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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 (show CAT Proteins) 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 (show GATA1 Proteins) and Nrf2a (show NFE2L2 Proteins) play differential roles in regulating the heme degradation enzymes hmox1a/bvra (show BLVRA Proteins)/bvrb (show BLVRB Proteins) during an early developmental period of heightened cellular stress.
Bach1 (show BACH1 Proteins) regulates the liver specificity and transience of the Nrf2a (show NFE2L2 Proteins)-dependent induction of hmox1a and that heme mediates this regulation through Bach1 (show BACH1 Proteins) 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 (show HMOX2 Proteins) has an activity high enough to substitute for HO1 under aerobic conditions.
co-expression patterns of NGF (show NGFB Proteins) and heme oxygenase-1 might be used as prognostic indicators for gastric carcinoma patients
These results suggest that HO-1 is involved in oxygen-glucose deprivation-evoked upregulation of apical junctional complex proteins, which is partly mediated by MMP9 (show MMP9 Proteins) pathway.
HMOX-1, an anti-oxidase, is a bona fide transcriptional target gene of HSF4 (show HSF4 Proteins) in HLECs (human lens epithelial cells). HSF4 (show HSF4 Proteins) directly binds to the HSE (show HSD17B6 Proteins) element in HMOX-1 promoter to mediate its mRNA transcription and protein accumulation.
The regulated HO-1 expression of Bone marrow stromal cells provides a new putative target for chronic myeloid leukemia (show BCL11A Proteins) therapy.
Dihydromyricetin (DMY) protects HUVECs from ox-LDL-induced oxidative injury by activating Akt (show AKT1 Proteins) and ERK1/2, which subsequently activates Nrf2 (show GABPA Proteins)/HO-1 signaling, thereby up-regulating antioxidant enzymes and anti-apoptotic proteins.
The interaction between ALAD (show ALAD Proteins) rs1800435 and the HMOX1 rs2071746, HMOX1 rs2071747 was not associated with essential tremor.
Docosahexaenoic acid (DHA) activates Nrf2 (show GABPA Proteins), possibly through modification of critical Keap1 (show KEAP1 Proteins) cysteine 288 residue and PKCdelta (show PKCd Proteins)-mediated phosphorylation of Nrf2 (show GABPA Proteins), leading to upregulation of HO-1 and NQO1 (show NQO1 Proteins) expression.
These results suggest that RYR (show RYR1 Proteins) extract serves as alternative and complementary medicine in the treatment of these diseases, by inducing HO-1, thereby decreasing the vascular complications of diabetes
These results indicate that TNFRI (show TNFRSF1A Proteins)-Fc and hHO-1 overexpression may apparently induce free iron in the liver and exert oxidative stress by enhancing reactive oxygen species production and block normal postneonatal liver metabolism.
Mice overexpressing human HO-1 specifically in astrocytes are protected from collagenase-induced intracerebral hemorrhage, as examined by striatal cell viability, neurological deficits and mortality.
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 (show MYLIP Proteins)-506 acts as a tumor suppressor via regulation of ROCK1 (show ROCK1 Proteins) expression and may thus be a promising therapeutic target for HCC (show FAM126A Proteins)
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 (show GRIN2C Proteins) regulates Ca2 (show CA2 Proteins)+ 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 (show VEGFA Proteins), a specific endothelial cell growth factor (show FGF1 Proteins).
Interaction of soluble factors in plasma possibly generated during PICSO are not responsible for upregulation of HO-1 and VEGF (show VEGFA Proteins) 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 (show NFE2L2 Proteins) 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 (show TXN Proteins) 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 (show SOD3 Proteins).
Splenic Ly6C(hi) monocytes contribute to adverse late post-ischemic left ventricular remodeling in heme oxygenase-1 deficient mice.
findings suggest that HO-1 protects against I/R-induced hepatic injury via regulation of mitochondrial QC by PGAM5 (show PGAM5 Proteins) signaling.
this study shows that heme oxygenase 1 affects granulopoiesis in mice through control of myelocyte proliferation
HO-1(pos) /CD169(neg) macrophages in jejunal serosa and at Auerbach's plexus up-regulated by lipopolysaccharide
The results demonstrated that restoration of Brg1 (show SMARCA4 Proteins) during reperfusion could enhance Nrf2 (show NFE2L2 Proteins)-mediated inducible expression of HO-1 during hepatic ischemia-reperfusion injury to effectively increase antioxidant ability to combat against hepatocytes damage.
report that TLR signaling involving MyoD88 has a negative role in egress of HSPCs from BM into PB as TLR signaling enhances expression of HO-1 in hematopoietic cells
These findings indicate that the HO-1/EBP (show EBP Proteins) interaction plays a protective role in alleviating the dysfunction of oxidative stress and cardiac systolic function induced by cholesterol stimulation.
Taken together, these findings suggest that 2,3,5,4'-Tetrahydroxystilbene-2-O-beta-D-glucoside (TSG (show TWSG1 Proteins)) enhances mitochondrial biogenesis and function mainly via activation the HO-1. TSG (show TWSG1 Proteins) can be developed as a potential drug for treatment of inflammatory diseases.
The in vitro study illustrated that the anti-inflammatory effects of RA-XII were partially reversed following Nrf2 (show NFE2L2 Proteins) and HO-1 inhibition. Together, these findings strongly suggested that RA-XII is a potential agent against acute kidney injury.
mRNA and protein levels of heme oxygenase-1 (HO-1)aresignificantly increased by Melaleuca alternifolia oil via p38 (show CRK Proteins) and JNK (show MAPK8 Proteins) MAPK (show MAPK1 Proteins) activation.
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 (show NFE2L2 Proteins)).
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 (show HSP70 Proteins) 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.
Statins showed anti-atherosclerotic effects mediated by HO-1/eNOS (show NOS3 Proteins), 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