Anti-Potassium Channel Kir3.4 Antibody, clone 8F4.1

Evaluated by Western Blotting in human adrenal gland tissue lysate.

Western Blotting Analysis: 0.5 µg/mL of this antibody detected potassium channel Kir3.4 in 10 µg of human adrenal gland tissue lysate.

Detect K(+) channel Kir3.4 using this mouse monoclonal Anti-Potassium Channel Kir3.4, clone 8F4.1, Cat. No. MABS1721, validated for use in Immunohistochemistry (Paraffin) and Western Blotting.

Immunohistochemistry Analysis: A 1:50 dilution from a representative lot detected potassium channel Kir3.4 in human adrenal gland and kidney tissue sections.

Research Category
Signaling

Clone 8F4.1 detects human potassium channel Kir3.4 by targeting an epitope within the C-terminal cytoplasmic domain.

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

G protein-activated inward rectifier potassium channel 4 (UniProt P48544; also known as Cardiac inward rectifier, CIR, Heart KATP channel, Inward rectifier K(+) channel Kir3.4, GIRK-4, IRK-4, KATP-1, Potassium channel, inwardly rectifying subfamily J member 5) is encoded by the KCNJ5 (also known as GIRK4, LQT13) gene (Gene ID 3762) in human. Inward rectifier K+ channels (Kirs) modulate cell membrane potential and are classified as K+ transport channels (Kir1.x, Kir4.x, Kir5.x, Kir7.x), classic Kir (Kir2.x), G-protein-gated Kirs (Kir2.x and Kir3.x), and ATP-sensitive Kirs (Kir6.x). Kirs mediate diverse physiological functions of both excitable and nonexcitable epithelial cells, such as cell adhesion-migration, volume regulation, apoptosis, and proliferation. While a large fraction of Kir3.4 (GIRK4; KCNJ5) subunits is processed to the cell membrane to form homomultimers, Kir3.4 subunits also assemble into heteromeric channels with Kir3.1 (GIRK1; KCNJ3) subunits in atrial myocytes or Kir3.2 (GIRK2; KCNJ6) in the cerebellum. Upon agonist activation of appropriate GPCRs, heteroterameric Kir3.4 channels are opened via interaction with subunits of the pertussis toxin-sensitive class (Gi/o) G-proteins, resulting in membrane hyperpolarization and/or reduced excitability. Whereas homotetrameric Kir3.4 channels can be activated by high intracellular Na+ independent of G-protein. Human Kir3.4 is a 419-amino acid multi-pass membrane (a.a. 87-111, 136-147, 164-185) protein that contains two small extraceullar regions (a.a. 112-135 and 155-163) and a pore-forming domain (a.a. 148-154), having both its N- and C-terminal ends exposed intracellularly (a.a. 1-86 and a.a. 186-419).

~47 kDa observed. 47.67 kDa calculated. Uncharacterized bands may be observed in some lysate(s).

GST-tagged human potassium channel Kir3.4 C-terminal end fragment.

Concentration: Please refer to lot specific datasheet.

Format: Purified

Protein G purified

Purified mouse IgG1 in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Stable for 1 year at 2-8°C from date of receipt.