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>   首页   >   产品   >   一抗   >   心血管   >   GIRK1/KCNJ3 Rabbit pAb   

GIRK1/KCNJ3 Rabbit pAb

GIRK1/KCNJ3 Rabbit pAb

     
  • 1 - GIRK1/KCNJ3 Rabbit pAb AP52214
    Sample:
    Heart (Mouse) Lysate at 40 ug
    Heart (Rat) Lysate at 40 ug
    Primary: Anti- GIRK1'KCNJ3 (AP52214) at 1/1000 dilution
    Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
    Predicted band size: 55 kD
    Observed band size: 53 kD
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB
Primary Accession P48549
Reactivity Mouse, Rat
Predicted Human, Dog, Pig, Rabbit, Guinea Pig
Host Rabbit
Clonality Polyclonal
Calculated MW 56603 Da
Physical State Liquid
Immunogen KLH conjugated synthetic peptide derived from human GIRK1
Epitope Specificity 81-180/501
Purity affinity purified by Protein A
Buffer 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
SUBCELLULAR LOCATION Membrane; Multi-pass membrane protein.
SIMILARITY Belongs to the inward rectifier-type potassium channel (TC 1.A.2.1) family. KCNJ3 subfamily.
SUBUNIT Associates with GIRK2, GIRK3 or GIRK4 to form a G-protein activated heteromultimer pore-forming unit. The resulting inward current is much larger.
Important Note This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
Background Descriptions 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.
Additional Information
Gene ID 3760
Other Names G protein-activated inward rectifier potassium channel 1, GIRK-1, Inward rectifier K(+) channel Kir3.1, Potassium channel, inwardly rectifying subfamily J member 3, KCNJ3, GIRK1
Dilution WB=1:500-2000
StorageStore at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
Protein Information
Name KCNJ3
Synonyms GIRK1
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. This potassium channel is controlled by G proteins (PubMed:8804710, PubMed:8868049). This receptor plays a crucial role in regulating the heartbeat (By similarity).
Cellular Location Membrane; Multi-pass membrane protein
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

BACKGROUND

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.

REFERENCES

Chan K.W.,et al.J. Gen. Physiol. 107:381-397(1996).
Schoots O.,et al.Brain Res. Mol. Brain Res. 39:23-30(1996).
Wagner V.,et al.Submitted (OCT-2009) to the EMBL/GenBank/DDBJ databases.
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Hillier L.W.,et al.Nature 434:724-731(2005).

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