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kainate receptor

vr.tr.kainate-receptor · thing-q3454536

Enable an AI agent to identify a kainate receptor assembly, assess its functional state, and select interpretable measurements or experimental perturbations.

Thing Registry Physical world and living systems PHY.MAT

Bundle → Layer → Finding → Questions Filled

5 bundles · 9 layers · 15 findings · 24 questions

Molecular identity and assembly Identify the receptor population through its constituent proteins and their assembled configuration.

Subunit identity

Resolve species, nomenclature and sequence variants.

Resolved GluK components

Record current subunit names alongside accessions and historical labels. Human GluK1 corresponds to GRIK1. [IUPHAR/BPS GluK1](https://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=450)

  1. Which GluK subunits, species and accessions identify the receptor under consideration? definition
  2. Which splice forms, editing states or engineered sequence changes were established in the preparation? provenance

Assembly resolution

Separate detected components from demonstrated co-assembly.

Functional complex evidence

Record homomeric or heteromeric assignment, proposed stoichiometry and evidence that the components form the same functional complex.

  1. What evidence distinguishes co-assembly from subunits merely being expressed in the same cell? provenance
  2. Does the observation describe an isolated subunit, one receptor assembly or a mixture of receptor populations? boundary
Membrane context and partners Describe where the receptor is available and which proteins accompany it.

Surface availability

Distinguish total receptor material from receptors delivered to the plasma membrane.

Surface delivery evidence

Track total abundance and surface abundance separately; ligand-binding-site mutations have affected expression and surface delivery in recombinant kainate-receptor experiments. [Primary study](https://pubmed.ncbi.nlm.nih.gov/30302614/)

  1. Which assay establishes plasma-membrane availability rather than total cellular subunit abundance? measurement
  2. Could a reduced response reflect impaired surface delivery, and what measurement would distinguish it from altered gating? action

Local environment

Specify cellular compartment and associated proteins.

Compartment and auxiliary context

Record presynaptic, postsynaptic or other localization and whether NETO-family or other partners were tested, detected or experimentally supplied.

  1. What evidence places this receptor population in the stated cell type and membrane compartment? provenance
  2. Which auxiliary proteins are present, and is their association with this receptor demonstrated or assumed? provenance
Gating and ion permeation Describe stimulus-dependent channel states and the ion flow they permit.

Activation and desensitization

Resolve the time course of opening, response decay and recovery.

Stimulus-linked state transitions

Associate kinetic measurements with ligand identity, concentration, application speed and pulse history instead of treating response amplitude as a complete functional description.

  1. What ligand pulse and solution-exchange conditions produced the measured activation and desensitization? measurement
  2. What paired-pulse or washout experiment distinguishes desensitization from persistent blockade or receptor loss? action

Conductance and selectivity

Connect ion transport measurements to receptor composition and recording conditions.

Variant-dependent permeation

Retain editing and assembly context when recording channel conductance; recombinant experiments demonstrate dependence on Q/R editing and subunit co-assembly. [Primary study](https://pubmed.ncbi.nlm.nih.gov/8730589/)

  1. What conductance, reversal potential and permeability measurements were obtained, with which ionic solutions and voltages? measurement
  2. Were relevant editing states determined directly, and how do they limit interpretation of calcium permeability or rectification? boundary
Pharmacology and functional attribution Relate experimental perturbations to receptor-specific effects with explicit limits.

Ligand response

Distinguish binding, activation, inhibition and modulation.

Assay-qualified pharmacology

Record ligand identity, concentration range, assay endpoint and receptor composition; keep binding affinity distinct from functional potency and efficacy.

  1. Does the reported parameter measure binding, peak current, steady-state current or a downstream endpoint? definition
  2. Which selectivity controls distinguish this ligand's kainate-receptor effect from activity at neighbouring glutamate receptors? action

Causal attribution

Separate receptor-level observations from cellular and circuit interpretations.

Mechanism and transfer limits

Attach pharmacological, genetic and recording evidence to each functional claim, identifying whether it supports direct channel current, an indirect response or a proposed non-ionotropic mechanism.

  1. Which independent controls establish that the observed effect depends on the identified kainate receptor population? provenance
  2. What evidence separates ion flux through the receptor from downstream signalling or network-mediated effects? boundary
  3. Which preparation differences must be resolved before transferring this finding to native tissue? action
Evidence and external alignment What the world already says about this thing, gathered so the model can be checked against it.

Reported evidence

Findings from the breadth pass, kept separate from the structural claims.

Check these first

Recalled without web access and unsourced; every item is a lead to verify.

  1. Which of these check these first hold for the sense of kainate receptor this model covers, and on what evidence? provenance

Kinds and varieties

Recalled without web access and unsourced; every item is a lead to verify.

  1. Which of these kinds and varieties hold for the sense of kainate receptor this model covers, and on what evidence? provenance

Identifiers and schemes

Recalled without web access and unsourced; every item is a lead to verify.

  1. Which of these identifiers and schemes hold for the sense of kainate receptor this model covers, and on what evidence? provenance

Real-world use

Recalled without web access and unsourced; every item is a lead to verify.

  1. Which of these real-world use hold for the sense of kainate receptor this model covers, and on what evidence? provenance

Typical measurements

Recalled without web access and unsourced; every item is a lead to verify.

  1. Which of these typical measurements hold for the sense of kainate receptor this model covers, and on what evidence? provenance

Failure modes and hazards

Recalled without web access and unsourced; every item is a lead to verify.

  1. Which of these failure modes and hazards hold for the sense of kainate receptor this model covers, and on what evidence? provenance

Neighbouring kinds and how to tell them apart

Recalled without web access and unsourced; every item is a lead to verify.

  1. Which of these neighbouring kinds and how to tell them apart hold for the sense of kainate receptor this model covers, and on what evidence? provenance

Classifiers Filled

Family
Thing Registry
Category
Physical world and living systems
Entry kind
thing
Plane
PHY
Domain
PHY.MAT
Other names and narrower kinds
Glutamate ionotropic receptor kainate type subunit 3, Glutamate ionotropic receptor kainate type subunit 4, Glutamate receptor, ionotropic, kainate 3, Glutamate receptor, ionotropic, kainate 2 (beta 2), Glutamate receptor, ionotropic, kainate 5 (gamma 2), Glutamate receptor, ionotropic, kainate 4, Glutamate receptor ionotropic, kainate 1

What it is Filled

A kainate receptor is a tetrameric ionotropic glutamate receptor assembled from GluK1-GluK5 subunits that mediates glutamate-activated cation conductance and modulates synaptic transmission in the nervous system.

In scope

  • GluK subunit composition, assembly and molecular variants
  • Receptor membrane localization and associated proteins
  • Ligand binding, activation, desensitization and recovery
  • Ion permeation and electrophysiological properties under recorded conditions
  • Pharmacological responses and evidence attributing an observed effect to kainate receptors

Out of scope

  • Kainic acid, glutamate and other ligands as chemical substances
  • GRIK genes and their transcriptional regulation as independent entities
  • AMPA, NMDA and metabotropic glutamate receptor families
  • Whole-neuron, synaptic circuit and organism models
  • Disease diagnosis, treatment recommendations and clinical drug dosing

Why it exists Filled

Enable an AI agent to identify a kainate receptor assembly, assess its functional state, and select interpretable measurements or experimental perturbations.

Distinguishing features Filled

  • Identify the complex through GluK-family subunits; a response to kainate alone is insufficient to establish receptor identity.
  • Distinguish an assembled receptor from a GRIK gene, transcript or isolated GluK protein.
  • Check assembly compatibility: GluK4 or GluK5 alone does not establish a functional channel; these subunits require partners from GluK1-GluK3. [IUPHAR/BPS](https://doi.org/10.2218/gtopdb%2Ff75%2F2019.4)
  • Distinguish ion conduction through the receptor from downstream signalling attributed to receptor activation.
  • Separate ligand-bound desensitized receptors from open channels; ligand occupancy does not by itself demonstrate current flow.

What robots and AI may and may not do Filled

Must not

  • Recommend compounds acting on these receptors for personal use.
  • Present early research as proven treatment for epilepsy or pain.
  • Interpret a person's genetic test on a receptor gene as a diagnosis.
  • Assist in making or using neurotoxins that act on these receptors to harm people or animals.

Only with a human decision

  • Using receptor research in decisions about patient treatment.

May

  • Explain the structure and roles of kainate receptors from scientific sources.
  • Summarise research on these receptors with citations.

Moral aspects Filled

  • Brain research can lead to treatments but also to harmful substances; dual use needs care.
  • Animal research on seizures raises welfare questions.

Who is affected

  • Patients with epilepsy and neurological conditions
  • Laboratory animals
  • Research participants

Owners Filled

Steward

Nobody owns the receptors; researchers answer for their data.

Master systems

  • Protein and gene databases

Links to other meta-models Filled

parent

  • Q24779507 - registry parent class

What else AI and robots need to interact with it Filled

Identity and identifiers required Filled

  • Vercy registry: vr.tr.kainate-receptor
  • Wikidata: Q3454536 (https://www.wikidata.org/wiki/Q3454536)

Direct properties required Filled

  • Subunit composition: GluK1-GluK5 identities, copy numbers where established, species and protein accessions
  • Sequence and processing variants: Splice isoform, Q/R editing status where applicable, mutations, tags and unknown status
  • Associated auxiliary proteins: NETO1, NETO2, other experimentally supported partners, absent or untested
  • Membrane localization: Intracellular, surface, presynaptic, postsynaptic, extrasynaptic or unresolved
  • Functional channel state: Resting, activated/open, desensitized, blocked or unresolved
  • Ligand response parameters: EC50, IC50 or Kd in mol/L; efficacy relative to a named reference; assay conditions required
  • Channel kinetics: Activation, deactivation, desensitization and recovery times in ms or s
  • Ion conduction: Conductance in pS, reversal potential in mV, relative permeability ratios and current-voltage relation
  • Experimental preparation: Native tissue or recombinant system, organism, cell type and recording protocol

Recognition required Filled

  • Resolved molecular structures show four subunits surrounding a central membrane-spanning ion pore, a feature shared with other ionotropic glutamate receptors.
  • Extracellular amino-terminal and ligand-binding domains form a layered assembly above the membrane-spanning region.
  • Assignment to the kainate receptor class requires identification of GluK1-GluK5 subunits because overall molecular shape alone does not reliably distinguish related receptor classes.

Capabilities and actions required Filled

  • Resolve historical subunit names to current GluK identities while retaining the original terminology.
  • Assess whether a proposed subunit combination has evidence for functional assembly.
  • Compare receptor responses after matching composition, auxiliary proteins and assay conditions.
  • Select binding or electrophysiological measurements appropriate to the unresolved receptor property.
  • Evaluate agonist, antagonist or genetic perturbations for their ability to distinguish kainate-receptor effects.
  • Flag unsupported transfers from recombinant assemblies to native receptor populations.

Hazards and failure modes required Filled

  • Overactivation of these receptors is linked to seizures and nerve cell damage.
  • Naturally occurring toxins acting on related receptors can contaminate shellfish.

Standards and interfaces required Filled

  • IUPHAR/BPS receptor nomenclature, International Union of Basic and Clinical Pharmacology.

Context of use required Filled

  • Kainate receptors occur in neuronal membranes, where they contribute to excitatory signaling and regulation of synaptic transmission.
  • They are studied in neuroscience and pharmacology to relate receptor composition to ion currents, synaptic function and neurological disease.

Sources Filled

  1. Wikidata item Q3454536: kainate receptor - identity and sense of the item
  2. Wikipedia: Kainate receptor - general description of the item

Open questions

  • Does the registry intend this entry to cover all taxonomic kainate-receptor homologues, or primarily the vertebrate GluK1-GluK5 family?
  • Which native subunit stoichiometries are directly established for the cell types of interest, and which remain inferred from expression?
  • How completely are editing states, splice variants and auxiliary-protein associations characterized in the intended preparations?
  • Which reported non-ionotropic effects have evidence that separates them from ion conduction and indirect network activity?
  • Which ligand and genetic-control combinations provide adequate receptor attribution in the intended experimental system?

Machine files

Provenance

thing registry research (pass 2) · unreviewed

Built from: models/things/publications/thing-q3454536/spec.json