anti-Sodium Channel, Voltage-Gated, Type III, beta Subunit (SCN3B) Antikörper

Mouse (Murine) Sodium Channel, Voltage-Gated, Type III, beta Subunit (SCN3B) Interaktionspartner

1. beta1-beta3 is more likely to form a di-polymer than beta1-beta1 based on molecular interaction analysis, including potential energy analysis

2. This study demonistrated that scn3b gene expression in mouse dorsal raphe nucleus

3. These data suggest that the SOD1G93A mutation results in increased expression of the beta3 subunit of voltage-gated Na+ channels in the spinal cord..

4. deficiency in Scn3b results in significant atrial electrophysiological and intracardiac conduction abnormalities

5. SCN3B mediates a p53-dependent apoptotic pathway and may be a candidate for gene therapy combined with anticancer drugs.

6. Bipolar electrogram and monophasic action potential recordings from the ventricles of Langendorff-perfused Scn3b(-/-) hearts demonstrated ventricular tachycardias induced by programmed electrical stimulation.

Human Sodium Channel, Voltage-Gated, Type III, beta Subunit (SCN3B) Interaktionspartner

1. Contribution of Cardiac Sodium Channel beta-Subunit Variants to Brugada Syndrome.

2. In a nonreferred nationwide Danish cohort of SIDS cases, up to 5/66 (7.5%) of SIDS cases can be explained by genetic variants in the sodium channel complex genes.

3. SCN1-3B the gene that encode respectively a- and b-subunits of the cardiac fast voltage-gated sodium channel, have been linked to atrial fibrillation.

4. The Val110Ile mutation of SCN3B is a relatively common cause of SCN5A-negative BrS in Japan, which has a reduced sodium current because of the loss of cell surface expression of Nav1.5.

5. the beta3 subunit can mediate trans homophilic-binding via its Ig domain and the beta3-Ig domain can associate heterophilically with the beta1 subunit

6. three mutations in SCN3B were investigated electrophysiologically and all led to loss of function in the sodium current, supporting the hypothesis that decreased sodium current enhances atrial fibrillation susceptibility

7. The researchers found evidence of an association between SCN3B subunit mutations and sudden infant death syndrome pathogenesis.

8. The sodium channel {beta}3-subunit induces multiphasic gating in NaV1.3 and affects fast inactivation via distinct intracellular regions.

9. This study identifies the first atrial fibrillation(AF) -associated mutation in SCN3B, and suggests that mutations in SCN3B may be a new pathogenic cause of AF.

10. Study provides molecular and cellular evidence implicating mutations in SCN3B as a cause of idiopathic ventricular fibrillation.

11. SCN3B mediates a p53-dependent apoptotic pathway and may be a candidate for gene therapy combined with anticancer drugs.

12. In patients with temporal lobe epilepsy, Na(v)beta3 levels were dramatically reduced in the hippocampus, but not in the cortex of non-hippocampal sclerosis patients when compared to hippocampal sclerosis patients.

13. beta3 does not participate in trans homophilic cell-cell adhesion or associate with contactin.