Pikachurin: Difference between revisions

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==PIKACHURIN GENE==
==PIKACHURIN GENE==


This is a default text for your page '''Pikachurin'''. Click above on '''edit this page''' to modify. Be careful with the < and > signs.
 
You may include any references to papers as in: Hu H, Li J, Zhang Z, Yu M (February 2011). "Pikachurin interaction with dystroglycan is diminished by defective O-mannosyl glycosylation in congenital muscular dystrophy models and rescued by LARGE overexpression". Neurosci. Lett. 489 (1): 10–5.
http://www.uniprot.org/uniprot/Q63HQ2.


== Function ==Has a Dual function of photoreceptor visual synapse formation and visual perception
== Function ==Has a Dual function of photoreceptor visual synapse formation and visual perception
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</StructureSection>
</StructureSection>
== References ==
== References ==
1)Hu H, Li J, Zhang Z, Yu M (February 2011). "Pikachurin interaction with dystroglycan is diminished by defective O-mannosyl glycosylation in congenital muscular dystrophy models and rescued by LARGE overexpression". Neurosci. Lett. 489 (1): 10–5.
2)http://www.uniprot.org/uniprot/Q63HQ2
<references/>
<references/>

Revision as of 21:48, 7 October 2016

PIKACHURIN GENE

== Function ==Has a Dual function of photoreceptor visual synapse formation and visual perception

== Disease ==Visual Impairments were seen in mice with deleted pikachurin gene. Congenital muscular dystrophies (CMD) such as muscle-eye-brain disease caused by defective glycosylation of α-dystroglycan (α-DG) exhibit defective photoreceptor synaptic function.

Relevance

Structural highlights

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</StructureSection>

References

1)Hu H, Li J, Zhang Z, Yu M (February 2011). "Pikachurin interaction with dystroglycan is diminished by defective O-mannosyl glycosylation in congenital muscular dystrophy models and rescued by LARGE overexpression". Neurosci. Lett. 489 (1): 10–5.

2)https://www.uniprot.org/uniprot/Q63HQ2

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