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Human Polyclonal TMPRSS6 Primary Antibody für WB - ABIN1881891
Altamura, DAlessio, Selle, Muckenthaler: A novel TMPRSS6 mutation that prevents protease auto-activation causes IRIDA. in The Biochemical journal 2010
Show all 2 Pubmed References
The role of TMPRSS6 A736V variants in the pathogenesis of iron deficiency anemia (IDA) in celiac disease (CD) patients was studied at diagnosis and after 1 year of gluten-free diet. A736V allele frequencies were similar among patients and controls.A736V was significantly increased in IDA persistent than in IDA not persistent. TMPRSS6 predicts oral iron response modulating hepcidin action on iron absorption.
Children with TT genotype of TMPRSS6 rs855791 had an increased risk of cow's milk protein allergy.
The associations between polymorphisms of TMPRSS6 and the levels of serum ferritin and soluble transferrin receptor are observed in pregnant women.
TMPRSS6 polymorphisms are associated with increased many iron-related hematological parameters in Turkish patients but may not be risk factors for iron deficiency anemia
results suggest that mother and child have a novel variety of iron-refractory iron deficiency anemia as a result of two TMPRSS6 mutations
Isolated heterozygous mutations of TMPRSS6 are unlikely to cause IRIDA, but when combined with a mutation in ALK2, the heterozygosity for the inactive MT2(I212T) may leave enough membrane hemojuvelin to allow persistent hepcidin activation.
These findings suggest that the expression of matriptase-2 may be both a prognostic marker and a potential therapeutic target for this cancer.
Data (including data from studies using knockout mice) suggest that MT2/TMPRSS6 suppresses hepcidin expression in hepatocytes independently of HJV; MT2/TMPRSS6 cleaves ALK2, ALK3, ACTRIIA, BMPR2, HFE, and, to a lesser extent, HJV and TFR2; thus, MT2/TMPRSS6 suppresses hepcidin expression by cleaving multiple components of the hepcidin induction pathway. (MT2/TMPRSS6 = matriptase-2; HJV = hemojuvelin)
In examining iron variant associations with glucose homeostasis, an iron-raising variant of TMPRSS6 was associated with lower HbA1c levels (P = 8.66 x 10-10).
Studies in colonic T84 cell monolayers revealed that barrier disruption by the colitis-associated Th2-type cytokines, IL-4 and IL-13, down-regulates matriptase as well as prostasin through phosphorylation of the transcriptional regulator STAT6
TMPRSS6 gene sequencing in 20 cases with IRIDA phenotype revealed 9 potentially deleterious intronic and two benign exonic variations in 12/20 cases (60%).
Study suggests that deregulated pericellular matriptase activity in OSCC may transactivate PAR-2 on fibroblasts in the surrounding tissue and thus promote their recruitment to the perimeter of the tumor, contributing to a microenvironement that favors tumor growth of oral squamous cell carcinoma.
All cases were either homozygous or compound heterozygous for missense or frameshift mutations in the TMPRSS6 gene, 2 of the mutations being novel (Cys410Ser and Leu689Pro)
TMPRSS6 expression is significantly downregulated in human masticatory mucosa during wound healing
Matriptase-2 deficiency causes iron deficiency anemia during the early postnatal development, but not during fetal development in humans.
Iron refractory iron deficiency anemia is caused by mutations of TMPRSS6 which encodes matriptase-2, a serine protease expressed on cell membranes of hepatocytes which is involved in the hepcidin regulatory pathways by processing hemojuvelin protein.
Combination of Tmprss6- ASO and the iron chelator deferiprone improves erythropoiesis and reduces iron overload in a mouse model of beta-thalassemia intermedia.
Data show that p.V736A TMPRSS6 variant (rs855791) influences the susceptibility to hepatic iron accumulation in NTDT patients, and the risk allele is 736(A).
A novel splicing mutation of TMPRSS6 exon 9 (c.1113G>A) was found in an iron-refractory iron deficiency anemia patient and his father.
N-glycan branching regulates HAI-2 through different subcellular distribution and subsequently access to different target proteases
The study describes a role for C and hepcidin in obesity and highlights the relevance of iron regulation in the control of adipose tissue function.
Erythroferrone and matriptase-2 independently regulate hepcidin expression.
Data (including data from studies using knockout mice) suggest that Mt2/Tmprss6 suppresses hepcidin expression in hepatocytes independently of Hjv; Mt2/Tmprss6 cleaves Alk2, Alk3, ActRIIA, Bmpr2, Hfe, and, to a lesser extent, Hjv and Tfr2; thus, Mt2/Tmprss6 suppresses hepcidin expression by cleaving multiple components of the hepcidin induction pathway. (Mt2/Tmprss6 = matriptase-2; Hjv = hemojuvelin)
The results provide support for the interaction between TMPRSS6 and hemojuvelin in vivo; they also suggest that hemojuvelin could be cleaved by another as yet unknown protease in the absence of functional TMPRSS6.
the function of matriptase-2 is dominant over that of ERFE and is essential in facilitating hepcidin suppression by attenuating the BMP-SMAD signaling.
role of fetuin-A in iron homeostasis and provide new insights into the mechanism of how matriptase-2 might modulate hepcidin expression
TMPRSS6 inhibition via decreased STAT5 phosphorylation may be an additional mechanism by which inflammation stimulates hepcidin expression to regulate iron homeostasis and immunity.
matriptase-2 (encoded by Tmprss6)-is responsible for hepcidin repression throughout development, with its deficiency leading to increased hepcidin levels triggering iron deficiency and anemia starting in utero
The iron-regulatory serine protease matriptase-2 is expressed in the retina, and absence of this enzyme leads to iron deficiency.
Loss of matriptase-2 increases bone morphogenetic protein-dependent signaling, while paradoxically decreasing liver hemojuvelin protein content.
Results confirm the anti-inflammatory status of Tmprss6 KO mice and identify new potential target pathways/genes of Tmprss6.
Tmprss6 gene knockdown reduces iron overload in an animal model of hemochromatosis and improves both iron overload and anemia in mice affected by beta-thalassemia.
Double mutant mice lacking functional Hfe or Tfr2 and Tmprss6 exhibited a severe iron deficiency microcytic anemia phenotype mimicking the phenotype of single mutant mice lacking functional Tmprss6 demonstrating that Hfe and Tfr2 are not substrates for Tmprss6.
Preventing iron overload improves beta-thalassemia and strengthens the essential role of Tmprss6 for Hamp suppression, providing a proof of concept that Tmprss6 manipulation can offer a novel therapeutic option in this condition.
The data do not provide support for the concept that matriptase-2 cleaves membrane hemojuvelin and may indicate that, in vivo, the role of matriptase-2 in the regulation of hepcidin gene expression is more complex.
Heterozygous loss of Tmprss6 in Hfe(-/-) mice reduced systemic iron overload, whereas homozygous loss caused systemic iron deficiency and elevated hepatic expression of hepcidin and other Bmp/Smad target genes
Loss of TMPRSS6 is associated with iron-deficiency anemia and involves up-regulation of Bmp/Smad signaling.
identification, characterization and comparative mRNA expression analysis with mouse hepsin in adult and embryonic tissues
identification, structural features, enzymology, expression pattern and potential roles of TMPRSS6 [review]
The protein encoded by this gene is a type II transmembrane serine proteinase that is found attached to the cell surface. The encoded protein may be involved in matrix remodeling processes in the liver.
transmembrane protease serine 6
, transmembrane serine protease 6
, membrane-bound mosaic serine proteinase matriptase-2
, type II transmembrane serine protease 6
, matriptase 2
, transmembrane protease, serine 6