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anti-Mouse (Murine) IREB2 Antikörper:
anti-Rat (Rattus) IREB2 Antikörper:
anti-Human IREB2 Antikörper:
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Mouse (Murine) Polyclonal IREB2 Primary Antibody für GS, ICC - ABIN151305
Regan, Chen, Li, Zhang, Benvenisti-Zarom, Chen-Roetling: Neurons lacking iron regulatory protein-2 are highly resistant to the toxicity of hemoglobin. in Neurobiology of disease 2008
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Human Polyclonal IREB2 Primary Antibody für ICC, IF - ABIN151304
Maeda, Hasegawa, Hyodo, Ito, Asano, Yuang, Funasaka, Shimokata, Hasegawa, Hamaguchi, Senga: ARHGAP18, a GTPase-activating protein for RhoA, controls cell shape, spreading, and motility. in Molecular biology of the cell 2011
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Human Polyclonal IREB2 Primary Antibody für ELISA, IHC - ABIN4327648
Wang, Di, DAgostino, Torti, Torti: Excess capacity of the iron regulatory protein system. in The Journal of biological chemistry 2007
Increased intracellular growth due to compromised expressions of Fpn and FBXL5 by specific siRNAs reveals that Leishmania donovani uses a novel strategy of manipulating IRP2-FBXL5 axis to inhibit host Fpn expression.
The Irp2(-/-) mice develop microcytic anemia, erythropoietic protoporphyria and a progressive neurological disorder, indicating that Irp2 has important functions in the nervous system and erythropoietic homeostasis
Irp2 mRNA transcription is promoted by circadian clock genes, including BMAL1, and the CLOCK heterodimer.
Irp2 increased mitochondrial iron loading and levels of cytochrome c oxidase, which led to mitochondrial dysfunction and subsequent experimental COPD.
IRP1 and IRP2 mutant mice rapidly succumb to systemic infection with Salmonella Typhimurium, a pathogenic bacterium that multiplies within macrophages, with increased bacterial burdens in liver and spleen.
aged Irp2-/- mice show marked iron deposition in white matter and in oligodendrocytes while iron content is significantly reduced in neurons. mice show impairments in locomotion, exploration, motor coordination/balance and nociception .
misregulation of iron metabolism from loss of Irp2 causes lower motor neuronal degeneration with significant spinal cord axonopathy
A wide network of mRNAs and proteins with iron-dependent regulation, IRP-dependent regulation, or both.
The FBXL5-IRP2 axis is integral to control of iron metabolism in vivo.
Iron regulatory protein 1 outcompetes iron regulatory protein 2 in regulating cellular iron homeostasis in response to nitric oxide.
Mice lacking both IRP2 in their hepatocytes suffer from mitochondrial iron deficiency and dysfunction associated with alterations of the ISC and heme biosynthetic pathways, leading to liver failure and death.
IRP2 binding activity reduces ferritin expression in the striatum after an intracerebral hemorrhage, preventing an optimal response to elevated local iron concentrations
A mechanism is proposed by which iron may regulate copper levels in the brain, mediated by IRP2 and amyloid beta protein precursor.
A comparative study of the roles of iron regulatory proteins 1 and 2 in regulating iron metabolism.
targeted mutagenesis; mice that are homozygous for the correctly modified IRP1 or IRP2 alleles, respectively, display a strong reduction (90%, IRP1(-/-)) or nondetectable levels (IRP2(-/-)) of the targeted proteins
IRP2 dominates regulation of iron homeostasis because it alone registers iron concentrations and modulates its RNA-binding activity at physiological oxygen tensions
IRP2 mutations may be a cause of refractory microcytic anemia and bone marrow iron depletion in patients with normal transferrin saturations, elevated serum ferritins, elevated red cell protoporphyrin IX levels, and adult-onset neurodegeneration
IRP2 has roles in body iron distribution and microcytosis
examined the expression levels of iron regulatory proteins (IRPs), ferritins, and binding activities of IRPs to iron-responsive element (IRE) in scrapie-infected mice
Data show that IRP2 are thus essential for intestinal function and organismal survival and coordinate the synthesis of key iron metabolism proteins in the duodenum.
All four variants were significantly associated (P < 1.4 x 10(-6)) with blood DNA methylation of IREB2, CHRNA3 and PSMA4, of which two, including IREB2 and PSMA4, were also differentially methylated in Chronic obstructive pulmonary disease cases and controls
rs16969858 in IREB2 was significantly associated with COPD but in the univariate analysis only, and the multivariate analysis did not show any association.
Five of these SNPs acted as cis-eQTLs, being associated with the transcription of IREB2 (rs2568494, rs16969968, rs11634351, rs6495309), PSMA4 (rs6495309) and ERCC1 (rs735482), out of 10,821 genes analyzed in lung. For these three genes, we obtained experimental evidence of differential allelic expression in lung tissue, pointing to the existence of in-cis genomic variants that regulate their transcription.
Iron loading caused cell proliferation in cancer cell lines, which were less able to regulate IREB2 expression than primary bronchial epithelial cells (PBECs). Iron chelation resulted in a return of proliferation rates to baseline levels; knockdown of IREB2 had a similar effect. IRP2-positive tumours were larger and higher percentage staining related to poorer survival.
The rs13180 (IREB2), rs16969968 (CHRNA5) and rs1051730 (CHRNA3) were significantly associated with Chronic obstructive pulmonary disease (COPD) in additive model [Padj =0.00001, odds ratio (OR)=0.64; Padj =0.0001, OR=1.41 and Padj =0.0001, OR=1.47]. The C-G haplotype by rs13180 and rs1051730 was a protective factor for COPD in our population (Padj =0.0005, OR=0.61).
IRP2 expression was associated with mutations in BRAF.
The current results revealed that there was significant association between IREB2 gene rs2568494 polymorphism with susceptibility to Chronic Obstructive Pulmonary Disease.
This study confirms that the IREB2 variants contribute to an increased risk of lung cancer, whereas FAM13A predisposes to increased susceptibility to chronic obstructive pulmonary disease.
IREB2 - candidate gene for Chronic Obstructive Pulmonary Disease identified by Genome-wide association studies.
Irp2 expression is increased in airway epithelial cells exposed to cigarette smoke.
IRP2 can regulate the expression of TfR and Fn by changing its own protein expression and thereby regulate iron metabolism.
Genetic variants near IREB2 and GALC likely contribute to genetic susceptibility to PAE associated with COPD.
Haplotypes of IREB2 carrying major alleles of rs2568494 (G), rs2656069 (A), rs10851906 (A), rs965604 (C) and minor alleles of rs1964678 (T), rs12593229 (T) showed negative correlation with lung function amongst South Indian male smokers with COPD.
IRE2 is located within genes previously associated with chronic obstructive pulmonary disease susceptibility.
Ascorbate-induced up-regulation of cellular ferroportin levels was associated with increased levels of the iron regulatory protein IRP2, and the hypoxia-inducible factor HIF2alpha.
dysregulation of IRP2 is an early nodal point underlying altered iron metabolism in breast cancer and may contribute to poor outcome of some patients with breast cancer
IREB2 polymorphisms were associated with chronic obstructive pulmonary disease in non-smoking Chinese Han subjects
A replication of association between two SNPs previously associated with COPD (CHRNA3/5 and IREB2), as well as an association with COPD of one locus initially associated with lung function (ADCY2).
Ggenetic polymorphisms of the iron regulatory protein 1 and 2 genes may be associated with development of age-related macular degeneration.
The data showed that IREB2 and CHRNA3 are potential genetic modifiers of chronic obstructive pulmonary disease in individuals with severe alpha-1 antitrypsin deficiency and may be sex-specific in their impact.
RNA-binding proteins that bind iron-responsive elements (IREs)
iron-responsive element binding protein 2
, iron regulatory protein 2
, Iron-responsive element-binding protein 2
, iron-responsive element-binding protein 2-like
, IRE-BP 2
, iron-responsive element-binding protein 2
, iron-regulatory protein 2