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GCM2 is a homolog of the Drosophila glial cells missing gene, which is thought to act as a binary switch between neuronal and glial cell determination. De plus, nous expédions GCM2 Anticorps (33) et GCM2 Protéines (2) et beaucoup plus de produits pour cette protéine.
Overexpression of gcm2 mRNA resulted in a significant increase in the numbers of ecac (Montrer TRPV6 Kits ELISA)-expressing ionocytes and Ca2 (Montrer CA2 Kits ELISA)+ uptake.
PTH1 (Montrer PTH Kits ELISA) morphants failed to express gcm2. Coinjection of PTH1 (Montrer PTH Kits ELISA) morpholino with gcm2 capped RNA rescued the phenotypes observed in the PTH1 (Montrer PTH Kits ELISA) morphants, suggesting that the defects in PTH1 (Montrer PTH Kits ELISA)-deficient fish were caused, at least in part, by the suppression of gcm2.
Results suggest that an acquisition of enhancers for the expression of gcm2 contributes to a diversity of ionocytes in zebrafish during evolution.
role of Shh (Montrer SHH Kits ELISA) signalling in patterning the pharyngeal pouches and in restricting the expression of the parathyroid marker Gcm2 in the pharyngeal epithelium
Results suggest a role for glial cells missing 2 during the evolution of divergent pharyngeal morphologies.
Gcm-2 is required for the formation of the internal gill buds in zebrafish
The transcription factor, glial cell missing 2, is involved in differentiation and functional regulation of H+-ATPase (Montrer ATP6AP1 Kits ELISA)-rich cells in zebrafish.
Our results demonstrate that germline-activating mutations affecting the C-terminal conserved inhibitory domain of GCM2 can cause familial isolated hyperparathyroidism.
Gata3 (Montrer GATA3 Kits ELISA) interacted with Gcm2 and MafB (Montrer MAFB Kits ELISA), two known transcriptional regulators of parathyroid development, and synergistically stimulated the PTH (Montrer PTH Kits ELISA) promoter.
The higher frequency of GCM2 282D in primary hyperparathyroidismand enhanced transcriptional activity of this variant supports the notion that it could contribute causally to parathyroid tumorigenesis
we identified the genetic defect in 35% of hypoparathyroidism patients in our cohort and discovered novel GCM2 mutations including submicroscopic deletion that was undetectable by array comparative genomic hybridization
Four single nucleotide polymorphisms of GCMB gene were found in the GCMB gene (c.-44T > C [rs16870746], c.91-242A > G [rs9379881], c.343+163G > A [rs9393726], and c.583-72A > T [rs2076257]) in our cohort.
First described GCM2 mutation in exon 3 in patients with severe congenital hypoparathyroidism.
Data suggest that replacement of cysteine 106 with arginine (C106R) would interfere with DNA binding of glial cells missing B (GCMB).
We conclude that mutations in the transcription factor GCMB do not seem to play a major role in the pathogenesis of primary hyperparathyroidism.
These results indicate that GCMB and vitamin D receptor (Montrer VDR Kits ELISA) are involved in the positive and negative regulation of parathyroid hormone (Montrer PTH Kits ELISA) gene expression, respectively.
Gcm2 is a useful adjunct marker for the diagnosis of parathyroid lesions.
results suggest that MafB (Montrer MAFB Kits ELISA) regulates later steps of parathyroid development, that is, separation from the thymus and migration toward the thyroid. MafB (Montrer MAFB Kits ELISA) also regulates the expression of PTH (Montrer PTH Kits ELISA) in cooperation with Gcm2
Gcm2 (glial cells missing 2) are involved in the epigenetic regulation of Hes5 (Montrer HES5 Kits ELISA) transcription by DNA demethylation independently of DNA replication.
GCM (Montrer GCM1 Kits ELISA) domain as a new type of Zn-coordinating, sequence-specific DNA-binding domain.
Gcm2 is required for the differentiation and survival of parathyroid precursor cells in the parathyroid/thymus primordia.
This gene is a homolog of the Drosophila glial cells missing gene, which is thought to act as a binary switch between neuronal and glial cell determination. The protein encoded by this gene contains a conserved N-terminal GCM motif that has DNA-binding activity. The protein is a transcription factor that acts as a master regulator of parathyroid development. It has been suggested that this transcription factor might mediate the effect of calcium on parathyroid hormone expression and secretion in parathyroid cells. Mutations in this gene are associated with hypoparathyroidism.
chorion-specific transcription factor GCMb
, glial cells missing 2
, gcmB transcription factor
, glial cell missing-like protein
, transcription factor glial cells missing-2
, transcription factor Glial cells missing-2
, glial cells missing protein homolog 2
, glial cells missing homolog 2
, GCM motif protein 2
, glial cells missing homolog b
, glide/gcm protein homolog