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This locus encodes a LEM domain-containing protein. De plus, nous expédions LEM Domain Containing 3 Anticorps (27) et LEM Domain Containing 3 Kits (4) et beaucoup plus de produits pour cette protéine.
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studies demonstrated that lower levels of MAN1 in differentiating MSC (Montrer MSC Protéines) are associated with higher osteogenesis and lower adipogenesis. High levels of MAN1 only affected adipogenesis.
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 Protéines) promoter and enhances its transcription.
a nuclear envelope-localized mechanism of inactivating TGF-beta (Montrer TGFB1 Protéines) signaling in which MAN1 competes with transcription factors for binding to Smad2 (Montrer SMAD2 Protéines) and Smad3 (Montrer SMAD3 Protéines) and facilitates their dephosphorylation by PPM1A (Montrer PPM1A Protéines).
The absence of direct binding of BAF (Montrer BANF1 Protéines) 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 Protéines) 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.
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 Protéines) is upregulated and Smad2 (Montrer SMAD2 Protéines)/3 signaling is abnormally activated, resulting in increased extracellular matrix deposition, a hallmark of the resolution phase of angiogenesis.
The nuclear envelope protein (Montrer SUN2 Protéines) MAN1 regulates TGFbeta (Montrer TGFB1 Protéines) signaling and vasculogenesis in the embryonic yolk sac (Montrer ADCY10 Protéines).
Man1 regulates left-right asymmetry by controlling Nodal signaling in a node-independent manner
Genome-wide analysis combined with linkage results revealed LEMD3 and WIF1 (Montrer WIF1 Protéines) as the candidates for porcine ear size.
LEM proteins, involved in signalling essential for organ development during early embryogenesis and suggests that loss of MAN1 may cause muscle and retina specific diseases
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 protein 3
, inner nuclear membrane protein Man1
, integral inner nuclear membrane protein
, integral inner nuclear membrane protein MAN1
, LEM domain containing 3
, Smad1 antagonistic effector
, LEM domain containing 3 S homeolog
, nuclear membrane protein XMAN1