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- Table of Contents
Facts about GRB10-interacting GYF protein 2.
May act cooperatively with GRB10 to regulate tyrosine kinase receptor signaling, including IGF1 and insulin receptors (PubMed:12771153). .
Human | |
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Gene Name: | GIGYF2 |
Uniprot: | Q6Y7W6 |
Entrez: | 26058 |
Belongs to: |
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GIGYF family |
DKFZp686J17223; FLJ23368; GRB10 interacting GYF protein 2; GRB10-interacting GYF protein 2; GYF domain containing 2; GYF2; KIAA0642DKFZp686I15154; PARK11; Parkinson disease (autosomal recessive, early onset) 11; PERQ amino acid rich, with GYF domain 2; PERQ amino acid rich, with GYF domain 3; PERQ amino acid-rich with GYF domain-containing protein 2; PERQ2; PERQ3; TNRC15; trinucleotide repeat containing 15; Trinucleotide repeat-containing gene 15 protein
Mass (kDA):
150.07 kDA
Human | |
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Location: | 2q37.1 |
Sequence: | 2; NC_000002.12 (232697331..232860605) |
This article explores the benefits of using the GIGYF2 Marker. Learn how GDNF protects cells from MPP toxicity, how it has been linked to ParkinsonaEUR(tm)s disease, and how NR4A2 mutations affect the expression of the GIGYF2 gene. These benefits are applicable to all scientists around the world.
GDNF possesses neuroprotective properties. GDNF administered intranigrally reduces the loss and degeneration of nigral DA neurons and attenuates decreases in nigrostriatal DA levels. GDNF exhibits protective effects on nigrostriatal DA and 5-HT systems. These findings are the first evidence of the neuroprotective properties of GDNF.
GDNF is known to increase the length and number of "axons" of serotonin neurons. It is also known to increase the rate of building dopamine from tyrosine, and improve mitochondrial function. GDNF also protects against MPP toxicity by improving the functioning of a protein called RET. Finally, GDNF helps the brain create new connections and learn.
In this Phase I study, human GDNF was delivered via convection-enhanced delivery by an adeno-associated virus, serotype 2 vector. The study will include two hemispheres of patients and will administer up to 450 microliters of the injected drug through bilateral catheters. If there are any screening failures, up to 76 subjects will be included. This study will evaluate four escalating dose levels in six patient cohorts.
The anti-GDNF antibody from Boster Bio is tested in a WB application on Human and Rat cells. It has been validated using known positive and negative samples, and is guaranteed for high affinity and specificity. Moreover, the Boster Bio Anti-GDNF Antibody can be stored at -20°C for a year or at 4°C for a month. It contains 0.05mg BSA, 0.1mg Thimerosal, and 0.01% NaN3.
After confirming that Boster Bio GDNF protects against the toxicity caused by MPPs, the study used a human plasma cell culture to confirm that the supplement is effective in reducing MPP toxicity. To further confirm the safety of the boster bio GDNF, animal studies are required. The results are consistent with previous studies that have implicated GDNF in preventing nitric oxide (MPP) toxicity in rats.
Several complementary approaches to brain health are effective in increasing GDNF levels in the blood. While preliminary research shows promising results, further large-scale studies are needed to confirm the findings. As always, you should consult a doctor before making any drastic changes. Among these complementary approaches are calorie restriction, exercise, and dietary supplements. SSRI medications are known to increase GDNF levels.
De novo deletions of the NR4A2 gene have been identified in three unrelated individuals with language and developmental delays. These de novo deletions have not been previously reported in the Database of Genomic Variants. In addition, two of these cases also had prominent speech impairment. Hence, this gene is not only associated with ParkinsonaEUR(tm)s disease, but also with other neurodevelopmental disorders.
The role of Nr4a2 in neurological disorders has been explored in recent years. Previous research has shown that this gene is involved in learning and memory, as well as hippocampal synaptic plasticity. Additionally, it is implicated in various neuropsychiatric disorders, such as schizophrenia, autism spectrum disorder, and ParkinsonaEUR(tm)s disease.
Interestingly, NR4A2 is regulated by the CREB protein, which regulates the expression of several genes. The gene has a putative role in learning and memory processes. Researchers also hope to develop novel drugs for ParkinsonaEUR(tm)s disease through targeting the NR4A2 gene. But the long road ahead is still long.
While the NR4a2 protein has been considered an orphan nuclear receptor for a long time, the latest research suggests that the gene may be a druggable target in the future. For example, drugs targeting the protein should have increased specificity, improved blood-brain barrier permeability, and better pharmacokinetics than existing drugs. Although the protein is considered an orphan nuclear receptor, recent studies have suggested that endogenous ligands may bind to the receptor and regulate its activity.
In addition to its role in neurodegeneration, Nr4a2 has been found to contribute to active-dependent synaptic plasticity, learning, and memory. However, further studies are needed to understand more fully the role of this protein in ParkinsonaEUR(tm)s disease. So, the question remains, can we identify a genetic variant with NR4A2 mutations in ParkinsonaEUR(tm)s disease?
Age-dependent memory problems have been linked with the presence of NR4A2 mutations. In aged mice, Nr4a2 expression decreased. The deletion of HDAC3 in the hippocampal region alleviated the problem in aged mice. It was also associated with hippocampal-dependent spatial memory deficits in APPSw,Ind mice.
PMID: 12771153 by Giovannone B., et al. Two novel proteins that are linked to insulin-like growth factor (IGF-I) receptors by the Grb10 adapter and modulate IGF-I signaling.
PMID: 19279319 by Nichols W.C., et al. Variation in GIGYF2 is not associated with Parkinson disease.