Record Information
Version2.0
Creation Date2009-06-19 21:58:17 UTC
Update Date2014-12-24 20:23:08 UTC
Accession NumberT3D1094
Identification
Common NameBarium bromate
ClassSmall Molecule
DescriptionBarium bromate is a chemical compound of barium and bromine. Barium is a metallic alkaline earth metal with the symbol Ba, and atomic number 56. It never occurs in nature in its pure form due to its reactivity with air, but combines with other chemicals such as sulfur or carbon and oxygen to form barium compounds that may be found as minerals. Bromine is a halogen element with the symbol Br and atomic number 35. Diatomic bromine does not occur naturally, but bromine salts can be found in crustal rock. (7, 6)
Compound Type
  • Barium Compound
  • Bromate Compound
  • Industrial/Workplace Toxin
  • Inorganic Compound
  • Synthetic Compound
Chemical Structure
Thumb
Synonyms
Synonym
Barium bromic acid
Bromic acid, barium salt
Chemical FormulaBaBr2O6
Average Molecular Mass393.131 g/mol
Monoisotopic Mass391.711 g/mol
CAS Registry Number13967-90-3
IUPAC Name(bromyloxy)bario bromate
Traditional Name(bromyloxy)bario bromate
SMILESO=[Br](=O)O[Ba]O[Br](=O)=O
InChI IdentifierInChI=1S/Ba.2BrHO3/c;2*2-1(3)4/h;2*(H,2,3,4)/q+2;;/p-2
InChI KeyInChIKey=VEASZGAADGZARC-UHFFFAOYSA-L
Chemical Taxonomy
Description belongs to the class of inorganic compounds known as alkaline earth metal bromates. These are inorganic compounds in which the largest oxoanion is bromate, and in which the heaviest atom not in an oxoanion is a lanthanide.
KingdomInorganic compounds
Super ClassMixed metal/non-metal compounds
ClassAlkaline earth metal oxoanionic compounds
Sub ClassAlkaline earth metal bromates
Direct ParentAlkaline earth metal bromates
Alternative Parents
Substituents
  • Alkaline earth metal bromate
  • Inorganic oxide
  • Inorganic salt
Molecular FrameworkNot Available
External DescriptorsNot Available
Biological Properties
StatusDetected and Not Quantified
OriginExogenous
Cellular Locations
  • Cytoplasm
  • Extracellular
Biofluid LocationsNot Available
Tissue LocationsNot Available
PathwaysNot Available
ApplicationsNot Available
Biological RolesNot Available
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceWhite powder.
Experimental Properties
PropertyValue
Melting PointNot Available
Boiling PointNot Available
SolubilityNot Available
LogPNot Available
Predicted Properties
PropertyValueSource
logP0.81ChemAxon
pKa (Strongest Basic)-8.5ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count4ChemAxon
Hydrogen Donor Count0ChemAxon
Polar Surface Area86.74 ŲChemAxon
Rotatable Bond Count4ChemAxon
Refractivity25.94 m³·mol⁻¹ChemAxon
Polarizability13.81 ųChemAxon
Number of Rings0ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
SpectraNot Available
Toxicity Profile
Route of ExposureOral (8) ; inhalation (8) ; dermal (8)
Mechanism of ToxicityBarium is a competitive potassium channel antagonist that blocks the passive efflux of intracellular potassium, resulting in a shift of potassium from extracellular to intracellular compartments. The intracellular translocation of potassium results in a decreased resting membrane potential, making the muscle fibers electrically unexcitable and causing paralysis. Some of these barium's effects may also be due to barium induced neuromuscular blockade and membrane depolarization. Bromine is a powerful oxidizing agent and is able to release oxygen free radicals from the water in mucous membranes. These free radicals are also potent oxidizers and produce tissue damage. In additon, the formation of hydrobromic and bromic acids will result in secondary irritation. The bromide ion is also known to affect the central nervous system, causing bromism. This is believed to be a result of bromide ions substituting for chloride ions in the in actions of neurotransmitters and transport systems, thus affecting numerous synaptic processes. (8, 9, 1, 6)
MetabolismBarium compounds are absorbed via ingestion and inhalation, the extent of which depends on the individual compound. In the body, the majority of the barium is found in the bone, while small amounts exists in the muscle, adipose, skin, and connective tissue. Barium is not metabolized in the body, but it may be transported or incorporated into complexes or tissues. Barium is excreted in the urine and faeces. Bromine is mainly absorbed via inhalation, but may also enter the body through dermal contact. Bromine salts can be ingested. Due to its reactivity, bromine quickly forms bromide and may be deposited in the tissues, displacing other halogens. (8, 6)
Toxicity ValuesNot Available
Lethal Dose1 to 15 grams for an adult human (barium salts). (2)
Carcinogenicity (IARC Classification)No indication of carcinogenicity (not listed by IARC). (5)
Uses/SourcesNot Available
Minimum Risk LevelIntermediate Oral: 0.2 mg/kg/day (Barium) (4) Chronic Oral: 0.2 mg/kg/day (Barium) (4)
Health EffectsThe health effects of the different barium compounds depend on how well the compound dissolves in water or the stomach contents. At low doses, barium acts as a muscle stimulant, while higher doses affect the nervous system, causing cardiac irregularities, tremors, weakness, anxiety, dyspnea, paralysisand possibly death. Barium may also cause gastrointestinal disturbances, damage the kidneys and cause decreases in body weight. Bromine vapour causes irritation and direct damage to the mucous membranes. Elemental bromine also burns the skin. The bromide ion is a central nervous system depressant and chronic exposure produces neuronal effects. This is called bromism and can result in central reactions reaching from somnolence to coma, cachexia, exicosis, loss of reflexes or pathologic reflexes, clonic seizures, tremor, ataxia, loss of neural sensitivity, paresis, papillar edema of the eyes, abnormal speech, cerebral edema, delirium, aggressiveness, and psychoses. Bromate is also a potential carcinogen. (6, 10, 7, 8, 9)
SymptomsIngesting excess barium may cause vomiting, abdominal cramps, diarrhea, difficulties in breathing, increased or decreased blood pressure, numbness around the face, and muscle weakness. High levels may result in changes in heart rhythm or paralysis and possibly death. Bromine vapour causes irritation and direct damage to the mucous membranes. Symptoms include lacrimation, rhinorrhoea, eye irritation with mucous secretions from the oropharyngeal and upper airways, coughing, dyspnoea, choking, wheezing, epistaxis, and headache. The bromide ion is a central nervous system depressant producing ataxia, slurred speech, tremor, nausea, vomiting, lethargy, dizziness, visual disturbances, unsteadiness, headaches, impaired memory and concentration, disorientation and hallucinations. This is called bromism. (8, 9, 6)
TreatmentEYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention. INHALATION: supply fresh air. If required provide artificial respiration.
Normal Concentrations
Not Available
Abnormal Concentrations
Not Available
DrugBank IDNot Available
HMDB IDNot Available
PubChem Compound ID61706
ChEMBL IDNot Available
ChemSpider ID55607
KEGG IDNot Available
UniProt IDNot Available
OMIM ID
ChEBI IDNot Available
BioCyc IDNot Available
CTD IDC078336
Stitch IDBarium bromate
PDB IDNot Available
ACToR IDNot Available
Wikipedia LinkNot Available
References
Synthesis ReferenceNot Available
MSDST3D1094.pdf
General References
  1. Ziouzenkova O, Orasanu G, Sharlach M, Akiyama TE, Berger JP, Viereck J, Hamilton JA, Tang G, Dolnikowski GG, Vogel S, Duester G, Plutzky J: Retinaldehyde represses adipogenesis and diet-induced obesity. Nat Med. 2007 Jun;13(6):695-702. Epub 2007 May 27. [17529981 ]
  2. Gosselin RE, Smith RP, and Hodge HC (1984). Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins.
  3. Golomb, BA (1999). A Review of the Scientific Literature As It Pertains to Gulf War Illnesses. Volume 2: Pyridostigmine Bromide. Washington, DC: RAND.
  4. ATSDR - Agency for Toxic Substances and Disease Registry (2001). Minimal Risk Levels (MRLs) for Hazardous Substances. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
  5. International Agency for Research on Cancer (2014). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. [Link]
  6. ATSDR - Agency for Toxic Substances and Disease Registry (2007). Toxicological profile for barium. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
  7. Wikipedia. Bromine. Last Updated 9 June 2009. [Link]
  8. International Programme on Chemical Safety (IPCS) INCHEM (1992). Poison Information Monograph for Bromine. [Link]
  9. Wikipedia. Potassium bromide. Last Updated 9 June 2009. [Link]
  10. Wikipedia. Bromate. Last Updated 26 May 2009. [Link]
Gene Regulation
Up-Regulated GenesNot Available
Down-Regulated GenesNot Available

Targets

General Function:
Voltage-gated chloride channel activity
Specific Function:
Voltage-gated chloride channel. Chloride channels have several functions including the regulation of cell volume; membrane potential stabilization, signal transduction and transepithelial transport.
Gene Name:
CLCN1
Uniprot ID:
P35523
Molecular Weight:
108625.435 Da
References
  1. Simchowitz L: Interactions of bromide, iodide, and fluoride with the pathways of chloride transport and diffusion in human neutrophils. J Gen Physiol. 1988 Jun;91(6):835-60. [3047312 ]
  2. Pusch M, Jordt SE, Stein V, Jentsch TJ: Chloride dependence of hyperpolarization-activated chloride channel gates. J Physiol. 1999 Mar 1;515 ( Pt 2):341-53. [10050002 ]
General Function:
Voltage-gated chloride channel activity
Specific Function:
Voltage-gated chloride channel. Chloride channels have several functions including the regulation of cell volume; membrane potential stabilization, signal transduction and transepithelial transport. May be important in urinary concentrating mechanisms.
Gene Name:
CLCNKA
Uniprot ID:
P51800
Molecular Weight:
75284.08 Da
References
  1. Simchowitz L: Interactions of bromide, iodide, and fluoride with the pathways of chloride transport and diffusion in human neutrophils. J Gen Physiol. 1988 Jun;91(6):835-60. [3047312 ]
  2. Pusch M, Jordt SE, Stein V, Jentsch TJ: Chloride dependence of hyperpolarization-activated chloride channel gates. J Physiol. 1999 Mar 1;515 ( Pt 2):341-53. [10050002 ]
General Function:
Voltage-gated chloride channel activity
Specific Function:
Voltage-gated chloride channel. Chloride channels have several functions including the regulation of cell volume; membrane potential stabilization, signal transduction and transepithelial transport. May be important in urinary concentrating mechanisms.
Gene Name:
CLCNKB
Uniprot ID:
P51801
Molecular Weight:
75445.3 Da
References
  1. Simchowitz L: Interactions of bromide, iodide, and fluoride with the pathways of chloride transport and diffusion in human neutrophils. J Gen Physiol. 1988 Jun;91(6):835-60. [3047312 ]
  2. Pusch M, Jordt SE, Stein V, Jentsch TJ: Chloride dependence of hyperpolarization-activated chloride channel gates. J Physiol. 1999 Mar 1;515 ( Pt 2):341-53. [10050002 ]
General Function:
Phosphatidylinositol-4,5-bisphosphate binding
Specific Function:
In the kidney, probably plays a major role in potassium homeostasis. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. This channel is activated by internal ATP and can be blocked by external barium.
Gene Name:
KCNJ1
Uniprot ID:
P48048
Molecular Weight:
44794.6 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
Voltage-gated potassium channel activity
Specific Function:
This receptor is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium (By similarity). Subunit of ATP-sensitive potassium channels (KATP). Can form cardiac and smooth muscle-type KATP channels with ABCC9. KCNJ11 forms the channel pore while ABCC9 is required for activation and regulation.
Gene Name:
KCNJ11
Uniprot ID:
Q14654
Molecular Weight:
43540.375 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
Inward rectifier potassium channel activity
Specific Function:
Inward rectifying potassium channel that is activated by phosphatidylinositol 4,5-bisphosphate and that probably participates in controlling the resting membrane potential in electrically excitable cells. Probably participates in establishing action potential waveform and excitability of neuronal and muscle tissues. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium.
Gene Name:
KCNJ12
Uniprot ID:
Q14500
Molecular Weight:
49000.6 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
Inward rectifier potassium channel activity
Specific Function:
This potassium channel is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by external barium (By similarity).
Gene Name:
KCNJ8
Uniprot ID:
Q15842
Molecular Weight:
47967.455 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
8. ATP-sensitive potassium channel (Protein Group)
General Function:
Phosphatidylinositol-4,5-bisphosphate binding
Specific Function:
In the kidney, probably plays a major role in potassium homeostasis. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. This channel is activated by internal ATP and can be blocked by external barium.
Included Proteins:
P48048 , P78508 , Q14654 , Q14500 , Q9UNX9 , Q99712 , Q15842
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
9. ATP-sensitive potassium channel (Protein Group)
General Function:
Phosphatidylinositol-4,5-bisphosphate binding
Specific Function:
In the kidney, probably plays a major role in potassium homeostasis. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. This channel is activated by internal ATP and can be blocked by external barium.
Included Proteins:
P48048 , P78508 , Q14654 , Q14500 , Q9UNX9 , Q99712 , Q15842
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
10. ATP-sensitive potassium channel (Protein Group)
General Function:
Phosphatidylinositol-4,5-bisphosphate binding
Specific Function:
In the kidney, probably plays a major role in potassium homeostasis. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. This channel is activated by internal ATP and can be blocked by external barium.
Included Proteins:
P48048 , P78508 , Q14654 , Q14500 , Q9UNX9 , Q99712 , Q15842
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
Titin binding
Specific Function:
Calmodulin mediates the control of a large number of enzymes, ion channels, aquaporins and other proteins by Ca(2+). Among the enzymes to be stimulated by the calmodulin-Ca(2+) complex are a number of protein kinases and phosphatases. Together with CCP110 and centrin, is involved in a genetic pathway that regulates the centrosome cycle and progression through cytokinesis.
Gene Name:
CALM1
Uniprot ID:
P0DP23
Molecular Weight:
16837.47 Da
References
  1. Kursula P, Majava V: A structural insight into lead neurotoxicity and calmodulin activation by heavy metals. Acta Crystallogr Sect F Struct Biol Cryst Commun. 2007 Aug 1;63(Pt 8):653-6. Epub 2007 Jul 28. [17671360 ]
General Function:
G-protein activated inward rectifier potassium channel activity
Specific Function:
This potassium channel is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. This receptor plays a crucial role in regulating the heartbeat.
Gene Name:
KCNJ3
Uniprot ID:
P48549
Molecular Weight:
56602.84 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
Inward rectifier potassium channel activity
Specific Function:
This potassium channel may be involved in the regulation of insulin secretion by glucose and/or neurotransmitters acting through G-protein-coupled receptors. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium.
Gene Name:
KCNJ6
Uniprot ID:
P48051
Molecular Weight:
48450.96 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
G-protein activated inward rectifier potassium channel activity
Specific Function:
This receptor is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium (By similarity).
Gene Name:
KCNJ9
Uniprot ID:
Q92806
Molecular Weight:
44019.45 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
G-protein activated inward rectifier potassium channel activity
Specific Function:
This potassium channel is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by external barium.
Gene Name:
KCNJ5
Uniprot ID:
P48544
Molecular Weight:
47667.3 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
Inhibitory extracellular ligand-gated ion channel activity
Specific Function:
Component of the heteropentameric receptor for GABA, the major inhibitory neurotransmitter in the vertebrate brain. Functions also as histamine receptor and mediates cellular responses to histamine. Functions as receptor for diazepines and various anesthetics, such as pentobarbital; these are bound at a separate allosteric effector binding site. Functions as ligand-gated chloride channel (By similarity).
Gene Name:
GABRA1
Uniprot ID:
P14867
Molecular Weight:
51801.395 Da
References
  1. Suzuki S, Kawakami K, Nakamura F, Nishimura S, Yagi K, Seino M: Bromide, in the therapeutic concentration, enhances GABA-activated currents in cultured neurons of rat cerebral cortex. Epilepsy Res. 1994 Oct;19(2):89-97. [7843172 ]
General Function:
Gaba-gated chloride ion channel activity
Specific Function:
Component of the heteropentameric receptor for GABA, the major inhibitory neurotransmitter in the vertebrate brain. Functions also as histamine receptor and mediates cellular responses to histamine. Functions as receptor for diazepines and various anesthetics, such as pentobarbital; these are bound at a separate allosteric effector binding site. Functions as ligand-gated chloride channel.
Gene Name:
GABRB3
Uniprot ID:
P28472
Molecular Weight:
54115.04 Da
References
  1. Suzuki S, Kawakami K, Nakamura F, Nishimura S, Yagi K, Seino M: Bromide, in the therapeutic concentration, enhances GABA-activated currents in cultured neurons of rat cerebral cortex. Epilepsy Res. 1994 Oct;19(2):89-97. [7843172 ]
General Function:
Inhibitory extracellular ligand-gated ion channel activity
Specific Function:
Component of the heteropentameric receptor for GABA, the major inhibitory neurotransmitter in the vertebrate brain. Functions also as histamine receptor and mediates cellular responses to histamine. Functions as receptor for diazepines and various anesthetics, such as pentobarbital; these are bound at a separate allosteric effector binding site. Functions as ligand-gated chloride channel.
Gene Name:
GABRG2
Uniprot ID:
P18507
Molecular Weight:
54161.78 Da
References
  1. Suzuki S, Kawakami K, Nakamura F, Nishimura S, Yagi K, Seino M: Bromide, in the therapeutic concentration, enhances GABA-activated currents in cultured neurons of rat cerebral cortex. Epilepsy Res. 1994 Oct;19(2):89-97. [7843172 ]
General Function:
Inward rectifier potassium channel activity
Specific Function:
Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. KCNJ13 has a very low single channel conductance, low sensitivity to block by external barium and cesium, and no dependence of its inward rectification properties on the internal blocking particle magnesium.
Gene Name:
KCNJ13
Uniprot ID:
O60928
Molecular Weight:
40529.195 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
Inward rectifier potassium channel activity
Specific Function:
Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. KCNJ16 may be involved in the regulation of fluid and pH balance.
Gene Name:
KCNJ16
Uniprot ID:
Q9NPI9
Molecular Weight:
47948.585 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
Voltage-gated potassium channel activity involved in cardiac muscle cell action potential repolarization
Specific Function:
Probably participates in establishing action potential waveform and excitability of neuronal and muscle tissues. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium or cesium.
Gene Name:
KCNJ2
Uniprot ID:
P63252
Molecular Weight:
48287.82 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
Pdz domain binding
Specific Function:
Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium and cesium (By similarity).
Gene Name:
KCNJ4
Uniprot ID:
P48050
Molecular Weight:
49499.61 Da
References
  1. Alagem N, Dvir M, Reuveny E: Mechanism of Ba(2+) block of a mouse inwardly rectifying K+ channel: differential contribution by two discrete residues. J Physiol. 2001 Jul 15;534(Pt. 2):381-93. [11454958 ]
General Function:
Voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarization
Specific Function:
Potassium channel that plays an important role in a number of tissues, including heart, inner ear, stomach and colon (By similarity) (PubMed:10646604). Associates with KCNE beta subunits that modulates current kinetics (By similarity) (PubMed:9312006, PubMed:9108097, PubMed:8900283, PubMed:10646604, PubMed:11101505, PubMed:19687231). Induces a voltage-dependent by rapidly activating and slowly deactivating potassium-selective outward current (By similarity) (PubMed:9312006, PubMed:9108097, PubMed:8900283, PubMed:10646604, PubMed:11101505). Promotes also a delayed voltage activated potassium current showing outward rectification characteristic (By similarity). During beta-adrenergic receptor stimulation participates in cardiac repolarization by associating with KCNE1 to form the I(Ks) cardiac potassium current that increases the amplitude and slows down the activation kinetics of outward potassium current I(Ks) (By similarity) (PubMed:9312006, PubMed:9108097, PubMed:8900283, PubMed:10646604, PubMed:11101505). Muscarinic agonist oxotremorine-M strongly suppresses KCNQ1/KCNE1 current (PubMed:10713961). When associated with KCNE3, forms the potassium channel that is important for cyclic AMP-stimulated intestinal secretion of chloride ions (PubMed:10646604). This interaction with KCNE3 is reduced by 17beta-estradiol, resulting in the reduction of currents (By similarity). During conditions of increased substrate load, maintains the driving force for proximal tubular and intestinal sodium ions absorption, gastric acid secretion, and cAMP-induced jejunal chloride ions secretion (By similarity). Allows the provision of potassium ions to the luminal membrane of the secretory canaliculus in the resting state as well as during stimulated acid secretion (By similarity). When associated with KCNE2, forms an heterooligomer complex leading to currents with an apparently instantaneous activation, a rapid deactivation process and a linear current-voltage relationship and decreases the amplitude of the outward current (PubMed:11101505). When associated with KCNE4, inhibits voltage-gated potassium channel activity (PubMed:19687231). When associated with KCNE5, this complex only conducts current upon strong and continued depolarization (PubMed:12324418). Also forms an heterotetramer with KCNQ5; has a voltage-gated potassium channel activity (PubMed:24855057). Binds with phosphatidylinositol 4,5-bisphosphate (PubMed:25037568).Isoform 2: Non-functional alone but modulatory when coexpressed with the full-length isoform 1.
Gene Name:
KCNQ1
Uniprot ID:
P51787
Molecular Weight:
74697.925 Da
References
  1. Gibor G, Yakubovich D, Peretz A, Attali B: External barium affects the gating of KCNQ1 potassium channels and produces a pore block via two discrete sites. J Gen Physiol. 2004 Jul;124(1):83-102. [15226366 ]
General Function:
Voltage-gated potassium channel activity
Specific Function:
Probably important in the regulation of neuronal excitability. Associates with KCNQ3 to form a potassium channel with essentially identical properties to the channel underlying the native M-current, a slowly activating and deactivating potassium conductance which plays a critical role in determining the subthreshold electrical excitability of neurons as well as the responsiveness to synaptic inputs. KCNQ2/KCNQ3 current is blocked by linopirdine and XE991, and activated by the anticonvulsant retigabine. Muscarinic agonist oxotremorine-M strongly suppress KCNQ2/KCNQ3 current in cells in which cloned KCNQ2/KCNQ3 channels were coexpressed with M1 muscarinic receptors.
Gene Name:
KCNQ2
Uniprot ID:
O43526
Molecular Weight:
95846.575 Da
References
  1. Gibor G, Yakubovich D, Peretz A, Attali B: External barium affects the gating of KCNQ1 potassium channels and produces a pore block via two discrete sites. J Gen Physiol. 2004 Jul;124(1):83-102. [15226366 ]
General Function:
Voltage-gated potassium channel activity
Specific Function:
Probably important in the regulation of neuronal excitability. Associates with KCNQ2 or KCNQ5 to form a potassium channel with essentially identical properties to the channel underlying the native M-current, a slowly activating and deactivating potassium conductance which plays a critical role in determining the subthreshold electrical excitability of neurons as well as the responsiveness to synaptic inputs.
Gene Name:
KCNQ3
Uniprot ID:
O43525
Molecular Weight:
96741.515 Da
References
  1. Gibor G, Yakubovich D, Peretz A, Attali B: External barium affects the gating of KCNQ1 potassium channels and produces a pore block via two discrete sites. J Gen Physiol. 2004 Jul;124(1):83-102. [15226366 ]
General Function:
Potassium channel activity
Specific Function:
Probably important in the regulation of neuronal excitability. May underlie a potassium current involved in regulating the excitability of sensory cells of the cochlea. KCNQ4 channels are blocked by linopirdin, XE991 and bepridil, whereas clofilium is without significant effect. Muscarinic agonist oxotremorine-M strongly suppress KCNQ4 current in CHO cells in which cloned KCNQ4 channels were coexpressed with M1 muscarinic receptors.
Gene Name:
KCNQ4
Uniprot ID:
P56696
Molecular Weight:
77099.99 Da
References
  1. Gibor G, Yakubovich D, Peretz A, Attali B: External barium affects the gating of KCNQ1 potassium channels and produces a pore block via two discrete sites. J Gen Physiol. 2004 Jul;124(1):83-102. [15226366 ]
General Function:
Voltage-gated potassium channel activity
Specific Function:
Probably important in the regulation of neuronal excitability. Associates with KCNQ3 to form a potassium channel which contributes to M-type current, a slowly activating and deactivating potassium conductance which plays a critical role in determining the subthreshold electrical excitability of neurons. May contribute, with other potassium channels, to the molecular diversity of a heterogeneous population of M-channels, varying in kinetic and pharmacological properties, which underlie this physiologically important current. Insensitive to tetraethylammonium, but inhibited by barium, linopirdine and XE991. Activated by niflumic acid and the anticonvulsant retigabine. Muscarine suppresses KCNQ5 current in Xenopus oocytes in which cloned KCNQ5 channels were coexpressed with M(1) muscarinic receptors.
Gene Name:
KCNQ5
Uniprot ID:
Q9NR82
Molecular Weight:
102178.015 Da
References
  1. Gibor G, Yakubovich D, Peretz A, Attali B: External barium affects the gating of KCNQ1 potassium channels and produces a pore block via two discrete sites. J Gen Physiol. 2004 Jul;124(1):83-102. [15226366 ]