CAML promotes prolactin-dependent proliferation of breast cancer cells by facilitating prolactin receptor signaling pathways

Breast Cancer Research and Treatment

Volumn 130, Issue 1, 2011, Pages 19-27

  Lim, Ji Hong ^a   Kim, Tae You ^a   Kim, Woo Ho ^a   Park, Jong Wan ^a  

^a Seoul National University   (South Korea)

Author keywords

Breast cancer; Calcium modulating cyclophilin ligand; Cell proliferation; Prolactin receptor; Stat5

Indexed keywords

CALCIUM ION; CALCIUM MODULATING CYCLOPHILIN LIGAND PROTEIN; CELL MEMBRANE PROTEIN; CYCLOPHILIN B; MITOGEN ACTIVATED PROTEIN KINASE 1; PROLACTIN; PROLACTIN RECEPTOR; PROTEIN CAML; STAT5 PROTEIN; UNCLASSIFIED DRUG;

ADULT; AGED; ARTICLE; BREAST CANCER; BREAST CARCINOGENESIS; CALCIUM MOBILIZATION; CANCER CELL CULTURE; CANCER TISSUE; CELL PROLIFERATION; CELL STRAIN HEK293; CLINICAL ARTICLE; CONTROLLED STUDY; FEMALE; HUMAN; HUMAN CELL; HUMAN TISSUE; IMMUNOHISTOCHEMISTRY; LEUKEMIA CELL; MALE; PRIORITY JOURNAL; PROTEIN FUNCTION; PROTEIN PROTEIN INTERACTION; SIGNAL TRANSDUCTION;

ADAPTOR PROTEINS, SIGNAL TRANSDUCING; ADULT; AGED; AGED, 80 AND OVER; BREAST NEOPLASMS; CELL LINE, TUMOR; CELL PROLIFERATION; FEMALE; GENE EXPRESSION REGULATION, NEOPLASTIC; HCT116 CELLS; HEK293 CELLS; HL-60 CELLS; HUMANS; JURKAT CELLS; MIDDLE AGED; PROLACTIN; PROTEIN BINDING; RECEPTORS, PROLACTIN; SIGNAL TRANSDUCTION; STAT5 TRANSCRIPTION FACTOR; TRANSCRIPTION, GENETIC;

EID: 82455205647     PISSN: 01676806     EISSN: 15737217     Source Type: Journal    
DOI: 10.1007/s10549-010-1274-4     Document Type: Article

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