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<span>Lafora disease is the most severe teenage-onset progressive epilepsy, a unique form of glycogenosis with perikaryal accumulation of an abnormal form of glycogen, and a neurodegenerative disorder exhibiting an unusual generalized organellar disintegration. The disease is caused by mutations of the EPM2A gene, which encodes two isoforms of the laforin protein tyrosine phosphatase, having alternate carboxyl termini, one localized in the cytoplasm (endoplasmic reticulum) and the other in the nucleus. To date, all documented disease mutations, including the knockout mouse model deletion, have been in the segment of the protein common to both isoforms. It is therefore not known whether dysfunction of the cytoplasmic, nuclear, or both isoforms leads to the disease. In the present work, we identify six novel mutations, one of which, c.950insT (Q319fs), is the first mutation specific to the cytoplasmic laforin isoform, implicating this isoform in disease pathogenesis. To confirm this mutation's deleterious effect on laforin, we studied the resultant protein's subcellular localization and function and show a drastic reduction in its phosphatase activity, despite maintenance of its location at the endoplasmic reticulum.
I got my information from </span>https://www.ncbi.nlm.nih.gov/pubmed/14722920
Answer:Amphibians evolved during the middle of the Devonian period (416 to 359 million years ago) from the lobe-finned fish of the vertebrate class Sarcopterygii. Species within the genus Ichthyostega (members of the Labyrinthodontia subclass) are considered by some scientists to be the earliest amphibians.
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When a nerve impulse reaches the end of an axon, the axon releases chemicals called neurotransmitters. Neurotransmitters travel across the synapse between the axon and the dendrite of the next neuron.
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The binding allows the nerve impulse to travel through the receiving neuron.
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