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DTor and DFMRP immunoreactivities were partially colocalized in several cellular organelles in larval muscles
Fmr1 protein associates with ninaE (zeige RHO Proteine) mRNA and represses its translation.
Our data strongly support a gain-of-function pathogenic mechanism of PQBP1 (zeige PQBP1 Proteine) c.459_462delAGAG and c.463_464dupAG mutations, and suggest that therapeutic strategies to restore FMRP function may be beneficial for those patients
dFMRP cooperates with Piwi in maintaining genome integrity by silencing heterochromatic genes and suppressing transposon expression.
results show Fragile X Mental Retardation Protein (FMRP) shapes neuron class-specific calcium signaling in excitatory vs. inhibitory neurons in developing learning/memory circuitry, and that FMRP mediates activity-dependent regulation of calcium signaling specifically during the early-use critical period.
results support a model whereby dFMRP can modulate the neurotoxicity caused by TDP-43 (zeige TARDBP Proteine) overexpression
demonstrate that Zfrp8 genetically interacts with Fmr1 and tral (zeige LSM14A Proteine) in an antagonistic manner. Zfrp8 and FMRP both control heterochromatin packaging, also in opposite ways
dFmr1 protein is essential for proper cardiac function and establish the fly as a new model for studying the role(s) of FraX proteins in the heart.
These results show that dfmr1 acts in a neuron type-specific activity-dependent manner for sculpting dendritic arbors during early-use, critical period development of learning and memory circuitry in the Drosophila brain.
upon the stimulation of replication stress, dFMR1 is associated with chromatin in a domain-specific manner, which is essential for its ability to induce the phosphorylation of H2Av (zeige H2AFV Proteine).
The results show that SMNDC1 (zeige SMNDC1 Proteine) mRNA 5'-UTR forms an intramolecular, parallel G quadruplex structure comprised of three G quartet planes, which is bound specifically by FMRP both in vitro and in mouse brain lysates.
The results of this study findings reveal domain-specific functions of FMRP in the regulation of axonal complexity that may be controlled by differential expression of FMRP splice forms.
our study shows that increased expression of FMRP, an important RNA binding protein, is associated with increased astrocytoma proliferation.
The characterization of the expression levels of the different FMR1 isoforms is fundamental for understanding the regulation of the FMR1 gene as imbalance in their expression could lead to an altered functional diversity with neurotoxic consequences. Their characterization will also help to elucidating the mechanism(s) by which "toxic gain of function" of the FMR1 mRNA may play a role in Fragile X-associated tremorAtaxia.
FMR1 CGG repeat length may have a role in determining X-chromosome inactivation which could represent a possible mechanism for previously observed association of low age adjusted ovarian reserve with FMR1 variations in repeat length.
Authors found that 5hmC enrichment at the FMR1 locus in FXS cells is specific to neurons by utilizing a nuclei sorting technique to separate neuronal and glial DNA fractions from post-mortem brain tissues. This FMR1 5hmC enrichment was not present in cellular models of FXS including fibroblasts, lymphocytes and reprogrammed neurons.
Mutation intolerant genes and targets of FMRP are associated with schizophrenia.
FMR1 mutation is associated with Fragile X syndrome.
High or low numbers of CGGs in FMR1 gene is associated with poorer health and functional outcomes during aging..
There is no robust evidence in this large study that variation within the normal range of FMR1 repeat alleles influences timing of menopause in the general population, which contradicts findings from some earlier, mainly smaller studies. The FMR1 CGG repeat polymorphism in the normal range is unlikely to contribute to genetic susceptibility to early menopause.
We identified thousands of clustered RNA editing sites in the zebrafish transcriptome and showed that Fmrp biochemically interacts with the Adar2a protein. The expression levels of the adar (zeige ADAR Proteine) genes and Adar2 (zeige ADARB1 Proteine) protein increased in fmr1-/- zebrafish
Loss-of-function fmr1 mutants carrying an anti-fmr1 miRNA transgene show abnormal neuronal morphology and connectivity similar to that seen in human fragile X syndrome.
Using the Fmr1 null mouse model of fragile X syndrome, brain regions, gene networks, and molecular pathways responsive to a social stimulus have been identified.
This study demonstrated that In vivo recordings from barrel cortex revealed that Fmr1 KO mice show an enlargement in the cortical area activated by whisker deflections.
The data of this study suggested that NMDAR (zeige GRIN1 Proteine) hypofunction in the DG may partly contribute to learning and memory impairment in female Fmr1(+/-) mice
This study shown a clear reduction in the frequency and duration of calls for FMR1 KOs compared with WT across all days and also a significant difference in vocalizations between male and female mice.
APP levels then decrease progressively as a function of age in close relationship with the gradual normalization of FMRP and hnRNP C levels.
Overexpression of Dgkkappa in neurons is able to rescue the dendritic spine defects of the Fragile X Mental Retardation 1 gene KO neurons.
Results indicate that direct inhibition of acetylcholinesterase (zeige AChE Proteine) activity and up-regulation of m1 muscarinic acetylcholine receptor (zeige CHRNB1 Proteine) expression in the striatum might contribute to the beneficial effects of alpha-asarone on locomotor hyperactivity in Fmr1 knock out mice.
neurogenesis is also accelerated in the embryonic brain of Fmr1-knockout mice, indicating that cellular model recapitulates the molecular alterations present in vivo.
Casein kinase II (zeige CSNK2A1 Proteine) (CK2 (zeige CSNK2A1 Proteine)) phosphorylates murine FMRP S499. Phosphorylation of FMRP S499 permits phosphorylation of additional, nearby residues. Evidence suggests that these nearby residues are modulated by mGluR (zeige GRM8 Proteine)-I and PP2A (zeige PPP2R2B Proteine) pathways; that FMRP is peritranslationally phosphorylated by CK2 (zeige CSNK2A1 Proteine), which allows for secondary phosphorylation of secondary residues in an activity-dependent manner.
The protein encoded by this gene binds RNA and is associated with polysomes. The encoded protein may be involved in mRNA trafficking from the nucleus to the cytoplasm. A trinucleotide repeat (CGG) in the 5' UTR is normally found at 6-53 copies, but an expansion to 55-230 repeats is the cause of fragile X syndrome. Expansion of the trinucleotide repeat may also cause one form of premature ovarian failure (POF1). Multiple alternatively spliced transcript variants that encode different protein isoforms and which are located in different cellular locations have been described for this gene.
, Fragile-X mental retardation protein
, drosophila fragile X mental retardation protein
, fragile X
, fragile X mental retardation
, fragile X mental retardation 1
, fragile X mental retardation gene
, fragile X mental retardation protein
, fragile X protein
, fragile X related protein
, fragile X-related
, fragile x related
, fragile X mental retardation protein 1
, fragile X mental retardation protein 1 homolog
, fragile X mental retardation syndrome 1 homolog
, fragile X mental retardation-1 protein
, protein FMR-1
, ragile X mental retardation protein
, fragile X mental retardation 1 protein