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William Blalock


Istituto di Genetica Molecolare - Sede di Bologna

c/o Istituto Ortopedico Rizzoli

via di Barbiano 1/10

40136 Bologna

Telefono: 051 6366769 




1991:  Bachelor of Science (BS) in Biology from Wake Forest University, Winston-Salem, North Carolina 

1997: Master of Science (MS) in Biology from East Carolina University, Greenville, North Carolina.

2000: Doctor of Philosophy (PhD) in Microbiology and Immunology from Brody School of Medicine, East Carolina University, Greenville, North Carolina. 


Employment/ Training

2000-2005: Post-doctoral Research Associate, University of Florida Shands Cancer Center, Gainesville, Florida, USA.

2005-2007: Senior Scientist, Department of Innovative Therapy, Advanced Biotechnology Center/G. Gaslini Pediatric Institute, Genoa, Italy  

2007-2011: Senior Scientist, Cell Signaling Laboratory, Department of Human Anatomical Sciences, University of Bologna, Bologna, Italy.

2011-Present: Research Scientist, III Level, Institute of Molecular Genetics, National Research Council of Italy, UOS Bologna, Bologna, Italy.


Key Areas of Research

Inflammation, stress, nuclear signaling, acute leukemia, bone marrow failure disorders, osteosarcoma



Research Interests

My research is focused on inflammatory/stress-mediated signaling in the nucleus and how this signaling influences the progression of cancer and neuromuscular degeneration.  In particular, I am characterizing the role of the stress-activated kinase, PKR, in the nucleus.  Constitutive activation of PKR has been demonstrated in myelodysplastic syndromes, leukemia, breast cancer, melanoma, Alzheimer’s disease, Huntington’s corea and Creutzfeldt-Jakob syndrome.  In many of these diseases active PKR is localized exclusively to the nucleus.  PKR can influence diverse signaling pathways and thus multiple cellular functions, including eIF2alpha (translation), NF-kappaB (transcription/inflammation/angiogenesis), and p53 (DNA repair/transcription/cell cycle).  The majority of effort is being directed toward understanding the role of PKR signaling in the development and progression of cancer. Using proteomic methods (mass spectrometry, peptide arrays, HPLC, 2D electrophoresis), I am looking to identify the interactors and potentially novel substrates of PKR in the nucleus of cancer cells.  New interactors and substrates are to be validated by biological, molecular and cellular methods.  Moreover, as the kinases AKT and PKR are involved in converging signaling pathways which are induced by cytokines such as tumor necrosis factor (TNF)-alpha, insulin growth factor (IGF) and platelet derived growth factor (PDGF); and their signaling influences each other, we are examining proteins that serve as substrates and/or interactors of both kinases. 


Recent Publications

  • Bavelloni,A., Focaccia,E., Piazzi,M., Orsini,A., Ramazzotti,G., Cocco,L., Blalock,W. (co-corresponding) and Faenza,I. (co-corresponding).  Therapeutic potential of NVP-BKM120 in human osteosarcoma cells.  (2018).  J. Cell. Physiol. (In press).
  • Bavelloni,A., Focaccia,E., Piazzi,M., Errani,C., Blalock,W. (co-corresponding) and Faenza I. (co-corresponding).  Cell Cycle Arrest and Apoptosis Induced by Kinamycin F in Human Osteosarcoma Cells.  (2017).  Anticancer Res. 37: 4103-4109.
  • Blalock,WL. (co-corresponding), Piazzi,M., Gallo,A., Bavelloni,A., Focaccia,E. and Faenza,I (co-corresponding).  RNA processing and ribosome biogenesis in bone marrow failure disorders.  (2017).  RNA & Disease. 4: e1531.
  • Ramazzotti, G., Bavelloni, A., Blalock, W., Piazzi, M., Cocco, L. and Faenza, I.  BMP-2 Induced Expression of PLC?1 That Is a Positive Regulator of Osteoblast Differentiation. (2016) J. Cell. Physiol. 231: 623-629.
  • Bavelloni, A., Piazzi, M., Raffini, M., Faenza, I. and Blalock, WL.  Prohibitin 2: At a communications crossroads. (2015). IUBMB Life 67: 239-254.
  • Piazzi, M., Blalock, WL., Bavelloni, A., Faenza, I., Raffini, M., Tagliavini, F., Manzoli, L. and Cocco, L.  PI-PLC?1b affects Akt activation, cyclin E expression, and caspase cleavage, promoting cell survival in pro-B-lymphoblastic cells exposed to oxidative stress. (2014). FASEB J. 
  • Bavelloni, A., Dmitrienko, GI., Goodfellow, VJ., Ghavami, A., Piazzi, M., Blalock, W., Chiarini, F., Cocco, L. and Faenza, I. PLC?1a and PLC?1b selective regulation and cyclin D3 modulation reduced by kinamycin F during k562 cell differentiation. (2015).  J. Cell. Physiol. 230: 587-594. 
  • Bavelloni, A., Poli, A., Fiume, R., Blalock, W., Matteucci, A., Ramazzotti, G., McCubrey, JA., Cocco, L. and Faenza, I.  PLC-beta 1 regulates the expression of miR-210 during mithramycin-mediated erythroid differentiation in K562 cells. (2014). Oncotarget 5: 4222-4231. 
  • Bavelloni, A., Piazzi, M., Faenza, I., Raffini, M., D'Angelo, A., Cattini, L., Cocco, L. and Blalock WL. Prohibitin 2 represents a novel nuclear AKT substrate during all-trans retinoic acid-induced differentiation of acute promyelocytic leukemia cells. (2014). FASEB J. 28: 2009-2019. 
  • Blalock, WL. (corresponding), Piazzi, M. (co-first author), Bavelloni, A., Raffini, M., Faenza, I., D'Angelo, A., and Cocco, L.  Identification of the PKR nuclear interactome reveals roles in ribosome biogenesis, mRNA processing and cell division. (2014). J. Cell. Physiol.  229: 1047-1060. 
  • Faenza I, Blalock W., Bavelloni A, Shoser B, Fiume R, Pacella S, Piazzi M, D'Angelo A, and Cocco L.  A role for PLC?1 in myotonic dystrophies type 1 and 2. (2012). FASEB J. 26: 3042-3048. 
  • Blalock,WL., Bavelloni,A., Piazzi,M., Tagliavini,F., Faenza,I., Martelli,AM., Follo,MY. and Cocco,L. Multiple forms of PKR present in the nuclei of acute leukemia cells represent an active kinase that is responsive to stress. (2011). Leukemia 25: 236-245.

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