Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models

Skeletal Muscle

Table 2 Transgenic models of the IGF1-Akt pathway: effect on growth

Genotype¹	Viability	Phenotype	References
ASA-hIGF1	Viable	Muscle hypertrophy	[45, 47]
MLC1-IGF1	Viable	Muscle hypertrophy	[51]
MCK-d.n. IGF1 receptor²	Viable	Transient delay of postnatal muscle growth; unaffected overload-induced muscle hypertrophy; impaired muscle regeneration	[59–62]
HSA-Akt1, inducible	Viable	Muscle hypertrophy	[79]
MCK-myrAkt1, inducible	Viable	Muscle hypertrophy	[80]
MLC1f-myrAkt1, inducible	Viable	Muscle hypertrophy	[82]
HSA-FoxO1	Viable	Muscle atrophy	[90]

¹Promoters used to drive transgene expression: ASA = avian skeletal actin; HSA = human skeletal actin; MCK = muscle creatine kinase; MLC1 = myosin light chain 1 fast.
²This transgene acts as a dominant negative for both the insulin-like growth factor 1 receptor and the insulin receptor, thus causing diabetes.

ISSN: 2044-5040