - ABIN3042449
Xue, Guo, Li, Hao: Heme oxygenase-1 induction by hemin protects liver cells from ischemia/reperfusion injury in cirrhotic rats. dans World journal of gastroenterology 2007
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Hamster Polyclonal HMOX1 Primary Antibody pour IP, IHC - ABIN223113
Song, Shih, Chan, Zhang: Suppression of annexin A11 in ovarian cancer: implications in chemoresistance. dans Neoplasia (New York, N.Y.) 2009
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Human Monoclonal HMOX1 Primary Antibody pour BP, ELISA - ABIN257888
Machado, Malheiros, Adamy, Santos, Silva Filho, Nahas, Lemos: Protective response in renal transplantation: no clinical or molecular differences between open and laparoscopic donor nephrectomy. dans Clinics (São Paulo, Brazil) 2013
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Cow (Bovine) Monoclonal HMOX1 Primary Antibody pour ICC, IF - ABIN361697
Brydun, Watari, Yamamoto, Okuhara, Teragawa, Kono, Chayama, Oshima, Ozono: Reduced expression of heme oxygenase-1 in patients with coronary atherosclerosis. dans Hypertension research : official journal of the Japanese Society of Hypertension 2007
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Cow (Bovine) Polyclonal HMOX1 Primary Antibody pour WB - ABIN2782158
Hausmann, Paul, Kellermeier, Frey, Schölmerich, Falk, Menzel, Fried, Herfarth, Rogler: (GT)N dinucleotide repeat polymorphism of haem oxygenase-1 promotor region is not associated with inflammatory bowel disease risk or disease course. dans Clinical and experimental immunology 2008
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Human Polyclonal HMOX1 Primary Antibody pour ICC, IF - ABIN441348
Bakkar, Kousari, Kovalik, Li, Bowser: RBM45 Modulates the Antioxidant Response in Amyotrophic Lateral Sclerosis through Interactions with KEAP1. dans Molecular and cellular biology 2015
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Human Polyclonal HMOX1 Primary Antibody pour ELISA, IHC - ABIN6262336
Qiu, Ma, Wu, Ding: DL-3-n-butylphthalide improves ventricular function, and prevents ventricular remodeling and arrhythmias in post-MI rats. dans Naunyn-Schmiedeberg's archives of pharmacology 2018
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Human Polyclonal HMOX1 Primary Antibody pour FACS, WB - ABIN655187
Li, Yu, Xi, Yu, Liu, Wang, Song, Feng, Yan, Zhang, Xiao, Ma: Fasudil Enhances Therapeutic Efficacy of Neural Stem Cells in the Mouse Model of MPTP-Induced Parkinson's Disease. dans Molecular neurobiology 2018
Human Polyclonal HMOX1 Primary Antibody pour ELISA, WB - ABIN1992533
Tseng, Huang, Lai, Hwai, Hsiao, Jhou, Chuang, Tzeng: Dual immuno-renal targeting of 7-benzylidenenaltrexone alleviates lupus nephritis via FcγRIIB and HO-1. dans Journal of molecular medicine (Berlin, Germany) 2018
Human Polyclonal HMOX1 Primary Antibody pour ELISA, WB - ABIN561294
Hong, Kim, Kim, Lee, Shin, Son, Han, Sung, Kwon: Apoptosis induction of 2'-hydroxycinnamaldehyde as a proteasome inhibitor is associated with ER stress and mitochondrial perturbation in cancer cells. dans Biochemical pharmacology 2007
Results suggest that soybean HO-1 gene expression is not epigenetically regulated. Moreover, the low level of HO-1 promoter methylation suggests that this antioxidant enzyme can rapidly respond to environmental stress.
study evaluated the time-course of HO-1 and catalase gene expressions in nodules and roots of soybean plants subjected to cadmium treatment
Data suggest expression of hsp32 is up-regulated in kidney epithelial cells upon in vitro exposure to heavy metal water pollutants (Cd, As) or proteasomal inhibitors (MG132, withaferin A, celastrol); heat shock may be synergistic factor.
this study provides a better understanding of the role of the HO-1/Carbon monoxide system in controlling heart function in lower vertebrates.
The induced expression of HO-1 by fenofibrate appeared to be essential for mediating the protective effects of fenofibrate, as the inhibition of HO-1 activity significantly diminished the protective effects of fenofibrate against the GM-mediated death of sensory hair cells in cochlea
Suggest that Gata-1 and Nrf2a play differential roles in regulating the heme degradation enzymes hmox1a/bvra/bvrb during an early developmental period of heightened cellular stress.
Bach1 regulates the liver specificity and transience of the Nrf2a-dependent induction of hmox1a and that heme mediates this regulation through Bach1 inhibition based on its level in each tissue.
Data indicate that Heme oxygenase 1 (HY1) functioned negatively and acted upstream of ABSCISIC ACID-INSENSITIVE4 (ABI4) in drought signaling.
HY1 confers cadmium tolerance by decreasing nitric oxide production and improving iron homeostasis.
Data indicate that AtHO1 (HY1; heme oxygenase-1)-overexpressing plants generated more NO, whereas knock-down of AtHO1 expression reduced the level of nitric oxide (NO) in plants.
HY1 mutant exhibited progressive salt hypersensitivity.
Disrupting the binding of the AtHBP5 to haem oxygenase 1 (HY1) leads to oxidative stress.
Mutation of HY1 causes UV-C hypersensitivity by impairing carotenoid and flavonoid biosynthesis and the down-regulation of antioxidant defence.
HY1 and HY5 additively regulate the expression of light regulated genes and accumulation of chlorophyll and anthocyanin during early seedling development.
HY1 (Heme oxygenase 1) plays an important role in salt acclimation.
all members of the HO1 subfamily (HY1, HO3 and HO4) are active monomeric HOs and can convert haem to BV IXalpha using spinach Fd (ferredoxin) as an electron donor
HO2 has an activity high enough to substitute for HO1 under aerobic conditions.
Study found that plasma HO-1 levels were low in patients with peripheral artery disease, in contrast to high levels in patients with coronary artery disease.
HO-1 is over-expressed in sera of psoriasis patients and is correlated with psoriasis extent and severity.
Pregnant women who subsequently develop severe preeclampsia show higher expression of HO-1.
Our findings identify survivin as a target of HO-1 and a mediator of adipocyte-induced survival in the metastatic niche.
the role of HO-1 in nervous system pointing out different molecular mechanisms possibly responsible for HO-1 up-regulation in nervous system homeostasis and neurodegeneration.
HO-1 may serve as a prognostic marker and a new target to modulate chemotherapeutic effects in patients with small-intestinal adenocarcinomas
The T allele of heme oxygenase 1 gene SNP polymorphism (rs2071746) is a risk factor for esophageal varices development in cirrhotics.
Data show that the ferroptotic process induced by heme oxygenase-1 (HO-1). overexpression indicated that HO-1 is a key mediator of BAY 11-7085 (BAY)-induced ferroptosis that operates through cellular redox regulation and iron accumulation.
Heme oxygenase activity increases after exercise in healthy volunteers.
Results show that HO-1 is overexpressed in pancreatic cancer (PC) cells, induces cell proliferation and SHH signaling pathway activation as well as resistance to anticancer therapy.
the expression of hsa_circRNA0054633 has a protective effect against high glucoseinduced endothelial cell dysfunction by targeting ROBO1 and HO1.
the 14 kDa HO-1 is shown to promote cell proliferation and an increase in relative telomere lengths in vivo and in vitro.
HO-1 plays a key role in protecting tumor cells from apoptosis, in a process that involves Smad7 and HDAC4/5 in apoptosis of B-ALL cells
HO-1 might be a potential marker for prediction of ovarian cancer prognosis and a target for ovarian cancer treatment
HO-1 was an important cellular factor against Dengue virus replication.
our results demonstrate that Pc-induced expression of HO-1 is mediated by the PKCA-Nrf-2/HO-1 pathway, and inhibits UVB-induced apoptotic cell death in primary skin cells.
HO-1 regulates macrophage activation via the SIRT1-p53 signaling network and regulates hepatocellular death in liver ischemia-reperfusion injury.
In light of a pivotal role of NRF2 and BACH1 in response to oxidative stress and regulation of HO-1, we examined if smoke-induced HO-1 expression is modulated through the NRF2/BACH1 axis. We demonstrated that smoke causes significant nuclear translocation of NRF2, but only a slight decrease in nuclear BACH1.
downregulation of HO-1 gene expression in patients with inflammatory bowel disease.
This study demonstrated that HO-1 plays a vital role in the development of gastric cancer and may serve as a therapeutic target of this type of cancer
These results provide a unique insight into the molecular mechanisms underlying the antiviral effects of the stress-responsive protein HO-1 during Porcine reproductive and respiratory syndrome virus infection.
findings collectively suggest that miR-506 acts as a tumor suppressor via regulation of ROCK1 expression and may thus be a promising therapeutic target for HCC
Exogenous administration of CO exacerbated allergic symptoms, resulting in higher levels of both CO and heme oxygenase-1 expression, and a further reduction in H2S levels and CSE expression.
Down-regulation of HO-1 is associated with pulmonary arterial hypertension and right ventricular failure.
The study revealed the involvement of HO-1 in classical swine fever virus proliferation.
The protective properties of flavonoids, such as EGCG, against endothelial inflammation may be regulated in part though induction of HO-1 and subsequent activator protein-1 signaling.
Glutamate regulates Ca2+ signals in smooth muscle cells of newborn piglet brain slice arterioles through astrocyte- and heme oxygenase-dependent mechanisms.
obalt protoporphyrin prevents postictal cerebral vascular dysfunction by upregulating HO-1.
Data demonstrate that lipopolysaccharides evoke a heat shock response, with an increase heat shock proteins 70 and Hsp32) and of VEGF, a specific endothelial cell growth factor.
Interaction of soluble factors in plasma possibly generated during PICSO are not responsible for upregulation of HO-1 and VEGF mRNA.
the data were consistent with HO-1 acting as an anti-viral factor and these findings suggested that induction of HO-1 may be a useful prevention and treatment strategy against BVDV infection.
These findings suggest that bronchiolar epithelial cells and macrophages up-regulate Nrf2 expression early in the course of infection, which results in increased expression of HO-1 within these cells.
investigation of molecular mechanisms of microvascular complications in diabetes/hyperglycemia: regulation of HO-1 gene expression in aortic endothelial cells by advanced glycation end products
Sickle blood increases endothelial heme oxygenase activity.
data provide evidence for the involvement of the thioredoxin/thioredoxin receptor system, in the regulation of haem oxygenase-1 expression in aortic endothelial cells during pro-oxidant challenge
Heme oxygenase-1 induction modulates hypoxic pulmonary vasoconstriction through upregulation of ecSOD/SOD3.
Mice lacking Hmox1 exhibited a significant increase in concentrations of liver and brain gangliosides and in mRNA expression of the key enzymes of ganglioside metabolism
Ori might exhibit a protective role against H2O2-stimulated oxidative damage by the induction of HO-1 expression through the activation of the JNK- and PI3K/AKT-Nrf2 signaling pathways.
This is the first study to demonstrate the regulatory role of HO-1 in silicosis.
The HO-1-mediated pathway is involved in the suppressive effects of FNDC4 on inflammation and insulin resistance.
HO-1 enhanced STAT3 phosphorylation, which enriched to Il12b and Il23a loci and negatively regulated their transcription. These findings demonstrate the underlying mechanism through which a nutritional can interfere with the immune response. CUR silences IL-23/Th17-mediated pathology by enhancing HO-1/STAT3 interaction in dendritic cells.
HO-1 reduces HFD-induced AKT2 phosphorylation via ROS thresholding in mitochondria to reduce visceral adipose precursor proliferation. HO-1 influences adipogenesis in a cell-autonomous way by regulating events early in adipogenesis, during the process of mitotic clonal expansion, upstream of Cebpalpha and PPARgamma.
Involved in the Nrf2/HO-1 pathway.
Studied effect of Sargassum horneri (Turner) C. Agardh ethanol extract (SHE) on inflammation induced by fine dust in RAW 264.7 cells. Results suggest SHE protects the cells from oxidative stress in part by activating the nuclear factor erythroid derived 2 like 2 /heme oxygenase 1 (Nrf2/HO-1) signal pathway.
Our results reveal a previously unrecognized function of HO-1 in regulating SMC gene expressions during ESC-EB development.
HO-1 protects bone marrow mesenchymal stem cells from reactive oxygen species by secreting IL-10 upon iron overload.
Results show that renal myeloid cells upregulate HO-1 upon renal ischemia-reperfusion injury (IRI). Also, myeloid HO-1 mitigates both innate immune responses and oxidative stress upon renal IRI.
Findings demonstrate that myeloid HO-1 plays an anti-inflammatory role in the acute response to zymosan in vivo.
Genetic Hmox1 partial deficiency is sufficient to sensitize mice to the development of diabetic glomerular microvascular lesions. HO-1 exerts antioxidant effects in the kidney during diabetes mellitus. These have protective effects on the development of glomerular endothelial injury.
Inhibition of miR-92a attenuates oxidative stress and improves endothelial function through enhancing HO-1 expression and activity in db/db mouse aortas
n-propargyl caffeamide (PACA) attenuated LPS-induced NF-kB activation while activated Nrf2/HO-1 pathway. HO-1 inhibitor SnPP attenuated the effects of PACA on iNOS expression in LPS-challenged macrophages, possibly by regulating the cross-talk between HO-1 and NF-kB pathways.
Ablation of adipose tissue-HO-1 abridged PGC1 expression promoted mitochondrial dysfunction and contributed to an increase of pro-inflammatory visceral fat and abrogated beige-cell like phenotype.
These results suggested that schisandrin A has a protective effect against LPS-induced inflammatory and oxidative responses in RAW 264.7 cells by inhibiting the NF-kappaB, MAPK and PI3K/Akt pathways; these effects are mediated, at least in part, by the activation of the Nrf2/HO-1 pathway
Newborns appear to be protected from the pro-oxidative effects of free heme (FH), which may be mediated by heme binding and a higher absolute HO activity at baseline and after FH-mediated induction.
Rosiglitazone Regulates TLR4 and Rescues HO-1 and NRF2 Expression in Myometrial and Decidual Macrophages in Inflammation-Induced Preterm Birth.
this study shows that induction of heme oxygenas-1 attenuates NLRP3 inflammasome activation in lipopolysaccharide-induced mastitis in mice
The expression of oxidative stress markers were upregulated after light exposure but attenuated by cyanidin-3-glucoside and ferulic acid, which may be attributed to the elevated secretion and expression of heme oxygenase (HO-1) and nuclear factor erythroid-2 related factor 2 (Nrf2).
Kidneys from circulation-restricted fetuses showed reduced heme oxygenase-1 mRNA.
Ligustrazine injection possesses notable protective effects on ischemia/reperfusion injury in rabbits by increasing the expression of HO-1 in lung.
Results add new evidence for the importance of HO-1 in the genesis and development of atherosclerosis and provide several possible mechanisms underlying the anti-atherosclerosis effects of HO-1
the effect of HO-1 on the progression and stabilization of vulnerable plaques and the possible mechanism
Heme-L-lysinate could attenuate atherosclerotic progression through upregulating HO-1 and HSP70 expression and increasing CO production.
These results suggest that HO-1 is important in limiting in-stent stenosis and can be regarded as a new therapeutic target.
renal HO inhibits tubuloglomerular feedback probably via release of CO and biliverdin
Statins showed anti-atherosclerotic effects mediated by HO-1/eNOS, restoring the [NO]/[ONOO(-)] imbalance and reducing lipid peroxidation.
HO-1/CO system was activated and may be one of the protective signal pathway during pulmonary ischemia-reperfusion injury in rabbits.
HO-1 contributes to vascular repair by increasing circulating endothelial progenitor cells (EPCs) derived from the bone marrow.
Heme oxygenase, an essential enzyme in heme catabolism, cleaves heme to form biliverdin, which is subsequently converted to bilirubin by biliverdin reductase, and carbon monoxide, a putative neurotransmitter. Heme oxygenase activity is induced by its substrate heme and by various nonheme substances. Heme oxygenase occurs as 2 isozymes, an inducible heme oxygenase-1 and a constitutive heme oxygenase-2. HMOX1 and HMOX2 belong to the heme oxygenase family.
heme oxygenase (decycling) 1
, heme oxygenase 1
, heme oxygenase
, Heme oxygenase
, heat shock protein, 32-kD
, heat shock protein 32
, heme oxygenase (decyclizing) 1
, P32 protein
, heme oxygenase-1