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>   首页   >   产品   >   一抗   >   心血管   >   Rabbit Anti-GIRK1 Polyclonal Antibody   

Rabbit Anti-GIRK1 Polyclonal Antibody

Purified Rabbit Polyclonal Antibody (Pab)

     
  • 1 - Rabbit Anti-GIRK1 Polyclonal Antibody AP52214
    Mouse kidney lysate probed with Rabbit Anti-GIRK1 Polyclonal Antibody (AP52214) at 1:300 overnight in 4˚C. Followed by conjugation to the secondary antibody at 1:5000 90min in 37˚C
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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, E
Primary Accession P48549
Reactivity Human, Mouse, Rat, Dog
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 KGA; GIRK1; KIR3.1; 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
Dilution WB=1:500-2000,ELISA=1:5000-10000
Format0.01M TBS(pH7.4) with 1% BSA, 0.09% (W/V) sodium azide and 50% Glyce
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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