Browse our anti-IREB2 (IREB2) Antibodies

Mouse (Murine) Iron-Responsive Element Binding Protein 2 (IREB2) interaction partners

1. The Irp2(-/-) mice develop microcytic anemia, erythropoietic protoporphyria (show FECH Antibodies) and a progressive neurological disorder, indicating that Irp2 has important functions in the nervous system and erythropoietic homeostasis

2. Irp2 mRNA transcription is promoted by circadian clock genes, including BMAL1 (show ARNTL Antibodies), and the CLOCK heterodimer.

3. Irp2 increased mitochondrial iron loading and levels of cytochrome c oxidase, which led to mitochondrial dysfunction and subsequent experimental COPD.

4. IRP1 (show ACO1 Antibodies) 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.

5. 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 .

6. misregulation of iron metabolism from loss of Irp2 causes lower motor neuronal degeneration with significant spinal cord axonopathy

7. A wide network of mRNAs and proteins with iron-dependent regulation, IRP (show WNT2 Antibodies)-dependent regulation, or both.

8. The FBXL5 (show FBXL5 Antibodies)-IRP2 axis is integral to control of iron metabolism in vivo.

9. Iron regulatory protein 1 (show ACO1 Antibodies) outcompetes iron regulatory protein 2 in regulating cellular iron homeostasis in response to nitric oxide.

10. 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.

Human Iron-Responsive Element Binding Protein 2 (IREB2) interaction partners

1. 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.

2. The rs13180 (IREB2), rs16969968 (CHRNA5 (show CHRNA5 Antibodies)) and rs1051730 (CHRNA3 (show CHRNA3 Antibodies)) were significantly associated with Chronic obstructive pulmonary disease (COPD (show ARCN1 Antibodies)) 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 (show ARCN1 Antibodies) in our population (Padj =0.0005, OR=0.61).

3. IRP2 expression was associated with mutations in BRAF (show BRAF Antibodies).

4. The current results revealed that there was significant association between IREB2 gene rs2568494 polymorphism with susceptibility to Chronic Obstructive Pulmonary Disease.

5. 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.

6. IREB2 - candidate gene for Chronic Obstructive Pulmonary Disease identified by Genome-wide association studies.

7. Irp2 expression is increased in airway epithelial cells exposed to cigarette smoke.

8. IRP2 can regulate the expression of TfR (show TFRC Antibodies) and Fn by changing its own protein expression and thereby regulate iron metabolism.

9. Genetic variants near IREB2 and GALC (show GALC Antibodies) likely contribute to genetic susceptibility to PAE associated with COPD (show ARCN1 Antibodies).

10. 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 (show ARCN1 Antibodies).