Target intelligence / Profile preview

Cornichon family AMPA receptor auxiliary protein 2 (CNIH2)

Target
CNIH2
Molecular classification
Auxiliary subunit, Ion channel associated protein, AMPA receptor auxiliary protein
01

Overview

Cornichon family AMPA receptor auxiliary protein 2 (CNIH2) is a protein that acts as an auxiliary subunit for ionotropic glutamate receptors of the AMPA subtype[2][3][4]. It regulates the trafficking, membrane targeting, and gating properties of AMPA-selective glutamate receptors, promoting their localization to the cell surface and synapses, and thereby modulating excitatory neurotransmission in the central nervous system[7]. CNIH2 is classified as an auxiliary protein associated with ion channels, and although it is not the direct drug target (unlike the main AMPA receptor subunits), it plays an important modulatory role in glutamatergic neurotransmission and synaptic plasticity. Disease relevance is most likely in neurological and neuropsychiatric contexts, though there are no direct disease or drug associations confirmed in major genetic or protein databases at this time.

Other names
Protein cornichon homolog 2CNIH2CNILCNIH-2MGC50896CnilCornichon-like proteincornichon homolog 2
02

Mechanism of action

No drugs directly target CNIH2 according to current sources. Mechanistically, CNIH2 regulates AMPA receptor function, so drugs modulating AMPA receptors could be indirectly affected by CNIH2 status.

03

Biological functions

Regulation of AMPA receptor traffickingModulation of AMPA receptor gating propertiesPromotion of AMPA receptor targeting to membrane and synapses[7]
04

Disease associations

Neurodegenerative disease (potential role through modulation of synaptic function and excitatory neurotransmission; direct disease associations not strongly characterized in search results)Other (possible involvement in neurological and neuropsychiatric disorders by affecting glutamatergic signaling; more research needed)
05

Safety considerations

No notable safety concerns or therapeutic challenges directly reported for targeting CNIH2. Changes in AMPA receptor auxiliary protein function could potentially impact neuronal excitability and risk for seizures, but this is not directly documented as a clinical concern for CNIH2[3][7].

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