GRIK2 antibody - N-terminal region (ARP35515_T100)
- Known as:
- GRIK2 (anti-) - N-terminal region (ARP35515_T100)
- Catalog number:
- arp35515_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GRIK2 antibody - N-terminal region (ARP35515_T100)
Related genes to: GRIK2 antibody - N-terminal region (ARP35515_T100)
- Gene:
- GRIK2 NIH gene
- Name:
- glutamate ionotropic receptor kainate type subunit 2
- Previous symbol:
- GLUR6
- Synonyms:
- GluK2, MRT6
- Chromosome:
- 6q16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-26
- Date modifiied:
- 2016-02-05
- Gene:
- GRIK5 NIH gene
- Name:
- glutamate ionotropic receptor kainate type subunit 5
- Previous symbol:
- GRIK2
- Synonyms:
- GluK5, KA2
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-21
- Date modifiied:
- 2016-02-05
Related products to: GRIK2 antibody - N-terminal region (ARP35515_T100)
Related articles to: GRIK2 antibody - N-terminal region (ARP35515_T100)
- Autism spectrum disorder (ASD) is a genetically inherited, complex neuropsychiatric developmental condition that impacts a person's ability to learn, interact, and communicate. ASD is currently classified as a heterogeneous disorder, given that the pathophysiology of ASD is yet unknown. The GRIK gene family (GRIK1, GRIK2, GRIK3, GRIK4, and GRIK5) has genetic variants associated with many psychiatric illnesses including; depression, obsessive–compulsive disorder, and autism. The present study is the first to determine the possible association of GRIK1 rs363598 and intergenic rs360932 variants with susceptibility to ASD in Egyptian children and to correlate these variants with different parameters. - Source: PubMed
Publication date: 2025/12/01
Bassiony HebaBaiomy AhmedAhmed DoaaElaraby Nesma MAmmar Tamer H AAshaat Engy A - A growing body of evidence suggests an association between microdeletion/microduplication and schizophrenia/intellectual disability. Abnormal neurogenesis and neurotransmission have been implicated in the pathogenesis of these neuropsychiatric and neurodevelopmental disorders. The kainate/AMPA-type ionotropic glutamate receptor (GRIK = glutamate receptor, ionotropic, kainate) plays a critical role in synaptic potentiation, which is an essential process for learning and memory. Among the five known GRIK family members, haploinsufficiency of GRIK1, GRIK2, and GRIK4 are known to cause developmental delay, whereas the roles of GRIK3 and GRIK5 remain unknown. Herein, we report on a girl who presented with a severe developmental delay predominantly affecting her language and fine motor skills. She had a 2.6-Mb microdeletion in 1p34.3 involving GRIK3, which encodes a principal subunit of the kainate-type ionotropic glutamate receptor. Given its strong expression pattern in the central nervous system and the biological function of GRIK3 in presynaptic neurotransmission, the haploinsufficiency of GRIK3 is likely to be responsible for the severe developmental delay in the proposita. A review of genetic alterations and the phenotypic effects of all the GRIK family members support this hypothesis. The current observation of a microdeletion involving GRIK3, a kainate-type ionotropic glutamate receptor subunit, and the neurodevelopmental manifestation in the absence of major dysmorphism provides further clinical implication of the possible role of GRIK family glutamate receptors in the pathogenesis of developmental delay. - Source: PubMed
Publication date: 2013/11/25
Takenouchi ToshikiHashida NorikoTorii ChiharuKosaki RikaTakahashi TakaoKosaki Kenjiro - Kainate receptors, a subtype of ionotropic glutamate receptors, perform important functions in the spinal cord. This study aimed to examine the expression pattern of various kainate receptor subunits in the spinal cord over different stages of development. The regional distribution and levels of Grik1-5 mRNAs, which encode kainate receptor subunits, were examined in the spinal cord of embryonic, perinatal, and adult mice using in-situ hybridization and real-time PCR. At different developmental stages, the expression of Grik1-5 genes showed different regional distributions in the spinal cord. At E16.5, Grik2 and Grik3 were mainly expressed in the dorsal horns whereas Grik5 was expressed in the entire spinal cord. At P0 and P7, Grik2 expression accumulated at laminae II-IV, whereas Grik1 accumulated at the superficial laminae of the dorsal horns. At P30 and P60, the expression of Grik1-5 was concentrated in the superficial laminae of the dorsal horns. Development-related changes were observed in the expression pattern of Grik1-5. Grik5 was expressed in the entire spinal cord up to the perinatal period, whereas from P7 to adult stages, Grik5 expression was almost exclusively restricted to the dorsal horns. Similar observations were present with Grik1, Grik2, and Grik3. Consistently, quantitative determination of the expression levels of Grik1-5 was in accordance with the in-situ hybridization results. This age-related dynamic expression of kainate receptors may act as one driving force for the development of the anatomofunctional pattern and the maturation of the somatosensory circuitry in the spinal cord. - Source: PubMed
Cui ShaoqianDu PengZhou XiaozhongWang Huan