Phosphospecific Antibody

Glutamate [NMDA] receptor subunit epsilon-2 (N-methyl D-aspartate receptor subtype 2B receptor or NMDA NR2B) is a NMDA receptor subtype of glutamate-gated ion channels with high calcium permeability and voltage-dependent sensitivity to magnesium. NMDA NR2B forms heteromeric channel of a zeta subunit, a epsilon subunit (GRIN2A , GRIN2B, GRIN2C or GRIN2D) and a third subunit (GRIN3A or GRIN3B). NMDA NR2B is sprimarily found in the fronto-parieto-temporal cortex and hippocampus pyramidal cells.

NR2A (Glutamate [NMDA] receptor subunit epsilon-1 or NMDA NR2A) is a glutamate-gated ion channel with high calcium permeability and voltage-dependent sensitivity to magnesium. The NMDA channel is involved in long-term potentiation, an activity-dependent increase in synaptic transmission underlying memory and learning. NMDA NR2A is a heteromer composed of a zeta subunit (GRIN1), an epsilon subunit (GRIN2A, GRIN2B, GRIN2C or GRIN2D) and a third subunit (GRIN3A or GRIN3B). NMDA NR2A activation requires binding of agonist to both types of subunits.

The metabotropic glutamate receptor 7 (mGluR7) is a receptor for L-glutamate. L-glutamate is the major excitatory neurotransmitter in the central nervous system and activates both ionotropic and metabotropic glutamate receptors. Glutamatergic neurotransmission is involved in most aspects of normal brain function and can be perturbed in many neuropathologic conditions. The metabotropic glutamate receptors are a family of G protein-coupled receptors that have been divided into 3 groups on the basis of sequence homology, putative signal transduction mechanisms, and pharmacologic properties.

MEK1 (MAPKK1) catalyzes the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in MAP kinases. MEKI (MAPKK1) activates ERK1 and ERK2 MAP kinases, enzymes which are involved in numerous signal transduction pathways. Defects in MEK1 (MAPKK1) are a cause of cardiofaciocutaneous syndrome (CFC syndrome), also known as cardio-facio-cutaneous syndrome. CFC syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. The sites on MEK 1 that are phosphorylated by MAP kinase are Thr292 and Thr386.

Dual specificity mitogen-activated protein kinase kinase 1 (MEK1/2) catalyzes the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in MAP kinases. MEK1/2 activates ERK1 and ERK2 MAP kinases. Defects in MEK1/2 are a cause of cardiofaciocutaneous syndrome (CFC syndrome), also known as cardio-facio-cutaneous syndrome. CFC syndrome is characterized by distinctive facial appearance, heart defects and mental retardation.