Keratinocyte growth factor protects endometrial cells from oxygen glucose deprivation/re-oxygenation via activating Nrf2 signaling

Biochemical and Biophysical Research Communications

Volumn 501, Issue 1, 2018, Pages 178-185

  Shi, Xuting ^a   Liu, Hai yan ^b   Li, Shu ping ^a   Xu, Hong bin ^a  

^a THE AFFILIATED CHANGZHOU NO 2 PEOPLE S HOSPITAL OF NANJING MEDICAL UNIVERSITY   (China)

^b Maternal and Child Health Care Hospital of Yancheng City   (China)

Author keywords

Akt mTOR; Endometrial cells; Keratinocyte growth factor; Nrf2 signaling; Oxygen glucose deprivation re oxygenation

Indexed keywords

2 MORPHOLINO 8 PHENYLCHROMONE; EVEROLIMUS; GLUCOSE; HEME OXYGENASE 1; KERATINOCYTE GROWTH FACTOR; KERATINOCYTE GROWTH FACTOR RECEPTOR; OXYGEN; SERINE; SHORT HAIRPIN RNA; TRANSCRIPTION FACTOR NRF2; VISTUSERTIB; FGF7 PROTEIN, HUMAN; FIBROBLAST GROWTH FACTOR RECEPTOR 2; MESSENGER RNA; MTOR PROTEIN, HUMAN; NFE2L2 PROTEIN, HUMAN; NFE2L2 PROTEIN, MOUSE; PROTEIN KINASE B; TARGET OF RAPAMYCIN KINASE;

AKT/MTOR SIGNALING; ANIMAL CELL; APOPTOSIS; ARTICLE; CELL DEATH; CELL FUNCTION; CELL LINE; CELL NUCLEUS; CELL PROTECTION; CELL VIABILITY; CONTROLLED STUDY; CRISPR-CAS9 SYSTEM; ENDOMETRIUM CELL; GCLC GENE; GENE; GENE TARGETING; HO1 GENE; HUMAN; HUMAN CELL; INTRACELLULAR TRANSPORT; MOUSE; NONHUMAN; NOQ1 GENE; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; PROTEIN STABILITY; PROTEIN TRANSPORT; REOXYGENATION; SIGNAL TRANSDUCTION; T-HESC CELL; TRANSCRIPTION INITIATION; ANIMAL; ANTAGONISTS AND INHIBITORS; CELL CULTURE; CELL HYPOXIA; CELL SURVIVAL; DRUG EFFECT; ENDOMETRIUM; FEMALE; GENE KNOCKOUT; GENETICS; METABOLISM; NECROSIS; PATHOLOGY;

ANIMALS; CELL HYPOXIA; CELL LINE; CELL SURVIVAL; CELLS, CULTURED; CYTOPROTECTION; ENDOMETRIUM; FEMALE; FIBROBLAST GROWTH FACTOR 7; GENE KNOCKOUT TECHNIQUES; GLUCOSE; HUMANS; MICE; NECROSIS; NF-E2-RELATED FACTOR 2; OXYGEN; PROTO-ONCOGENE PROTEINS C-AKT; RECEPTOR, FIBROBLAST GROWTH FACTOR, TYPE 2; RNA, MESSENGER; SIGNAL TRANSDUCTION; TOR SERINE-THREONINE KINASES;

EID: 85046707994     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2018.04.208     Document Type: Article

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