anti-Solute Carrier Family 12 (Potassium-Chloride Transporter) Member 6 (SLC12A6) Antikörper

Human Solute Carrier Family 12 (Potassium-Chloride Transporter) Member 6 (SLC12A6) Interaktionspartner

1. Neurodegenerative deficits in hereditary motor and sensory neuropathy associated with agenesis of the corpus callosum are primarily caused by an axonopathy superimposed upon abnormal development, affecting peripheral but also central nervous system axons, all ultimately because of a genetic defect in the axonal cotransporter KCC3.

2. These results suggest that the function of the peripheral nervous system depends on finely tuned, kinase-regulated KCC3 activity and implicate abnormal cell volume homeostasis as a previously unreported mechanism of axonal degeneration.

3. These results suggest that the expression of KCC3 in ESCC may affect cellular invasion and be related to a worse prognosis in patients with ESCC.

4. SPAK (zeige STK39 Antikörper) may promote KCC3-mediated cervix tumor aggressiveness via the NF-kappaB (zeige NFKB1 Antikörper)/p38 MAPK (zeige MAPK14 Antikörper)/MMP2 (zeige MMP2 Antikörper) axis.

5. SLC12A6 has been shown to be causative in Andermann Syndrome.

6. serine residue 96 of human KCC3 is a third site that has to be dephosphorylated for full activation of the cotransporter during hypotonicity.

7. mis (zeige AMH Antikörper)-trafficking of mutant protein is an important pathophysiological feature of HMSN/ACC (zeige ACACA Antikörper) causative KCC3 mutations.

8. Neuropathic features of hereditary motor and sensory neuropathy/agenesis of corpus callosum in transgenic mouse lines are predominantly due to a neuronal KCC3 deficit, while the auditory impairment is due to loss of non-neuronal KCC3 expression.

9. The Wnk3 (zeige WNK3 Antikörper) protein isoforms have a similar effect on SLC12 cotransporters. NKCC1 (zeige SLC12A2 Antikörper)/2 and NCC (zeige SLC12A3 Antikörper) were inhibited, even in hypertonicity, while KCCs were activated, even in isotonic conditions.

10. KCC3 is the dominant isoform in erythrocytes, with variable expression of KCC1 (zeige SLC12A4 Antikörper) and KCC4 (zeige SLC12A7 Antikörper) that could result in modulation of KCC activity

Mouse (Murine) Solute Carrier Family 12 (Potassium-Chloride Transporter) Member 6 (SLC12A6) Interaktionspartner

1. electrophysiological studies using the threshold tracking technique indicated a reduced stimulus-response curve slope with an elevated rheobase, a decreased strength-duration time constant, diminished persistent Na(+) currents, and an outward deviation of threshold electrotonus in KCC3(-/-) nerves compared to wild-type nerves

2. These results suggest that the function of the peripheral nervous system depends on finely tuned, kinase-regulated KCC3 activity and implicate abnormal cell volume homeostasis as a previously unreported mechanism of axonal degeneration.

3. Kcc3 inactivation caused systemic vascular resistance and ventricular mass to increase while preventing extracellular fluid volume to accumulate.

4. The results establish that the parvalbumin (zeige PVALB Antikörper)-positive neuronal population is an important player in the pathogenic development of peripheral neuropathy associated with agenesis of the corpus callosum.

5. Data are consistent with a role for KCC3 in the proximal tubule glucose reabsorption mechanism.

6. KCC3 regulates NADPH oxidase (zeige NOX1 Antikörper) activity and neutrophils activation

7. KCC3 contributes to Cl(-) extrusion in adult sensory neurons

8. K+-Cl-cotransporter (zeige SLC12A4 Antikörper) KCC3 is expressed in neurons, interneurons and radial glial-like cells in the spinal cord.

9. KCC3 is the dominant isoform in erythrocytes, with variable expression of KCC1 (zeige SLC12A4 Antikörper) and KCC4 (zeige SLC12A7 Antikörper) that could result in modulation of KCC activity

10. This study demonstrated that the K(+)-Cl(-) cotransporter (zeige SLC12A4 Antikörper) activity of KCC3 contributes to the propagation of action potentials along peripheral nerves.