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Human Monoclonal SLC11A2 Primary Antibody for IHC (p), ELISA - ABIN562043
Foot, Dalton, Shearwin-Whyatt, Dorstyn, Tan, Yang, Kumar: Regulation of the divalent metal ion transporter DMT1 and iron homeostasis by a ubiquitin-dependent mechanism involving Ndfips and WWP2. in Blood 2008
Show all 4 Pubmed References
Mouse (Murine) Polyclonal SLC11A2 Primary Antibody for IF, WB - ABIN657723
Rose, Behm, Drgon, Johnson, Uhl: Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score. in Molecular medicine (Cambridge, Mass.) 2010
Show all 5 Pubmed References
Human Polyclonal SLC11A2 Primary Antibody for WB - ABIN4892577
Scheers, Almgren, Sandberg: Proposing a Caco-2/HepG2 cell model for in vitro iron absorption studies. in The Journal of nutritional biochemistry 2014
A compound heterozygote with hereditary hypochromic microcytic anemia was found to have 2 new DMT1 mutations: a C > T transition at nucleotide 1429 of exon 15 (R477W) and a G > C substitution at position +1 bp of the splice-donor site within intron 4 (ivs4 + 1 G/C). R477W was inherited from proband's mother, while ivs4 + 1 G/C was of paternal inheritance.
Solute carrier family-11 member-2 (SLC11A2) homozygous CC genotype for IVS4+44C/A showed significant correlation with Type-2 diabetes (T2DM) risk, suggesting that presence of C allele of IVS4+44C/A plays pathological roles.
E193 in hDMT1, is proposed to translocate protons in an inward-rectified manner by alternating contact with the solvent on each side of the membrane bilayer. Furthermore, molecular dynamics simulations provide insight into how H(+)-translocation through E193 is allosterically linked to intracellular gating, establishing a novel transport mechanism distinct from that of other H(+)-coupled transporters.
DMT1 was increased in myelodysplastic syndrome patients.
SLC11A2 expression is increased in the intestine of patients with type 2 diabetes in association with iron stores and serum hepcidin levels.
Results indicate that there is a dysregulation of DMT1 + IRE in IA testes, which might due to the up-regulation of IRP1 and HIF-1A.
celiac disease may unmask the contribution of the DMT1 IVS4+44C>A polymorphism to the risk of anemia.
These results suggest that the increased expression of DMT1 induces iron overload and iron overload induces osteoblast autophagy and apoptosis, thus affecting the pathological processes of osteoporosis. Clarifying the mechanisms underlying the effects of DMT1 will allow the identification of novel targets for the prevention and treatment of osteoporosis.
the cellular iron importer, divalent metal transporter 1 (DMT1), is highly expressed in colorectal cancer through hypoxia-inducible factor 2alpha-dependent transcription.
Divalent metal transporter-1 overexpression in endometriosis patients' endometrium can increase iron influx to endometrial cells, inducing oxidative stress-mediated proinflammatory signaling. In turn, endometriosis-related conditions, as iron overload and inflammation (IL-1beta), enhance endometriosis patients endometrial DMT1 expression, creating a vicious circle on DMT-1-modulated pathways.
X-ray crystallographic analysis of a 4-component complex comprising the VPS26 & VPS35 subunits of retromer, sorting nexin SNX3, & recycling signal from the divalent cation transporter DMT1-II; analysis identifies a binding site for canonical recycling signals at the interface between VPS26 & SNX3; shows cooperative interactions among the VPS subunits, SNX3 & cargo that couple signal-recognition to membrane recruitment.
Gene silencing of either CTR1 or DMT1 did not affect copper accumulation in cells, but deficiency in both CTR1 and DMT1 resulted in a complete inhibition of copper uptake.
These data suggest that iron uptake induces the production of ROS, which modify DMT1 endocytic cycling, thus changing the iron transport activity at the apical membrane.
We propose that DMT1 deficiency negatively affects metabolism and life span of mature erythrocytes; two other aspects of defective erythropoiesis which contribute to the pathophysiology of the disease
the TT genotype and T allele of the 1254T>C polymorphism may be a risk factor for Parkinson disease
Suggest role for divalent cation transporter DMT1 in the entry of Hg(II) into the intestinal epithelium.
Six months after RYGB surgery, patients exhibit an increase in DMT1 expression in the enterocytes of the tips of the villi at the proximal jejunum
In Parkinson's disease, increased iron levels are associated with increased Ndfip1 expression for the regulation of DMT1, including abnormal Ndfip1 activation in non-neuronal cell types such as astrocytes.
The DMT1 IVS4 C(+) allele occurred more frequently in WND than in the healthy controls.
DMT1 not only exports iron from endosomes, but also serves to import the metal into the mitochondria
Data suggest that maternal protein restriction during pregnancy and lactation influences growth of male and female offspring at weaning, reduces duodenum mucosal expression of iron transporters (DMT1 and FPN), and decreases serum Fe levels; serum ferritin levels tend to be lower, yet serum transferrin is greatly higher in male weaning piglets. (FPN = solute carrier family 40 [iron-regulated transporter] member 1)
The results indicate that global DMT1 overexpression causes decreased superoxide generation upon stimulation in inflammatory cells, which presumably delayed the promotional stage of crocidolite-induced mesothelial carcinogenesis. DMT1Tg mice with low-stamina inflammatory cells may be helpful to evaluate the involvement of inflammation in various pathologies
IL-6 likely up-regulates IRP1 and DMT1 expression and down-regulates FPN1 expression in BV2 microglial cells through JNK signaling pathways
Ndfip2 controls DMT1 in the liver with female mice showing a greater response to altered dietary iron than the male mice
PrP(C) promotes, and possibly regulates, the uptake of iron through DMT1 and Zip14 via its ferrireductase activity.
This study reveals a critical function for DMT1 in intestinal nonheme-iron absorption for normal growth and development, and that it is not required for the transport of copper, manganese, or zinc.
Misregulation of DMT1 is implicated in Parkinson's disease.
The Cu uptake in HEK293 cells that over-expressed the 2/-IRE isoform of DMT1 transporter supports our earlier contention that DMT1 transports Cu as Cu(1+).
Hepatocyte divalent metal-ion transporter-1 is dispensable for hepatic iron accumulation and non-transferrin-bound iron uptake in mice.
DMT-1 expression in hypothalamic subregions is cre recombinase sensitive, and that central-peripheral pathways may impact beta cell function in the Dmt1 null mouse.
CD61 regulates the expression of Slc11a2, which is involved in iron transportation in epithelial tissues.
that 1B/(-)IRE DMT1 expression and intracellular iron influx are early downstream responses to NF-kappaB/RelA activation and acetylation during brain ischemia and contribute to the pathogenesis of stroke-induced neuronal damage
The knockdown of ZIP8, ZIP14 or DMT1 by siRNA transfection significantly reduced the uptake of Cd(2+) and Mn(2+) from the apical membrane.
in b/b rats depressed liver hepcidin production and activated intestinal Hif2alpha starting at the C-pole resulted in increasing expression of iron transport genes, including DMT1 G185R, in an attempt to compensate for the anemia in Belgrade rats.
These data demonstrate that Ndfip1 is a critical mediator of DMT1 regulation in vivo, particularly under iron restricted conditions
Data suggest that reduced iron release from duodenal cells into circulation due to suppression of SLC11A2 plays a role in mitigating excessive iron uptake from the diet
Results suggest that divalent metal transporter 1 (DMT1) participates in inflammatory lung injury after bleomycin with DMT1 knockout mice having increased inflammation and damage following exposure.
Both Nramp1 and DMT1 are necessary for efficient macrophage iron recycling.
NRAMP2 is required for the detoxification of reactive oxygen species.
Under Mn-deficient conditions, increased accumulation of hydrogen peroxide (H2 O2 ) is partially responsible for the root growth inhibition and NRAMP2 is involved in remobilization of manganese (Mn) in Golgi for root growth.
The zebrafish mutant gene chardonnay (cdy) encodes divalent metal transporter 1 (DMT1). Whereas wild-type zebrafish DMT1 protein can transport iron, the truncated protein expressed in cdy mutants is not functional.
This gene encodes a member of the solute carrier family 11 protein family. The product of this gene transports divalent metals and is involved in iron absorption. Mutations in this gene are associated with hypochromic microcytic anemia with iron overload. A related solute carrier family 11 protein gene is located on chromosome 2. Multiple transcript variants encoding different isoforms have been found for this gene.
, NRAMP 2
, divalent cation transporter 1
, natural resistance-associated macrophage protein 2
, solute carrier family 11 (proton-coupled divalent metal ion transporters), member 2
, divalent metal transporter 1
, microcytic anemia, viable anaemia
, Solute carrier family 11 member 2 (natural resistance-associated macrophage protein 2)
, manganese transport protein