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Kir4.1 antibody - 472 005

Kir4.1 a K+- channel subtype
Guinea pig polyclonal purified antibody
Cat. No.: 472 005
Amount: 50 µg
Price: $450.00
Cat. No. 472 005 50 µg specific antibody, lyophilized. Affinity purified with the immunogen. Albumin and azide were added for stabilization. For reconstitution add 50 µl H2O to get a 1mg/ml solution in PBS. Then aliquot and store at -20°C to -80°C until use.
Applications
 
WB: 1 : 1000 up to 1 : 2000 (AP-staining) (see remarks) gallery  
IP: not tested yet
ICC: 1 : 500 up to 1 : 1000 gallery  
IHC: 1 : 500 up to 1 : 1000 gallery  
IHC-P: not tested yet
IHC-Fr: 1 : 500 up to 1 : 1000 gallery  
Immunogen Recombinant protein corresponding to residues near the carboxy terminus of human Kir4.1. (UniProt Id: P78508)
Reactivity Reacts with: mouse (Q9JM63), rat (P49655).
Other species not tested yet.
Specificity Specific for Kir4.1
Remarks

WB: Kir4.1 aggregates after boiling, making it necessary to run SDS-PAGE with non-boiled samples.

Data sheet 472_005.pdf
Cat. No.: 472 005
Amount: 50 µg
Price: $450.00
Background

Astrocyte membranes are highly permeable to K+ ions, leading to a hyperpolarized resting membrane potential and low input membrane resistance. The main player in mediating these properties is the Kir4.1 inward rectifying K+ channel [1, 2]. Without Kir4.1, astrocytes lack their signature K+ currents, which are sensitive to K+ blockers such as Ba2+ [3, 4]. The Kir4.1 channels are expressed throughout the brain, but are found in the highest concentrations in the olfactory bulb, cerebellum, brain stem, spinal cord and midbrain. While Kir4.1 is not expressed on neurons, it is expressed in a variety of CNS glia, including oligodendrocytes, and astrocytes. Protoplasmic astrocytes within the grey matter have higher Kir4.1 expression than fibrous astrocytes within the white matter [2, 5]. The expression of Kir4.1 increases with age, particularly within the first 10 days postnatally. This increase is associated with both an increase of the inward current in developing astrocytes and a shift away from oligodedroglial expression of Kir4.1 [6, 3].