PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32557691-13 2021 AMPK agonist AICAR was used to activate the AMPK pathway. AICA ribonucleotide 13-18 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 0-4 33861582-2 2021 AMPK agonist AICAR has been reported to improve cognition. AICA ribonucleotide 13-18 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 0-4 32557691-13 2021 AMPK agonist AICAR was used to activate the AMPK pathway. AICA ribonucleotide 13-18 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 44-48 32703218-10 2020 On the contrary, the activation of AMPK by metformin (Met) or 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) could overcome the KRAS-induced resistance to the anti-EGFR antibody in vivo and in vitro. AICA ribonucleotide 62-107 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 35-39 32703218-10 2020 On the contrary, the activation of AMPK by metformin (Met) or 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) could overcome the KRAS-induced resistance to the anti-EGFR antibody in vivo and in vitro. AICA ribonucleotide 109-114 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 35-39 32246808-5 2020 Pharmacologic activation of AMPK with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) or metformin during sepsis improved the survival, while AMPK inhibition with Compound C increased mortality, impaired mitochondrial respiration, decreased OCR, and disrupted TEC metabolic fitness. AICA ribonucleotide 38-83 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 28-32 32246808-5 2020 Pharmacologic activation of AMPK with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) or metformin during sepsis improved the survival, while AMPK inhibition with Compound C increased mortality, impaired mitochondrial respiration, decreased OCR, and disrupted TEC metabolic fitness. AICA ribonucleotide 85-90 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 28-32 31559637-9 2019 Furthermore, SIRT4 down-regulated 5" AMP-activated protein kinase (AMPK) signaling in Treg cells, whereas the AMPK agonist AICAR restored the expression of Foxp3 and interleukin-10 in SIRT4-overexpressing Treg cells. AICA ribonucleotide 123-128 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 110-114 21195169-8 2011 In addition, overexpression of wild-type phosphatase and tensin homologue deleted on chromosome 10 (PTEN) or pretreatment with aminoimidazole carboxamide ribonucleotide, an AMP-activated protein kinase (AMPK) activator, partially prevented Cd-induced ROS and activation of the mTOR pathway, as well as cell death. AICA ribonucleotide 127-168 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 173-201 19407487-3 2009 AICAR, one of the pharmacological AMPK activators, has been widely used to suppress cancer cell growth through activation of LKB1, an upstream kinase of AMPK. AICA ribonucleotide 0-5 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 34-38 19407487-3 2009 AICAR, one of the pharmacological AMPK activators, has been widely used to suppress cancer cell growth through activation of LKB1, an upstream kinase of AMPK. AICA ribonucleotide 0-5 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 153-157 32308539-8 2020 Furthermore, AICAR, an AMPK activator, increased CD9 expression under EF, while compound C, an AMPK inhibitor, decreased CD9 expression in keratinocytes. AICA ribonucleotide 13-18 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 23-27 31211863-9 2019 Attenuation or exacerbation of EtOH-induced oxidative stress by AICAR or Compound C, respectively, suggests a link between AMPK signaling, EtOH metabolism, and related oxidative stress. AICA ribonucleotide 64-69 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 123-127 26236947-4 2015 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR), an AMPK activator, caused growth arrest, inhibition of migration and invasion of TNBC cells. AICA ribonucleotide 0-45 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 58-62 26236947-4 2015 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR), an AMPK activator, caused growth arrest, inhibition of migration and invasion of TNBC cells. AICA ribonucleotide 47-52 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 58-62