Genomes and Genes
Rachel A Altura
Affiliation: Brown University
- XPO1 (CRM1) inhibition represses STAT3 activation to drive a survivin-dependent oncogenic switch in triple-negative breast cancerYan Cheng
Corresponding Author Rachel A Altura, Department of Pediatrics, Rhode Island Hospital, 593 Eddy Street, Providence, RI 02903
Mol Cancer Ther 13:675-86. 2014..Collectively, these data demonstrate that XPO1 inhibition by SINE compounds represses STAT3 transactivation to block the selective oncogenic properties of survivin and supports their clinical use in TNBC...
- EGF regulates survivin stability through the Raf-1/ERK pathway in insulin-secreting pancreatic β-cellsHaijuan Wang
Department of Pediatrics, Division of Pediatric Hematology Oncology, Brown University, Providence, RI 02903, USA
BMC Mol Biol 11:66. 2010..Here, we analyzed the effects of the β-cell mitogens IGF-1 and EGF on survivin regulation in the established pancreatic β-cell model cell lines, MIN6 and INS-1 and in primary mouse islets...
- Histone deacetylase 6 (HDAC6) deacetylates survivin for its nuclear export in breast cancerMatthew T Riolo
Department of Pediatrics, The Warren Alpert Medical School of Brown University and Rhode Island Hospital, Providence, Rhode Island 02903, USA
J Biol Chem 287:10885-93. 2012..Together, these data imply that HDAC6 deacetylates survivin to regulate its nuclear export, a feature that may provide a novel target for patients with ER+ breast cancer...
- Total Survivin and acetylated Survivin correlate with distinct molecular subtypes of breast cancerEvgeny Yakirevich
Department of Pathology, Brown University School of Medicine and Rhode Island Hospital, Providence, RI 02903, USA
Hum Pathol 43:865-73. 2012....
- Rapamycin induces the anti-apoptotic protein survivin in neuroblastomaAyman Samkari
Department of Pediatrics, Division of Hematology Oncology, The Warren Alpert Medical School of Brown University and Rhode Island Hospital 593 Eddy Street, Providence, RI, 02903, USA
Int J Biochem Mol Biol 3:28-35. 2012..Induction of survivin by rapamycin could therefore be a potential mechanism of neuroblastoma tumor cell resistance and rapamycin may not be an effective therapeutic agent for these tumors...
- Acetylation directs survivin nuclear localization to repress STAT3 oncogenic activityHaijuan Wang
Department of Pediatrics, Brown University and Rhode Island Hospital, Providence, Rhode Island 02903, USA
J Biol Chem 285:36129-37. 2010....
- Quantitative phosphoproteomic analysis identifies activation of the RET and IGF-1R/IR signaling pathways in neuroblastomaBradley D Denardo
Division of Pediatric Hematology Oncology, Department of Pediatrics, The Warren Albert School of Medicine at Brown University, Providence, Rhode Island, United States of America
PLoS ONE 8:e82513. 2013..Furthermore, application of this previously unexploited technology in the clinic opens the possibility of providing a new wide-scale molecular signature to assess disease progression and prognosis. ..
- The CRM1 nuclear export protein in normal development and diseaseKevin T Nguyen
Department of Pediatrics, Division of Pediatric Hematology Oncology, Hasbro Children s Hospital and The Warren Alpert Medical School at Brown University Providence, Rhode Island, USA
Int J Biochem Mol Biol 3:137-51. 2012..Whether all of these proteins together are responsible for this phenotype or whether specific proteins are required for this effect is unclear at this time...
- A novel missense mutation in MVK associated with MK deficiency and dyserythropoietic anemiaAyman Samkari
Division of Hematology Oncology, Department of Pediatrics, Hasbro Children s Hospital and Warren Alpert Medical School of Brown University, Providence, Rhode Island 02903, USA
Pediatrics 125:e964-8. 2010..Treatment with corticosteroids and colchicine directed at controlling the autoinflammatory disease resulted in improvement of the anemia...