High Affinity Choline Transporter (ChT) ELISA Kits

Human High Affinity Choline Transporter (ChT) Interaktionspartner

1. Here we describe an autosomal recessive presynaptic congenital myasthenic syndrome presenting with a broad clinical phenotype due to homozygous SLC5a7 missense mutations. Phenotype ranges from classical presentation of a congenital myasthenic syndrome in one patient (p.Pro210Leu), to severe neurodevelopmental delay with brain atrophy (p.Ser94Arg) and extend the clinical outcomes to infantile lethality (p.Val112Glu).

2. Impaired Presynaptic High-Affinity Choline Transporter Causes a Congenital Myasthenic Syndrome with Episodic Apnea: this study broadens the clinical spectrum of human diseases resulting from reduced CHT activity and highlights the complexity of cholinergic metabolism at the synapse

3. These data show that acute exposure of depolarized cells to insulin (zeige INS ELISA Kits) is coupled to transiently increased levels of CHT proteins at the cell surface, and that this is attenuated by chronic insulin (zeige INS ELISA Kits) exposure.

4. This study demonstrated a specific impairment in cognitive control associated with the Ile89Val polymorphism of SLC5A7.

5. This mini-review discusses structural requirements for both organic cationic transporters OCT1 (zeige POU2F1 ELISA Kits) and OCT2 versus the blood-brain barrier choline transporter (BBBCHT) are discussed and compared.

6. [review] The critical role of CHT in maintaining cholinergic transmission indicates that it could be a target for therapeutic intervention to promote acetylcholine synthesis, the accomplishment of which has not been adequately addressed.

7. CHT1 forms a homo-oligomer on the cell surface in cultured cells.

8. Our findings compel consideration of mutations in SLC5A7 or its functional partners in relation to unexplained motor neuronopathies.

9. Polymorphic variation in the CHT1 gene can predict early, subclinical measures of carotid atherosclerosis.

10. Nedd4-2 mediated ubiquitination regulates the cell surface expression of CHT1 in HEK293 cells.

Mouse (Murine) High Affinity Choline Transporter (ChT) Interaktionspartner

1. Our findings suggest that CHT protein levels preferentially impact the capacity for ACh (zeige FGFR3 ELISA Kits) release afforded by mobilization of reserve pool vesicles

2. These data provide evidence for an epithelium-independent non-vesicular, non-quantal ACh (zeige FGFR3 ELISA Kits) release in the mouse trachea involving low-affinity choline transporters.

3. bacterial artificial chromosome CHT mice thus represent a novel tool to examine both the positive and negative impact of constitutively elevated cholinergic signaling capacity

4. These findings reveal compensatory mechanisms that, in the context of moderate cognitive challenges, can overcome the performance deficits expected from the significantly reduced ACh (zeige FGFR3 ELISA Kits) capacity of CHT+/- cholinergic terminals.

5. CHT association with cholesterol-rich rafts is critical for its function

6. This study showed that a constitutive loss of CHT expression in hemizygous mice leads to a significant reduction in basal extracellular dopamine levels in the nucleus accumbens.

7. This study demonistrated that CHT support for neuromuscular signaling involves contributions to ACh (zeige FGFR3 ELISA Kits) synthesis as well as cholinergic synaptic vesicle availability.

8. CHT1 knockout mice have tachycardia and hypertension at rest.

9. CHT1 binds to Par-4 (zeige F2RL3 ELISA Kits) and inhibits choline uptake when its incorporation is reduced on the cell surface

10. CHT is an essential and regulated presynaptic component of cholinergic signaling