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This locus encodes a LEM domain-containing protein. De plus, nous expédions LEM Domain Containing 3 Anticorps (22) et LEM Domain Containing 3 Protéines (3) et beaucoup plus de produits pour cette protéine.
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Genome-wide analysis combined with linkage results revealed LEMD3 and WIF1 (Montrer WIF1 Kits ELISA) as the candidates for porcine ear size.
Letter/Case-Report: novel frameshift mutation in RNA recognition motif of LEMD3 in patient with Buschke-Ollendorff syndrome.
A novel mutation in LEMD3 splice site results in Buschke-Ollendorff syndrome.
Data indicate that the inner nuclear membrane protein MAN1 directly binds the transcription activator BMAL1 (Montrer ARNTL Kits ELISA) promoter and enhances its transcription.
a nuclear envelope-localized mechanism of inactivating TGF-beta (Montrer TGFB1 Kits ELISA) signaling in which MAN1 competes with transcription factors for binding to Smad2 (Montrer SMAD2 Kits ELISA) and Smad3 (Montrer SMAD3 Kits ELISA) and facilitates their dephosphorylation by PPM1A (Montrer PPM1A Kits ELISA).
The absence of direct binding of BAF (Montrer BANF1 Kits ELISA) to MAN1-C eliminates disruption of this interaction as the cause of the premature aging phenotype.
Genetic analyses of three generations of a family with Buschke-Ollendorff syndrome having a variable phenotype showed a novel c.2203C>T nonsense mutation at the LEMD3 locus. The mutation induced a change in the 735 arginine codon to a stop codon.
Buschke-Ollendorff syndrome in a three-generation family: influence of a novel LEMD3 mutation to tropoelastin (Montrer ELN Kits ELISA) expression.
We found a novel c.2203C > T (p.R735X) mutation in exon 9 of LEMD3, resulting in a premature stop codon at amino acid position 735.
Absence of LEMD3 mutation in the exons and splice sites of a family with BOS suggests that there is genetic heterogeneity for this disorder.
Binds to Smad2 (Montrer SMAD2 Kits ELISA) and Smad3 (Montrer SMAD3 Kits ELISA) and antagonizes signaling by transforming growth factor-beta
the heterozygous Lemd3 gene-trapped mouse is not a good model to study osteopoikilosis and the Buschke-Ollendorff syndrome.
In Man1-deficient embryos, the expression of Tgfb1 (Montrer TGFB1 Kits ELISA) is upregulated and Smad2 (Montrer SMAD2 Kits ELISA)/3 signaling is abnormally activated, resulting in increased extracellular matrix deposition, a hallmark of the resolution phase of angiogenesis.
The nuclear envelope protein MAN1 regulates TGFbeta (Montrer TGFB1 Kits ELISA) signaling and vasculogenesis in the embryonic yolk sac (Montrer ADCY10 Kits ELISA).
Man1 regulates left-right asymmetry by controlling Nodal signaling in a node-independent manner
This locus encodes a LEM domain-containing protein. The encoded protein functions to antagonize transforming growth factor-beta signaling at the inner nuclear membrane. Two transcript variants encoding different isoforms have been found for this gene. Mutations in this gene have been associated with osteopoikilosis, Buschke-Ollendorff syndrome and melorheostosis.
LEM domain containing 3
, inner nuclear membrane protein Man1
, Smad1 antagonistic effector
, LEM domain-containing protein 3
, integral inner nuclear membrane protein
, integral inner nuclear membrane protein MAN1