Overview

laforin


'laforin' can also refer to...

laforin

Laforin, the most common protein mutated in Lafora disease, regulates autophagy

The phosphatase activity of laforin is dispensable to rescue Epm2a−/− mice from Lafora disease

Laforin and malin knockout mice have normal glucose disposal and insulin sensitivity

Lafora disease proteins malin and laforin are recruited to aggresomes in response to proteasomal impairment

Laforin, defective in the progressive myoclonus epilepsy of Lafora type, is a dual-specificity phosphatase associated with polyribosomes

Modulation of functional properties of laforin phosphatase by alternative splicing reveals a novel mechanism for the EPM2A gene in Lafora progressive myoclonus epilepsy

Regulation of glycogen synthesis by the laforin–malin complex is modulated by the AMP-activated protein kinase pathway

Laforin preferentially binds the neurotoxic starch-like polyglucosans, which form in its absence in progressive myoclonus epilepsy

The malin–laforin complex suppresses the cellular toxicity of misfolded proteins by promoting their degradation through the ubiquitin–proteasome system

The Lafora disease gene product laforin interacts with HIRIP5, a phylogenetically conserved protein containing a NifU-like domain

Laforin, the dual-phosphatase responsible for Lafora disease, interacts with R5 (PTG), a regulatory subunit of protein phosphatase-1 that enhances glycogen accumulation

Laforin, a dual specificity phosphatase involved in Lafora disease, regulates insulin response and whole-body energy balance in mice

 

More Like This

Show all results sharing this subject:

  • Chemistry

GO

Show Summary Details

Quick Reference

A protein‐tyrosine phosphatase present in many tissues. Mutations lead to Lafora disease, a progressive myoclonus epilepsy with intellectual decline, accumulation of glycogen in brain, skin, and liver, and early death.

[...]

Subjects: Chemistry.


Reference entries

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.