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Sodium Channels

Receptors are found on the surface of cells and have numerous functions. They act as binding sites or antigens to antibodies and other ligands and can communicate signals within a cell or between cells and even allow for transport of molecules into and out of the cell. Receptors are made of proteins and act as ligands to other proteins, molecules, drugs or toxins. Basically, the ligand will bind to the receptor and form a ligand-receptor complex. Certain ligands can activate a receptor. These are called agonists. Other ligands will deactivate or block the receptor from having a certain action. These are called antagonists. Antibodies can serve as binding materials and can also be agonists or antagonists. Receptor structure varies depending on the classification of the certain receptor. There are receptors that merely sit on the surface of cells and receptors that go across the external cellular membrane. These include G-protein coupled receptors and ligand- gated ion channels. Sodium channels are also highly specialized membrane proteins which allow sodium ions to enter the cell under circumstances. The sodium channels are made of several subunits labeled alpha, beta 1, and beta 2. These ion channels can be either voltage gated or ligand gated. The state of the sodium channel is either opened (activated) or closed (deactivated or inactivated). When the channel is open, the sodium ions can flow freely across the membrane. Voltage activated channels are activated by a change in the membrane potential and ligand activated channels are triggered by the binding of a ligand to the protein's receptor site. Sodium channel antibodies bind against sodium channels and affect or block their activity.

Anti-nav1.5 antibody binds against the target nav1.5 (sodium channel protein cardiac muscle alpha subunit). SCN5A is a protein that mediates the sodium ion permeability of voltage-dependent membranes. SCN5A forms the Na selective channel that is responsible for the initial upstroke of the action potential. Nav 1.5 is localized only in the cell membrane and expressed in smooth muscle cells, cardiac muscle, and the brain. Defects in SCN5A are the cause of progressive familial heart block type 1A, long QT syndrome type 3, Brugada syndrome type 1, sick sinus syndrome type 1, and sudden infant death syndrome. Progressive familial heart block type 1A is an autosomal dominant cardiac bundle branch disorder that can progress into a complete heart block causing sudden death. Long QT syndrome type 3 is another type of rare heart condition causing an irregular ventricular heartbeat (TDP) which can lead to fainting and sudden death. Brugada syndrome is a genetic disease characterized by ECG abnormalities that can lead to sudden death. Brugada syndrome causes the ventricles in the heart to beat so fast that the blood is actually prevented from circulating efficiently in the body. Sick sinus syndromes are a group of disorders characterized by heart arrhythmias caused by the malfunction of the sinus node. The sinus node is the pacemaker of the heart that is responsible for generating electrical impulses. Sudden infant death syndrome, or SIDS, is the leading cause of death for babies between 1 month and 1 year old. Most experts believe that SIDS occurs to babies that have an underlying immature or abnormal heart function. Anti-epithelial sodium channel alpha antibody binds against the target non-voltage gated sodium channel 1 subunit alpha. SCNN1A mediates the diffusion of luminal sodium and water. SCCNN1A is localized in the cell membrane and highly expressed in the kidney and lung. It is also expressed, in lower amounts, in the pancreas, liver, and heart. Defects in epithelial sodium channel alpha are the cause of autosomal recessive pseudohypoaldosteronism type 1 and bronchiectasis. Pseudohypoaldosteronism type 1 is a disorder of electrolyte metabolism characterized large amounts of sodium being eliminated through the urine, sweat, stool, and saliva. Treatment involves sodium replacement. Bronchiectasis is a disease characterized by damage to the airways. This damage causes the airways to become widened and scarred. This widening and scarring prevents the airways from being able to clear themselves of mucous which can contain inhaled dust, bacteria, and other particles.

 
Product Number Title Applications Host Clonality
AC21-2638 Anti-Serotonin Transporter Antibody ELISA, WB Goat Polyclonal
AC21-2922 Anti-STOM Antibody ELISA, WB Goat Polyclonal
AC21-0701-01 Anti-Serotonin Transporter Antibody (AMCA) ELISA, WB Goat Polyclonal
AC21-0701-02 Anti-Serotonin Transporter Antibody (AP) ELISA, WB Goat Polyclonal
AC21-0701-03 Anti-Serotonin Transporter Antibody (APC) ELISA, WB Goat Polyclonal
AC21-0701-04 Anti-Serotonin Transporter Antibody (APC-Cy5.5) ELISA, WB Goat Polyclonal
AC21-0701-05 Anti-Serotonin Transporter Antibody (APC-Cy7) ELISA, WB Goat Polyclonal
AC21-0701-06 Anti-Serotonin Transporter Antibody (Avidin) ELISA, WB Goat Polyclonal
AC21-0701-07 Anti-Serotonin Transporter Antibody (Biotin) ELISA, WB Goat Polyclonal
AC21-0701-08 Anti-Serotonin Transporter Antibody (BPE) ELISA, WB Goat Polyclonal
AC21-0701-09 Anti-Serotonin Transporter Antibody (Cy3) ELISA, WB Goat Polyclonal
AC21-0701-10 Anti-Serotonin Transporter Antibody (Cy5) ELISA, WB Goat Polyclonal