![]() Mitä teet Sampossa Tehtäväni on johtaa ohjaus- ja tukipalveluiden vastuuyksikköä, jossa tiimien kanssa tarjoamme opinto-ohjaukseen, erityiseen tukeen, oppisopimukseen sekä markkinointiin ja viestintään liittyviä palveluja. However, such alterations do not progress once they have stabilized in early adulthood, emphasizing the role of collagen XIII in NMJ maturation. Kuka olet Riitta Moilanen, monessa mukana kehittämässä. We conclude that intrinsic alterations at the NMJ in Col13a1 −/− mice contribute to impaired and incomplete NMJ regeneration and functional recovery after peripheral nerve injury. Thus, collagen XIII could serve as a therapeutic agent in cases of injury-induced PNS regeneration and functional recovery. Shedding of the ectodomain is not required, as the transmembrane form of collagen XIII alone fully rescues the phenotype. This is mainly attributable to presynaptic defects that already existed in the absence of collagen XIII before injury. ![]() We show that collagen XIII-deficient male mice are unable to achieve complete NMJ regeneration and functional recovery. Sciatic nerve crush was performed to examine how the lack of collagen XIII or forced expression of its transmembrane form affects the neuromuscular synapse regeneration and functional recovery following injury. We show here that muscle defects in collagen XIII-deficient mice stabilize in adulthood, so that the disease is not progressive until very late. Mutations in COL13A1 have recently been found to cause congenital myasthenic syndrome, characterized by fatigue and chronic muscle weakness, which may be lethal. ![]() Its absence results in myasthenia: presynaptic and postsynaptic defects at the neuromuscular junction (NMJ), leading to destabilization of the motor nerves, muscle regeneration and atrophy. Collagen XIII occurs as both a transmembrane-bound and a shed extracellular protein and is able to regulate the formation and function of neuromuscular synapses.
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