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Study · Ex vivo tissue · rat · 2002

18 results

Activation of the ERK pathway and atypical protein kinase C isoforms in exercise- and aminoimidazole-4-carboxamide-1-beta-D-riboside (AICAR)-stimulated glucose transport.

Chen HC, Bandyopadhyay G, Sajan MP, Kanoh Y, Standaert M, Farese RV Jr, Farese RV

The Journal of biological chemistry26 Apr 2002Cited by 153 (Europe PMC)

Summary

Exercise increases glucose transport in muscle by activating 5'-AMP-activated protein kinase (AMPK), but subsequent events are unclear. Presently, we examined the possibility that AMPK increases glucose transport through atypical protein kinase Cs (aPKCs) by activating proline-rich tyrosine kinase-2 (PYK2), ERK pathway components, and phospholipase D (PLD). In mice, treadmill exercise rapidly activated ERK and aPKCs in mouse vastus lateralis muscles. In rat extensor digitorum longus (EDL) muscles, (a) AMPK activator, 5-aminoimidazole-4-carboxamide-1-beta-d-riboside (AICAR), activated PYK2, ERK and aPKCs; (b) effects of AICAR on ERK and aPKCs were blocked by tyrosine kinase inhibitor, genistein, and MEK1 inhibitor, PD98059; and (c) effects of AICAR on aPKCs and 2-deoxyglucose (2-DOG) uptake were inhibited by genistein, PD98059, and PLD-inhibitor, 1-butanol. Similarly, in L6 myotubes, (a) AICAR activated PYK2, ERK, PLD, and aPKCs; (b) effects of AICAR on ERK were inhibited by genistein, PD98059, and expression of dominant-negative PYK2; (c) effects of AICAR on PLD were inhibited by MEK1 inhibitor UO126; (d) effects of AICAR on aPKCs were inhibited by genistein, PD98059, 1-butanol, and expression of dominant-negative forms of PYK2, GRB2, SOS, RAS, RAF, and ERK; and (e) effects of AICAR on 2DOG uptake/GLUT4 translocation were inhibited by genistein, PD98059, UO126, 1-butanol, cell-permeable myristoylated PKC-zeta pseudosubstrate, and expression of kinase-inactive RAF, ERK, and PKC-zeta. AMPK activator dinitrophenol had effects on ERK, aPKCs, and 2-DOG uptake similar to those of AICAR. Our findings suggest that effects of exercise on glucose transport that are dependent on AMPK are mediated via PYK2, the ERK pathway, PLD, and aPKCs.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study18

10 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabEx vivo tissueMechanism

    In rat EDL muscle, AICAR activated PYK2.

    In plain wordsIn lab tests, AICAR activated PYK2 in rat muscle.

    Outcome
    IncreasePYK2 activation
    Study

    ratn: not reported in source

    extensor digitorum longus muscle
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In rat extensor digitorum longus (EDL) muscles, (a) AMPK activator, 5-aminoimidazole-4-carboxamide-1-beta-d-riboside (AICAR), activated PYK2, ERK and aPKCs;
  2. 02LabEx vivo tissueMechanism

    In rat EDL muscle, AICAR activated ERK.

    In plain wordsIn lab tests, AICAR activated ERK in rat muscle.

    Outcome
    IncreaseERK activation
    Study

    ratn: not reported in source

    extensor digitorum longus muscle
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In rat extensor digitorum longus (EDL) muscles, (a) AMPK activator, 5-aminoimidazole-4-carboxamide-1-beta-d-riboside (AICAR), activated PYK2, ERK and aPKCs;
  3. 03LabEx vivo tissueMechanism

    In rat EDL muscle, AICAR activated atypical protein kinase Cs.

    In plain wordsIn lab tests, AICAR activated atypical protein kinase Cs in rat muscle.

    Outcome
    IncreaseaPKC activation
    Study

    ratn: not reported in source

    extensor digitorum longus muscle
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In rat extensor digitorum longus (EDL) muscles, (a) AMPK activator, 5-aminoimidazole-4-carboxamide-1-beta-d-riboside (AICAR), activated PYK2, ERK and aPKCs;
  4. 04LabEx vivo tissueMechanism

    In laboratory muscle models, AICAR and dinitrophenol had similar effects on ERK.

    In plain wordsIn lab tests, AICAR and dinitrophenol had similar effects on ERK.

    Outcome
    No significant changeERK response compared with dinitrophenol
    Study

    n: not reported in source

    Comparator
    Dinitrophenol
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activator dinitrophenol had effects on ERK, aPKCs, and 2-DOG uptake similar to those of AICAR.
  5. 05LabEx vivo tissueMechanism

    In laboratory muscle models, AICAR and dinitrophenol had similar effects on atypical protein kinase Cs.

    In plain wordsIn lab tests, AICAR and dinitrophenol had similar effects on atypical protein kinase Cs.

    Outcome
    No significant changeaPKC response compared with dinitrophenol
    Study

    n: not reported in source

    Comparator
    Dinitrophenol
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activator dinitrophenol had effects on ERK, aPKCs, and 2-DOG uptake similar to those of AICAR.
  6. 06LabEx vivo tissueMechanism

    In laboratory muscle models, AICAR and dinitrophenol had similar effects on 2-DOG uptake.

    In plain wordsIn lab tests, AICAR and dinitrophenol had similar effects on sugar uptake.

    Outcome
    No significant changeGlucose uptake compared with dinitrophenol
    Study

    n: not reported in source

    Comparator
    Dinitrophenol
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activator dinitrophenol had effects on ERK, aPKCs, and 2-DOG uptake similar to those of AICAR.
  7. 07LabIn vitro (cells)Mechanism

    In L6 myotubes, AICAR activated PYK2.

    In plain wordsIn cells, AICAR activated PYK2.

    Outcome
    IncreasePYK2 activation
    Study

    n: not reported in source

    L6 myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Similarly, in L6 myotubes, (a) AICAR activated PYK2, ERK, PLD, and aPKCs;
  8. 08LabIn vitro (cells)Mechanism

    In L6 myotubes, AICAR activated ERK.

    In plain wordsIn cells, AICAR activated ERK.

    Outcome
    IncreaseERK activation
    Study

    n: not reported in source

    L6 myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Similarly, in L6 myotubes, (a) AICAR activated PYK2, ERK, PLD, and aPKCs;
  9. 09LabIn vitro (cells)Mechanism

    In L6 myotubes, AICAR activated PLD.

    In plain wordsIn cells, AICAR activated PLD.

    Outcome
    IncreasePLD activation
    Study

    n: not reported in source

    L6 myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Similarly, in L6 myotubes, (a) AICAR activated PYK2, ERK, PLD, and aPKCs;
  10. 10LabIn vitro (cells)Mechanism

    In L6 myotubes, AICAR activated atypical protein kinase Cs.

    In plain wordsIn cells, AICAR activated atypical protein kinase Cs.

    Outcome
    IncreaseaPKC activation
    Study

    n: not reported in source

    L6 myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Similarly, in L6 myotubes, (a) AICAR activated PYK2, ERK, PLD, and aPKCs;

Studies that did not test the peptide alone8

In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking AICAR (acadesine).

  1. 11LabNot a test of AICAR (acadesine) aloneEx vivo tissueMechanism

    In rat EDL muscle, genistein and PD98059 blocked AICAR-induced ERK activation.

    In plain wordsIn lab tests, genistein and PD98059 blocked AICAR-induced ERK activation in rat muscle.

    Outcome
    DecreaseInhibition of AICAR-induced ERK activation
    Study

    ratn: not reported in source

    extensor digitorum longus muscle
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    (b) effects of AICAR on ERK and aPKCs were blocked by tyrosine kinase inhibitor, genistein, and MEK1 inhibitor, PD98059;

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  2. 12LabNot a test of AICAR (acadesine) aloneEx vivo tissueMechanism

    In rat EDL muscle, genistein, PD98059 and 1-butanol inhibited AICAR-induced aPKC activation.

    In plain wordsIn lab tests, genistein, PD98059 and 1-butanol inhibited AICAR-induced aPKC activation in rat muscle.

    Outcome
    DecreaseInhibition of AICAR-induced aPKC activation
    Study

    ratn: not reported in source

    extensor digitorum longus muscle
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    (b) effects of AICAR on ERK and aPKCs were blocked by tyrosine kinase inhibitor, genistein, and MEK1 inhibitor, PD98059;
    1 context sentence
    Summary · context
    and (c) effects of AICAR on aPKCs and 2-deoxyglucose (2-DOG) uptake were inhibited by genistein, PD98059, and PLD-inhibitor, 1-butanol.

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  3. 13LabNot a test of AICAR (acadesine) aloneEx vivo tissueMechanism

    In rat EDL muscle, genistein, PD98059 and 1-butanol inhibited AICAR-induced 2-deoxyglucose uptake.

    In plain wordsIn lab tests, these inhibitors reduced AICAR-induced sugar uptake in rat muscle.

    Outcome
    DecreaseInhibition of AICAR-induced glucose uptake
    Study

    ratn: not reported in source

    extensor digitorum longus muscle
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    and (c) effects of AICAR on aPKCs and 2-deoxyglucose (2-DOG) uptake were inhibited by genistein, PD98059, and PLD-inhibitor, 1-butanol.

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  4. 14LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In L6 myotubes, genistein, PD98059 and dominant-negative PYK2 inhibited AICAR-induced ERK activation.

    In plain wordsIn cells, genistein, PD98059 and altered PYK2 inhibited AICAR-induced ERK activation.

    Outcome
    DecreaseInhibition of AICAR-induced ERK activation
    Study

    n: not reported in source

    L6 myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    (b) effects of AICAR on ERK were inhibited by genistein, PD98059, and expression of dominant-negative PYK2;

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  5. 15LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In L6 myotubes, UO126 inhibited AICAR-induced PLD activation.

    In plain wordsIn cells, UO126 inhibited AICAR-induced PLD activation.

    Outcome
    DecreaseInhibition of AICAR-induced PLD activation
    Study

    n: not reported in source

    L6 myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    (c) effects of AICAR on PLD were inhibited by MEK1 inhibitor UO126;

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  6. 16LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In L6 myotubes, chemical inhibitors and dominant-negative pathway proteins inhibited AICAR-induced aPKC activation.

    In plain wordsIn cells, chemical inhibitors and altered pathway proteins inhibited AICAR-induced aPKC activation.

    Outcome
    DecreaseInhibition of AICAR-induced aPKC activation
    Study

    n: not reported in source

    L6 myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    (d) effects of AICAR on aPKCs were inhibited by genistein, PD98059, 1-butanol, and expression of dominant-negative forms of PYK2, GRB2, SOS, RAS, RAF, and ERK;

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  7. 17LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In L6 myotubes, chemical inhibitors and kinase-inactive proteins inhibited AICAR-induced 2DOG uptake.

    In plain wordsIn cells, chemical inhibitors and inactive proteins inhibited AICAR-induced sugar uptake.

    Outcome
    DecreaseInhibition of AICAR-induced 2DOG uptake
    Study

    n: not reported in source

    L6 myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    and (e) effects of AICAR on 2DOG uptake/GLUT4 translocation were inhibited by genistein, PD98059, UO126, 1-butanol, cell-permeable myristoylated PKC-zeta pseudosubstrate, and expression of kinase-inactive RAF, ERK, and PKC-zeta.

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  8. 18LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In L6 myotubes, chemical inhibitors and kinase-inactive proteins inhibited AICAR-induced GLUT4 translocation.

    In plain wordsIn cells, chemical inhibitors and inactive proteins inhibited AICAR-induced movement of GLUT4.

    Outcome
    DecreaseInhibition of AICAR-induced GLUT4 translocation
    Study

    n: not reported in source

    L6 myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    and (e) effects of AICAR on 2DOG uptake/GLUT4 translocation were inhibited by genistein, PD98059, UO126, 1-butanol, cell-permeable myristoylated PKC-zeta pseudosubstrate, and expression of kinase-inactive RAF, ERK, and PKC-zeta.

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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