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genetic analyses of indel loci in ACE, DJ-1, and GIGYF2 genes, was performed to explore the potential contribution of insertion (I)/deletion (D) polymorphisms (indels) to the risk of PD in a Chinese population.
Full-length GIGYF2 coimmunoprecipitates with AGO2 in human cells, and upon tethering to a reporter mRNA, GIGYF2 exhibits strong, dose-dependent silencing activity, involving both mRNA destabilization and translational repression.
required, this finding may shed light on the GIGYF2-associated mechanisms that lead to PD and suggests insulin dysregulation as a disease-specific mechanism for both PD and cognitive dysfunction.
Results suggest that the N56S and N457T of GIGYF2 are risk factors for Parkinson's disease in Caucasians, but not in Asians
GIGYF2 and the zinc finger protein 598 (ZNF598) are identified as components of the 4EHP complex.
Our result indicated that SCNA, LRRK2, UCHL1, HtrA2 and GIGYF2 genes' mutations might not be a main reason for Chinese Autosomal dorminant Parkinson's disease
within the Chinese population, the c.297T>C p.Ala99Ala polymorphism of the GIGYF2 gene may be associated with an increased risk of developing Parkinson disease.
These data, together with those recently reported by other groups, suggest that GIGYF2 is unlikely to be the PARK11 gene.
No clearly pathogenic mutations are identified in GIGYF2 and ATP13A2 in Brazilian patients with early-onset Parkinson's disease.
The results of this study did not support a role for GIGYF2 in the genetic etiology of Belgian Parkinson disease.
GIGYF2 is unlikely to play a major role in PD in Japanese patients, similar to other populations.
our findings suggest that GIGYF2 variants are not a frequent cause of Parkinson's disease in the Spanish population, since we found no clearly segregating GIGYF2 variants
GIGYF2 variants are not associated with Parkinson's disease in the mainland Chinese Population.
The results of this study do not support a major role of GIGYF2 in parkinson disease.
We identified nine novel variants in GIGYF2 gene, which might be associated with PD in the Chinese population.
These data strongly support GIGYF2 as a PARK11 gene with a causal role in familial Parkinson disease.
Mutations in GIGYF2 are not strongly related to the development of the Parkinson's disease in Portuguese and North American populations.
This study suggested that reported mutations in GIGYF2 are not a common cause of Parkinson's disease in Norway and United States.
The results of this study concluded that neither of Asn56Ser and Asn457Thr variants plays a major role in the pathogenesis of parkinson disease.
We believe that variation in a gene other than GIGYF2 accounts for the previously reported linkage finding on chromosome 2q36-37.
Negative regulation of Grb10 Interacting GIGYF2 protein on IGF-1 receptor signaling pathway caused diabetic mice cognitive impairment.
Disruption of the eukaryotic translation initiation factor 4E - Gigyf2 complex leads to increased translation and perinatal lethality in mice.
Primary cultured embryo fibroblasts from Gigyf2 null mice exhibit decreased IGF1 signaling.
identification of proteins linked to insulin-like growth factor (IGF-I) receptors by the Grb10 adapter and modulate IGF-I signaling
The protein encoded by this gene interacts with GRB10 and may be involved in the regulation of tyrosine kinase receptor signaling. This gene contains CAG repeats, and the encoded protein contains stretches glutamine and glutamic acid residues. Defects in this gene are a cause of Parkinson disease type 11 (PARK11). Multiple transcript variants encoding several different isoforms have been found for this gene.
trinucleotide repeat containing 15
, GRB10 interacting GYF protein 2
, PERQ amino acid-rich with GYF domain-containing protein 2
, PERQ amino acid rich, with GYF domain 3
, Parkinson disease (autosomal recessive, early onset) 11
, trinucleotide repeat-containing gene 15 protein
, GRB10-interacting GYF protein 2