Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Grin3a. (This text reflects annotations as of Wednesday, January 23, 2013.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of September 27, 2007. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.

---

Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a subunit of the N-methyl-D-aspartate (NMDA) receptors, which belong to the superfamily of glutamate-regulated ion channels, and function in physiological and pathological processes in the central nervous system. This subunit shows greater than 90% identity to the corresponding subunit in rat. Studies in the knockout mouse deficient in this subunit suggest that this gene may be involved in the development of synaptic elements by modulating NMDA receptor activity. [provided by RefSeq, Jul 2008]

---

Summary text based on GO annotations supported by experimental evidence in mouse

• Researchers have inferred from direct assay, that the gene product of Grin3a
  • participates in the following biological processes:
    • calcium ion transmembrane transport ^[2]
  • performs the following molecular functions:
    • calcium channel activity ^[2]
  • is located in the following cellular components:
    • neuronal cell body ^[3]
    • postsynaptic membrane ^[2]
• The gene product of Grin3a has been shown to bind to the gene products of Grin1. ^[2] Researchers have inferred, based on physical interactions, that the gene product of Grin3a
  • participates in the following biological processes:
    • ionotropic glutamate receptor signaling pathway ^[2]
  • performs the following molecular functions:
    • N-methyl-D-aspartate selective glutamate receptor activity ^[2]
• Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of Grin3a
  • participates in the following biological processes:
    • calcium ion transmembrane transport ^[3]
    • calcium ion transport ^[3]
    • dendrite development ^[2]
    • ion transmembrane transport ^[3]
    • ionotropic glutamate receptor signaling pathway ^[3]
    • prepulse inhibition ^[1]
  • performs the following molecular functions:
    • calcium channel activity ^[3]
    • N-methyl-D-aspartate selective glutamate receptor activity ^[3]

---

Summary text based on GO annotations supported by experimental evidence in other organisms

• From comparative sequence analysis (see table for details), MGI curators have determined that the gene product of Grin3a:
  • participates in the following biological processes:
    • calcium ion transport
    • ionotropic glutamate receptor signaling pathway
    • response to ethanol
    • rhythmic process
  • performs the following molecular functions:
    • glycine binding
    • identical protein binding
    • ionotropic glutamate receptor activity
    • N-methyl-D-aspartate selective glutamate receptor activity
    • neurotransmitter binding
    • protein phosphatase 2A binding
  • is located in the following cellular components:
    • membrane
    • N-methyl-D-aspartate selective glutamate receptor complex
    • neuron projection
    • neuronal cell body
    • postsynaptic membrane
    • synapse

---

Summary text for additional MGI annotations

• Automated translation to GO terms of SwissProt keywords that describe Grin3a indicates that it:
  • participates in the following biological processes:
    • ion transport
    • transport
  • performs the following molecular functions:
    • ion channel activity
  • is located in the following cellular components:
    • cell junction
    • integral to membrane
    • plasma membrane

---

References

1. Brody SA et al. (2005) A developmental influence of the N-methyl-D-aspartate receptor NR3A subunit on prepulse inhibition of startle. Biol Psychiatry, 57:1147-52. (PubMed:15866554)
2. Das S et al. (1998) Increased NMDA current and spine density in mice lacking the NMDA receptor subunit NR3A. Nature, 393:377-81. (PubMed:9620802)
3. Sucher NJ et al. (2003) N-methyl-D-aspartate receptor subunit NR3A in the retina: developmental expression, cellular localization, and functional aspects. Invest Ophthalmol Vis Sci, 44:4451-6. (PubMed:14507892)

---

---

Gene Ontology Evidence Code Abbreviations:

EXP Inferred from experiment

IC Inferred by curator

IDA Inferred from direct assay

IEA Inferred from electronic annotation

IGI Inferred from genetic interaction

IMP Inferred from mutant phenotype

IPI Inferred from physical interaction

ISS Inferred from sequence or structural similarity

ISO Inferred from sequence orthology

ISA Inferred from sequence alignment

ISM Inferred from sequence model

NAS Non-traceable author statement

ND No biological data available

RCA Reviewed computational analysis

TAS Traceable author statement

---