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Kir4.1 antibody - 472 011

Kir4.1 a K+- channel subtype
Mouse monoclonal purified IgG
Cat. No.: 472 011
Amount: 100 µg
Price: $415.00
Cat. No. 472 011 100 µg purified IgG, lyophilized. Albumin and azide were added for stabilization. For reconstitution add 100 µl H2O to get a 1mg/ml solution in PBS. Then aliquot and store at -20°C to -80°C until use.
Antibodies should be stored at +4°C when still lyophilized. Do not freeze!
Applications
 
WB: 1 : 1000 up to 1 : 2000 (AP-staining) gallery  
IP: yes
ICC: 1 : 500 up to 1 : 1000 gallery  
IHC: 1 : 500 up to 1 : 1000 (see remarks) gallery  
IHC-P: 1 : 1000 up to 1 : 2000 gallery  
Clone Sy-84E10D9
Subtype IgG2a (κ light chain)
Immunogen Recombinant protein corresponding to residues near the carboxy terminus of human Kir4.1. (UniProt Id: P78508)
Reactivity Reacts with: mouse (Q9JM63), rat (P49655), human (P78508).
Other species not tested yet.
Remarks

IHC: Heat-mediated antigen retrieval (citrate buffer pH 6) is recommended.

Data sheet 472_011.pdf
Cat. No.: 472 011
Amount: 100 µg
Price: $415.00
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 in 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].