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Human Polyclonal GLRX5 Primary Antibody for IF (p), IHC (p) - ABIN1715024
Rychtarcikova, Lettlova, Tomkova, Korenkova, Langerova, Simonova, Zjablovskaja, Alberich-Jorda, Neuzil, Truksa: Tumor-initiating cells of breast and prostate origin show alterations in the expression of genes related to iron metabolism. in Oncotarget 2016
GLRX5 rs1007814 showed a statistically marginally significant difference between cases and controls in genotype frequency (case/control: CC 1 (显示 CCL14 抗体):6; CT 112 (显示 FAM46D 抗体):78; TT 752:505, P=0.049361), but no significant differences in allele distribution [odds ratio (OR)=0.852805]In men, we found a minor difference in the genotype frequency (case/control: CC 0:3; CT 72:36; TT 411:280, P=0.037370) and not in allele distribution (OR=1.142857)
Patients with GLRX5-associated variant nonketotic hyperglycemia had normal development with childhood-onset spastic paraplegia, spinal lesion, and optic atrophy.
crystal structure of GLRX5 revealed a tetrameric organization with the [2Fe-2S] clusters buried in the interior and shielded from the solvent by the conserved beta1-alpha2 loop
Glutaredoxin 5 deficiency causes sideroblastic anemia by specifically impairing heme biosynthesis and depleting cytosolic iron in human erythroblasts
No GLRX5 mutations were found among sixty CSA probands examined
Mutations in GLRX5 is associated with sideroblastic-like microcytic anemia and iron overload
Study reports a decrease of Grx (显示 GRX1 抗体) expression levels in pancreatic islets of diabetic mice which was accompanied by declining insulin (显示 INS 抗体) secretion, increase of reactive oxygen species (ROS (显示 ROS1 抗体)) production level, and cell cycle alterations. These data demonstrate the essential role of the Grx (显示 GRX1 抗体) system for the beta-cell during metabolic stress which may provide a new target for diabetes mellitus type 2 treatment.
Grx5 is an important determinant of osteoblast apoptosis and acts via a molecular pathway that involves regulation of ROS (显示 ROS1 抗体) production, cardiolipin oxidation, caspase (显示 CASP3 抗体) activity, Fe-S cluster formation, and MnSOD (显示 SOD2 抗体) activity.
the hypochromic anaemia in shiraz (sir) zebrafish mutants is caused by deficiency of glutaredoxin 5 (grx5), a gene required in yeast for Fe-S cluster assembly
This gene encodes a mitochondrial protein, which is evolutionarily conserved. It is involved in the biogenesis of iron-sulfur clusters, which are required for normal iron homeostasis. Mutations in this gene are associated with autosomal recessive pyridoxine-refractory sideroblastic anemia.
glutaredoxin 5 homolog
, glutaredoxin-related protein 5, mitochondrial
, monothiol glutaredoxin-5