KCNJ10 Antibodies

ATP-sensitive inward rectifier potassium channel 10 (KCNJ10)

May cause potassium buffering action of glial cells in the brain. 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.

Gene Information

Human
Gene Name:	KCNJ10
Uniprot:	P78508
Entrez:	3766

Family

Belongs to:
inward rectifier-type potassium channel (TC 1.A.2.1) family

Alternative Names

ATP-dependent inwardly rectifying potassium channel Kir4.1; ATP-sensitive inward rectifier potassium channel 10; BIRK-10; glial ATP-dependent inwardly rectifying potassium channel KIR4.1; Inward rectifier K(+) channel Kir1.2; inward rectifier K+ channel KIR1.2; KCNJ13-PEN; KIR1.2; KIR4.1; Potassium channel, inwardly rectifying subfamily J member 10; potassium inwardly-rectifying channel, subfamily J, member 10; SESAME

Molecular Weight

Mass (kDA):
42.508 kDA

Genomic Context

Human
Location:	1q23.2
Sequence:	1; NC_000001.11 (160037467..160070160, complement)

Tissue Specificity

Expressed in kidney (at protein level).

Subcellular Localizations

Membrane; Multi-pass membrane protein. Basolateral cell membrane. In kidney distal convoluted tubules, located in the basolateral membrane where it colocalizes with KCNJ16.

Diseases

• Complete Hearing Loss
• Sensorineural Hearing Loss (disorder)
• Epilepsy
• Ataxia
• Pendred's Syndrome
• Sesame Syndrome
• Alkalosis
• Deafness Congenital
• Electrolyte Imbalance
• Metabolic Alkalosis
• Epilepsy, Generalized

• Idiopathic Generalized Epilepsy
• Nodular Goiter
• Bartter Disease
• Goiter
• Epilepsy, Temporal Lobe
• Kidney Diseases

Interacting Proteins

• SIAH1

Pathways

• Transport
• Localization
• Secretion
• Ion Transport
• Ion Homeostasis
• Cell Death
• Pathogenesis
• Pigmentation
• Inner Ear Development
• Startle Response
• Reverse Transcription

• Water Transport
• Cellular Localization
• Ear Development
• Protein Folding
• Excretion
• Regulation Of Blood Pressure

PTMs

• Nitration

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/KCNJ10

Boster Bio - Best Uses Of The KCNJ10 Marker

This Boster Bio product overview will discuss the Boster Bio anti-Kir4.1 KCNJ10 marker and its advantages. We will also be discussing how it has rewarded its innovators. This is the place to go if your goal is to make your KCNJ10 antibody. Boster Bio Anti–Kir4.1 KCNJ10 antibody reacts against Human, Mouse, or Rat.

Boster Bio: Anti-Kir4.1 KCNJ10 Marker

The KCNJ10 gene is a candidate for use in the diagnosis of multiple sclerosis. It still needs to be validated in clinical practice. There are several limitations to the research. Its clinical utility is limited. It is also highly variable, making it difficult to determine its effectiveness in different patients. Therefore, it would be best to test this gene in people with multiple sclerosis.

Innovating Scientists Reward

There are many options for how to use the Boster Bio Anti-Kir4.1 KCNJ10 Labeler. These antibodies are high-affinity and have been widely cited for research. They have also been tested on Western Blotting, Immunohistochemistry, ELISA, and confocal microscopy. Boster Bio has an antibody to suit your research needs, no matter what your goals are.