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Cited by 96Muscle metabolism and nutritionMuscle Physiology and DisordersPI3K/AKT/mTOR signaling in cancer

Ecdysteroids Elicit a Rapid Ca2+ Flux Leading to Akt Activation and Increased Protein Synthesis in Skeletal Muscle Cells

Open access
Gorelick-Feldman, Jonathan, Cohick, Wendie, Raskin, Ilya·2010·Steroids
DOI 10.1016/j.steroids.2010.03.008PMC PMC3815456
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Abstract

Phytoecdysteroids, structurally similar to insect molting hormones, produce a range of effects in mammals, including increasing growth and physical performance. In skeletal muscle cells, phytoecdysteroids increase protein synthesis. In this study we show that in a mouse skeletal muscle cell line, C(2)C(12), 20-hydroxyecdysone (20HE), a common phytoecdysteroid in both insects and plants, elicited a rapid elevation in intracellular calcium, followed by sustained Akt activation and increased protein synthesis. The effect was inhibited by a G-protein coupled receptor (GPCR) inhibitor, a phospholipase C (PLC) inhibitor, and a phosphoinositide kinase-3 (PI3K) inhibitor.

Integrity signals

Registry

Crossref · 10.1016/j.steroids.2010.03.008

Cites

29 of 29 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 18 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    PTX pretreatment (1 μg/ml, 1 h) eliminates the 20HE-stimulated rise in protein synthesis in C2C12 myotubes.

    “Pretreatment with 1 μg/ml PTX, a G protein inhibitor, for 1 h completely abolished the 20HE-induced increase in protein synthesis in C2C12 myotubes (Fig. 7).”
    Quote in the paperSubstantial claim
    • Rests on an assumption: PTX specifically inhibits G-protein signaling in C2C12 myotubes without off-target effects.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.
  • Findingown data

    Treatment with extracellular chelator EGTA (3 mM) or intracellular chelator BAPTA-AM (25 μM) 1 h prior reduces 20HE-induced Akt phosphorylation.

    “Treatment with either the extracellular chelator, 3mM EGTA, or the intracellular chelator, 25μM BAPTA-AM, 1 h prior to treatment reduced 20HE-induced Akt phosphorylation (Fig. 5).”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.
  • Findingown data

    20HE activates Akt in C2C12 skeletal myotubes.

    “Exposure to 20HE activated Akt in C2C12 skeletal myotubes (Fig. 2).”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.
  • Findingown data

    0.1 μM 20HE significantly increases phosphorylation of Ser473 Akt by more than 3-fold in C2C12 myotubes.

    “0.1 μM 20HE significantly increased phosphorylation of Ser473 Akt by more than 3-fold.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.
  • Findingown data

    Pretreatment with 25 μM BAPTA-AM for 1 h similarly attenuates the 20HE-induced increase in protein synthesis.

    “The response to 20HE was similarly attenuated by pretreatment with 25μM BAPTA-AM for 1 h.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.
  • May combine two claims. 18
  • Classified as probably not a substantial claim. 7

  • May combine two claims.

    Findingown data

    Incubation in Ca2+-free medium with 3 mM EGTA slightly reduces and modifies the 20HE-induced intracellular Ca2+ response and decreases its duration in C2C12 myotubes.

    “Ca2+ free media containing the extracellular Ca2+ chelator, 3 mM EGTA, slightly reduced and modified the 20HE response and decreased its duration (Fig. 1C).”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    Akt activation increases with greater concentrations of 20HE, with maximal increases of approximately 5-fold at the highest concentration and a clear dose response at lower concentrations.

    “Activation of Akt continued to increase with greater concentrations of 20HE. Although maximal increases of approximately 5-fold were observed with the highest concentration of 20HE, and a clear dose response was observed at lower concentrations”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    IGF-1 still increases protein synthesis in cells pretreated with EGTA, but produces no increase in cells pretreated with BAPTA-AM.

    “While IGF-l still increased protein synthesis in cells pretreated with EGTA, IGF-1 produced no increase in cells pretreated with BAPTA-AM.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    In media containing 3 mM EGTA, the 20HE-induced increase in protein synthesis is only 8%, significantly lower than the 16% increase in Ca2+-containing media.

    “When cells were incubated in media containing 3 mM EGTA to chelate free Ca2+, the increase in protein synthesis was only 8%, significantly lower than the 16% when cells were exposed to 20HE in Ca2+ containing media.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    IGF-1-induced increase in protein synthesis is inhibited by both EGTA and BAPTA-AM.

    “The IGF-1 induced increase in protein synthesis was also inhibited by both EGTA and BAPTA-AM.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    Pretreatment with both EGTA and BAPTA-AM together eliminates the rise in protein synthesis caused by 20HE, producing a response not significantly different from either chelator alone or control and significantly lower than 20HE with either chelator alone.

    “When cells were pretreated for 1 h with both EGTA and BAPTAAM together, the 20HE-induced increase was completely abolished producing a response not significantly different from either EGTA and/or BAPTA-AM pretreatments or control while significantly lower then 20HE pretreated with either EGTA or BAPTA-AM.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    Intracellular Ca2+ in C2C12 myotubes peaks 35 seconds after 20HE treatment and begins to decline after 70 seconds.

    “Intracellular Ca2+ peaked 35 sec after treatment, and began to decline after 70 sec.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    Pretreatment with U-73122 significantly reduces IGF-1-induced increase in protein synthesis, while 2-APB causes only a slight decrease.

    “Pretreatment with U-73122 significantly reduced the IGF-1 induced increase in protein synthesis while 2-APB caused only a slight decrease.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: U-73122 specifically inhibits phospholipase C in C2C12 myotubes.
    • Rests on an assumption: 2-APB specifically inhibits IP3 receptors in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    In contrast, IGF-1 (100 ng/ml)-induced Akt activation is inhibited by LY but not by PTX.

    “In contrast, activation of Akt by 100 ng/ml IGF-1 was inhibited by LY but not PTX.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: PTX specifically inhibits G-protein signaling in C2C12 myotubes without off-target effects.
    • Rests on an assumption: LY-294002 specifically inhibits PI3K in C2C12 myotubes.
    • Rests on an assumption: Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    There is a significant difference in Akt activation between 0.5 μM and 1 μM 20HE, but no significant difference between 1 μM and higher concentrations.

    “with significant differences between 0.5 μM and 1 μM, there was no significant difference between 1 μM and higher concentrations.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    Treatment with 1 μM 20HE significantly increases Akt activation, which peaks after 2 h, decreases somewhat after 4 h, and remains greater than initial levels after 24 h.

    “Treatment with 1 μM 20HE significantly increased Akt activation which peaked after 2 h, decreased somewhat after 4 h, but remained greater than initial levels even after 24 h”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    20HE treatment produces significantly greater Akt phosphorylation than EGTA, BAPTA-AM, or control groups, while there is no significant difference between either EGTA or BAPTA-AM and control.

    “Although 20HE treatment was significantly greater than the EGTA, BAPTA-AM, or control groups, there was no significant difference between either EGTA or BAPTA-AM with the control.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    There are significant differences in Akt activation between 0 and 2 h, 2 and 4 h, and 0 and 24 h after 1 μM 20HE treatment.

    “with significant differences between 0 and 2 h, 2 and 4 h, and 0 and 24 h (Fig. 3A and 3B).”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    Pretreatment with U-73122 (10 μM) or 2-APB (10 μM) for 1 h reduces the protein synthesis response to 20HE, but the effect is not additive when both inhibitors are combined.

    “Pretreatment with either 10 μMU-73122, a PLC inhibitor, or 10 μM2-APB, an IP3R inhibitor, for 1 h reduced the protein synthesis response to 20HE, but the effect was not additive when both inhibitors were combined (Fig. 8).”
    Quote in the paperSubstantial claim
    • Rests on an assumption: U-73122 specifically inhibits phospholipase C in C2C12 myotubes.
    • Rests on an assumption: 2-APB specifically inhibits IP3 receptors in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • May combine two claims.

    Findingown data

    Pretreatment with both EGTA and BAPTA-AM together completely abolishes 20HE-induced Akt phosphorylation, although the response is not significantly different from either chelator alone.

    “Pretreatment with both EGTA and BAPTA-AM together completely abolished the 20HE-induced phosphorylation of Akt, although the response was not significantly different than either EGTA or BAPTA-AM alone.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.
    • Rests on an assumption: The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

  • Probably not a substantial claim: may not pass S1 (asserted), S3 (load-bearing), S4 (based).

    Interpretationown data

    The delayed Akt response may explain the delay in protein synthesis after 20HE treatment.

    “Therefore, the delayed Akt response may explain the delay in protein synthesis.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.

  • May combine two claims.

    Premisecitation

    In animals, ecdysteroids raise growth and endurance and are reported to lack adverse effects.

    “Ecdysteroids have been shown to increase growth and endurance in animals [1, 3] without negative side effects.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [1]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [3]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Ecdysteroids produce many non-genomic effects in invertebrates.

    “In addition to their classical nuclear receptor-mediated genomic response, ecdysteroids also produce many “non-genomic” effects in invertebrates [9, 10].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [9]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [10]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    High affinity membrane binding sites for 20HE have been described in rat erythrocytes using 20HE bound to magnetic nanoparticles.

    “High affinity membrane binding sites have already been described in rat erythrocytes using 20HE bound to magnetic nanoparticles [29].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [29]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    DopEcR, a membrane-bound GPCR in Drosophila, binds both ecdysteroids and dopamine.

    “A membrane-bound GPCR, DopEcR, has been identified in Drosophila which binds ecdysteroids in addition to dopamine [12].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [12]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The PLC-IP3R pathway is a major route for releasing internal Ca2+ in skeletal muscle.

    “An important pathway for release of internal Ca2+ in skeletal muscle is the PLC-IP3R pathway [24].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [24]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Interpretationown data

    The PLC pathway contributes to the 20HE-induced Ca2+ rise, but other sources of intracellular Ca2+ also exist.

    “This suggests that, although the PLC pathway may be involved, it is not the only source of intracellular Ca2+.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: U-73122 specifically inhibits phospholipase C in C2C12 myotubes.
    • Rests on an assumption: 2-APB specifically inhibits IP3 receptors in C2C12 myotubes.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Several mammalian steroid hormones raise Ca2+ entry in many cell types, among them cardiac myocytes and skeletal muscle.

    “Mammalian steroid hormones increased Ca2+ influx in a variety of cell types including cardiac myocytes [6] and skeletal muscle [7].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [6]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [7]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Estrogen and progesterone GPCRs have been cloned and characterized, and a putative membrane-bound AR has been described.

    “Estrogen and progesterone G-protein coupled receptors (GPCRs) have already been cloned and characterized and a putative membrane-bound AR has been described [8].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [8]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

24 of 24

  • The paper relies on this without support.

    PTX specifically inhibits G-protein signaling in C2C12 myotubes without off-target effects.

    “Pretreatment with 1 μg/ml PTX, a G protein inhibitor, for 1 h completely abolished the 20HE-induced increase in protein synthesis in C2C12 myotubes (Fig. 7).”
    “The G-protein inhibitor, PTX completely abolished the 20HE-induced increase in both Ca2+ (Fig. 1A) and protein synthesis (Fig. 8), and significantly reduced Akt activation (Fig. 5)”

  • The paper relies on this without support.

    U-73122 specifically inhibits phospholipase C in C2C12 myotubes.

    “Pretreatment with the phospholipase C (PLC) inhibitor, 10 μM U-73122, for 1 h prior to 1 μM 20HE treatment also reduced the intensity and duration of the intracellular Ca2+ flux as compared to the 20HE treatment alone (Fig. 1D).”

  • The paper relies on this without support.

    2-APB specifically inhibits IP3 receptors in C2C12 myotubes.

    “The inositol 3-phosphate receptor (IP3R) inhibitor, 2-APB, produced similar results (data not shown).”

  • The paper relies on this without support.

    LY-294002 specifically inhibits PI3K in C2C12 myotubes.

    “Pretreatment with either 10 μM LY, a PI3K inhibitor, or 1 μg/ml PTX, a G-protein inhibitor, for 1 h inhibited the 20HE-induced Akt activation in C2C12 myotubes (Fig. 4).”

  • The paper relies on this without support.

    Phosphorylation of Akt at Ser473 is a valid measure of Akt activation in C2C12 myotubes.

    “0.1 μM 20HE significantly increased phosphorylation of Ser473 Akt by more than 3-fold.”

  • The paper relies on this without support.

    The C2C12 myotube model is representative of skeletal muscle for the 20HE responses studied.

    “Using the murine skeletal muscle cell line C2C12, we have previously shown that treatment with ecdysteroids increases protein synthesis by up to 20% [4].”
6 of 6

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The effect of 20E on Ca2+ and Akt was prevented by inhibitors of GPCR, PLC, and PI3K, supporting involvement of a pathway inducing Ca2+ efflux from the sarcoplasmic reticulum.

    “This effect was prevented by inhibitors of G-protein-coupled receptor (GPCR), phospholipase C (PLC), and PI3K, supporting the involvement of the pathway inducing Ca2+ efflux from the sarcoplasmic reticulum.”

    From Molecular Targets of 20-Hydroxyecdysone in Mammals, Mechanism of Action: Is It a Calorie Restriction Mimetic and Anti-Aging Compound? (2025) · cites this paper as [9]

    The Intracellular Ca2+ results report that a G-protein inhibitor abolished the 20HE-induced Ca2+ increase, while a PLC inhibitor reduced its intensity and duration rather than preventing it. The Akt Activation results report inhibition by G-protein and PI3K inhibitors, but do not show that PI3K inhibition prevented the Ca2+ response. The Discussion describes release from the sarcoplasmic reticulum through the PLC-IP3 receptor pathway as a possible contributor, not an established sole mechanism. Page numbers were not provided in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • 20E-induced hypertrophy and protein synthesis were prevented by a GPCR inhibitor in differentiating C2C12 myoblasts.

    “First, 20E-induced hypertrophy and protein synthesis were prevented by GPCR inhibitor in differentiating C2C12 myoblasts [9,10].”

    From Molecular Targets of 20-Hydroxyecdysone in Mammals, Mechanism of Action: Is It a Calorie Restriction Mimetic and Anti-Aging Compound? (2025) · cites this paper as [9]

    The Results (Protein Synthesis; page not provided) report that pretreatment with PTX completely abolished the 20HE-induced increase in protein synthesis. But the Cell Culture section says the experiments used differentiated C2C12 myotubes, not differentiating myoblasts; the paper identifies PTX as a G-protein inhibitor and does not report that it prevented hypertrophy. (LLM, conf=0.90)

    Experimental — accuracy not yet measured

  • Some evidence indicates that ecdysteroids and 20HE activate Akt.

    “Some evidence indicates that ecdysteroids and 20HE activate Akt [18].”

    From Acute and chronic effects of <i>Rhaponticum carthamoides</i> and <i>Rhodiola rosea</i> extracts supplementation coupled to resistance exercise on muscle protein synthesis and mechanical power in rats (2020) · cites this paper as [18]

  • 20E elicited a rapid elevation in cytoplasmic Ca2+ followed by sustained activation of Akt and increased protein synthesis in C2C12 cells.

    “The same laboratory [9] showed that 20E elicited a rapid elevation in the cytoplasmic Ca2+ followed by a sustained activation of Akt and increased protein synthesis in C2C12 cells.”

    From Molecular Targets of 20-Hydroxyecdysone in Mammals, Mechanism of Action: Is It a Calorie Restriction Mimetic and Anti-Aging Compound? (2025) · cites this paper as [9]

  • 20E action through a membrane GPCR receptor is supported by pharmacological evidence.

    “Gorelick-Feldman et al. [194] provided pharmacological evidence for 20E action through a membrane GPCR receptor.”

    From Ecdysteroids (2021) · cites this paper as [194]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Calcium-chelator pretreatment times differ

    Major

    The signaling methods specify 30 minutes of EGTA or BAPTA-AM pretreatment, whereas the Akt results say the cells were pretreated for one hour.

  • EGTA concentration differs for the calcium-flux assay

    Major

    The assay methods specify 1.0 mM EGTA in calcium-free medium, but the calcium-flux results describe that medium as containing 3 mM EGTA.

  • Discussion points to the wrong PTX results figures

    Minor

    The discussion cites Fig. 8 for the PTX protein-synthesis result, but the results assign that experiment to Fig. 7. It also cites Fig. 5 for PTX effects on Akt, which the results assign to Fig. 4.

  • Discussion misidentifies the PTX calcium-flux panel

    Minor

    The discussion cites Fig. 1A for the PTX inhibition result, while the results identify Fig. 1B as the PTX panel.

4 of 4

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Authors
Gorelick-Feldman, J., Cohick, W., & Raskin, I.
Affiliations
Rutgers, The State University of New Jersey (US)
Corresponding author
Raskin, Ilya
ORCID
Venue
Steroids
Publisher
Elsevier BV
Published
2010-10
Volume
75
Issue
10
Pages
632-637
ISSN
0039-128X (ISSN-L)
DOI
10.1016/j.steroids.2010.03.008
PMC
PMC3815456
OpenAlex
W1978212980
Cited by
96
References
29
Citations by year
2026: 9 · 2025: 6 · 2024: 6 · 2023: 6 · 2022: 2 · 2021: 14 · 2020: 15 · 2019: 5 · 2018: 6 · 2017: 4 · 2016: 4 · 2015: 4 · 2014: 7 · 2013: 2 · 2012: 4
FWCI
1.12
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Steroids (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Fogarty International Center (U01TW006674)
  • National Center for Complementary and Integrative Health (P50AT002776)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords
phytoecdysteroids, 20-hydroxyecdysone, ecdysteroids, intracellular calcium flux, Akt activation, protein synthesis, skeletal muscle cells, C2C12 myoblasts, G protein-coupled receptors, phospholipase C, PI3K signaling, muscle growth
MeSH terms
Phosphoinositide-3 Kinase Inhibitors, Animals, Biological Transport, Boron Compounds, Calcium, Cell Line, Chelating Agents, Ecdysterone, Egtazic Acid, Estrenes, Type C Phospholipases, Phosphorylation, Pyrrolidinones, Blotting, Western, Muscle, Skeletal, Phosphatidylinositol 3-Kinases, Ecdysteroids, Proto-Oncogene Proteins c-akt, Mice

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