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IGF1 — MYOG
Text-mined interactions from Literome
Yang et al., J Cell Physiol 1999
:
The simultaneous decrease in IGFBP-3 mRNA and protein that accompanies
IGF-I induced
myogenin expression suggests that differentiation of myogenic cells may be preceded or accompanied by decreased production of IGFBP-3
Adi et al., J Cell Biochem 2000
:
Opposing early inhibitory and late stimulatory
effects of
insulin-like growth factor-I on
myogenin gene transcription ... The mechanisms by which
IGF-I initially inhibits and subsequently
stimulates myogenin expression are unknown ... In the first 24 h, we find that
IGF-I inhibits
myogenin gene transcription by > 80 % but has no effect on myogenin mRNA stability ... Similarly, in the first 24 h,
IGF-I markedly
inhibits myogenin promoter activity ; the sequence -145 to -9 of the myogenin gene is sufficient to confer this inhibitory effect of IGF-I ... In contrast, 48 h of treatment with
IGF-I results in an increase in
myogenin promoter activity that parallels the increase in myogenin steady-state mRNA ... These data indicate that the early inhibitory and late stimulatory effects of IGF-I on
myogenin expression are mediated at the level of transcription, and that these time dependent, opposing effects of
IGF-I on myogenin transcription are
mediated by distinct regions of the myogenin gene
Tureckova et al., J Biol Chem 2001
:
Induction of
myogenin by
IGF-I and myotube formation were prevented by the phosphatidylinositol (PI) 3-kinase inhibitor, LY294002, even when included 2 days after growth factor addition, whereas expression of active PI 3-kinase could promote differentiation in the absence of IGF-I
Adi et al., Endocrinology 2002
:
We have examined the role of extracellular signal regulated kinase ( Erk ) 1/2 signaling in mediating the early inhibitory and late stimulatory
effects of
IGF-I on the gene expression of
myogenin , a skeletal muscle-specific transcription factor essential for myogenic differentiation
Broussard et al., Endocrinology 2003
:
The inhibition by TNFalpha of
IGF-I induced protein synthesis and expression of
myogenin is not due to direct killing of myoblasts by TNFalpha
Broussard et al., J Immunol 2004
:
However, in the
presence of
IGF-I , 100-fold lower concentrations of IL-1beta ( 0.01 ng/ml ) significantly suppressed myoblast differentiation, protein synthesis, and
myogenin expression
Strle et al., Endocrinology 2004
:
Consistent with these data, neutral sphingomyelinase (N-SMase), an enzyme that catalyzes formation of ceramide from sphingomyelin, blocks
IGF-I induced protein synthesis and expression of both
myogenin and MyoD
Tiffin et al., Endocrinology 2004
(MAP Kinase Signaling System) :
Akt phosphorylation is not sufficient for
insulin-like growth factor stimulated
myogenin expression but must be accompanied by down-regulation of mitogen activated protein kinase/extracellular signal regulated kinase phosphorylation ... Initially,
IGF-I inhibits expression of
myogenin , a skeletal muscle-specific regulatory factor essential for myogenesis ... We find that even in the presence of phosphorylated Akt, it is only when ERK1/2 phosphorylation is inhibited that
IGF-I can
stimulate myogenin mRNA expression
Tsuchiya et al., Int J Oncol 2007
(Rhabdomyosarcoma, Alveolar...) :
In this study, we found that
IGF-I affected the induction of
myogenin and cell cycle progression in alveolar RMS cells, but not in embryonal RMS cells ...
IGF-I enhanced the induction of
myogenin protein in alveolar RMS SJ-Rh30 and KP-RMS-MS cells as it did in myoblast C2C12 cells, but not in embryonal RMS RD or KP-RMS-KH cells ...
IGF-I induction of
myogenin protein was blocked by anti-IGF-IR monoclonal antibody alphaIR-3 and the mTOR-specific inhibitor rapamycin ... In Rh30mTOR-rr cells, which stably express a rapamycin-resistant mutant mTOR, rapamycin did not inhibit
IGF-I induction of
myogenin protein ... These data suggest that
IGF-I induces
myogenin in alveolar RMS cells through the IGF-IR/mTOR pathway ... These findings suggest that the different
effects of
IGF-I on
myogenin induction and cell cycle progression in alveolar and embryonal RMS cells are due to a difference of phosphorylation status of 4E-BP1
Strle et al., J Neuroimmunol 2007
:
We found that IL-10 restores myogenesis by suppressing the ability of exogenous TNFalpha to inhibit
IGF-I induced
myogenin
Strle et al., Am J Physiol Endocrinol Metab 2008
(MAP Kinase Signaling System) :
Prototypical anti-inflammatory cytokine IL-10 prevents loss of
IGF-I induced
myogenin protein expression caused by IL-1beta ... Here we demonstrate that IL-10 plays a protective role in nonhematopoietic cells by suppressing the ability of exogenous IL-1beta to inhibit
IGF-I induced
myogenin and myosin heavy chain expression in myoblasts ... This conclusion is supported by the finding that a specific JNK inhibitor acts similarly to IL-10 to restore
IGF-I induced
myogenin expression, which is suppressed by IL-1beta
Huang et al., PloS one 2011
:
Mechanistically, we found that the expression of
myogenin , a myogenic transcription factor reported to transactivate miR-133, was
increased by
IGF-1 stimulation