Browse our anti-ALOX12B (ALOX12B) Antibodies

Human Arachidonate 12-Lipoxygenase, 12R Type (ALOX12B) interaction partners

1. The rare homozygous ALOX12B mutation found in Patient 5 causes a change in a conserved residue; Leu315 into a proline in the catalytic domain of 12R-LOX.

2. report adds information on the clinical picture of autosomal recessive congenital ichthyosis caused by ALOX12B mutations

3. We found that the contribution of the ALOX12B gene to the pathogenesis of Autosomal Recessive Congenital Ichthyosis to be as important as that of TGM1 in families of Arab Muslim origin

4. Loss-of-function mutations in the LOX genes ALOX12B and ALOXE3 have been found to represent the second most common cause of autosomal recessive congenital ichthyosis. [review]

5. This review covers the background to discovery of the two key lipoxygenases (LOX) involved in epidermal barrier function, 12R-LOX and eLOX3. [review]

6. Autosomal recessive congenital ichthyosis patients with NIPAL4 mutations and abnormal ichthyin expression showed increased 12R-LOX and eLOX-3 staining and a colocalization signal of these LOXs that was three times the normal intensity.

7. It was shown that 12R-lipoxygenase is involved in MUC5AC expression via ERK- and Sp1-signalling pathways.

8. co-overproduction of the two chaperones with 12R-LOX resulted in increased solubility of 12R-LOX and allowed the purification of milligram amounts of active enzyme for structural studies by X-ray diffraction

9. ALOX12B mutations are the leading cause of self-improving collodion ichthyosis in Scandinavia, followed by ALOXE3 mutations, and TGM1 mutations

10. 12-R-LOX and COX-2 play critical roles in the regulation of growth in epidermoid carcinoma

11. Lipoxygenase-3 (ALOXE3) and 12(R)-lipoxygenase (ALOX12B) are mutated in non-bullous congenital ichthyosiform erythroderma (NCIE) linked to chromosome 17p13.1.

12. Isoenzyme is characterized.

13. 12R-LOX hydrolase functions in the normal process of skin differentiation, and that the loss of function mutations are the basis of the LOX-dependent form of Non-bullous congenital ichthyosiform erythroderma.

14. Our data contribute to an enlargement of the spectrum of mutations for the development of efficient molecular genetic tests for analysis of at risk individuals whose carrier status is unknown.

15. Formation of a ligand for the nuclear receptor PPARalpha may be one possibility by which 12R-LOX and eLOX3 contribute to epidermal differentiation.

16. presented a novel form of ichthyosis in a patient, termed hepoxilin A(3) synthase-linked ichthyosis (HXALI), whose scales expressed high levels of 12R-LOX, but were deficient of HXA(3) synthase [hepoxilin A3 synthase]

17. clinical & molecular features of 2 cases of self-healing collodion phenotype that developed mild ichthyosiform erythroderma; both patients were compound heterozygous for novel ALOX12B mutations

18. mutation hotspots in ALOXE3 and allelic heterogeneity in ALOX12B may have roles in autosomal recessive congenital ichthyosis

Mouse (Murine) Arachidonate 12-Lipoxygenase, 12R Type (ALOX12B) interaction partners

1. Loss-of-function mutations in the LOX genes ALOX12B and ALOXE3 have been found to represent the second most common cause of autosomal recessive congenital ichthyosis. [review]

2. The 12R-LOX-eLOX-3 pathway plays a key role in the process of epidermal barrier acquisition by affecting lipid metabolism, as well as protein processing.

3. Alox12b-deficient mouse skin transplants have an ichthyosiform phenotype