Diana Resetca

ORCID: 0000-0003-0007-7828
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About
Contact & Profiles
Research Areas
  • Ubiquitin and proteasome pathways
  • Cytokine Signaling Pathways and Interactions
  • Genomics and Chromatin Dynamics
  • Protein Degradation and Inhibitors
  • Mass Spectrometry Techniques and Applications
  • Chronic Myeloid Leukemia Treatments
  • Biotin and Related Studies
  • Tuberculosis Research and Epidemiology
  • RNA modifications and cancer
  • Cancer Mechanisms and Therapy
  • Nanowire Synthesis and Applications
  • Biochemical and Molecular Research
  • Protein Kinase Regulation and GTPase Signaling
  • Cancer, Stress, Anesthesia, and Immune Response
  • Monoclonal and Polyclonal Antibodies Research
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • DNA Repair Mechanisms
  • Peptidase Inhibition and Analysis
  • Bioinformatics and Genomic Networks
  • Cancer, Hypoxia, and Metabolism
  • Chronic Lymphocytic Leukemia Research
  • Glycosylation and Glycoproteins Research
  • Enzyme Structure and Function
  • CAR-T cell therapy research
  • Virus-based gene therapy research

Princess Margaret Cancer Centre
2017-2021

University of Toronto
2011-2021

University Health Network
2017-2019

York University
2013-2014

Abstract The c-MYC (MYC) oncoprotein is deregulated in over 50% of cancers, yet regulatory mechanisms controlling MYC remain unclear. To this end, we interrogated the interactome using BioID mass spectrometry (MS) and identified PP1 (protein phosphatase 1) its subunit PNUTS phosphatase-1 nuclear-targeting subunit) as interactors. We demonstrate that endogenous interact across multiple cell types they co-occupy target gene promoters. Inhibiting by RNAi or pharmacological inhibition results...

10.1038/s41467-018-05660-0 article EN cc-by Nature Communications 2018-08-23

// Daniel P. Ball 1, * , Andrew M. Lewis Declan Williams 2, 3 Diana Resetca 4 Derek J. Wilson Patrick T. Gunning 1 Department of Chemical and Physical Sciences, University Toronto Mississauga, Ontario, L5L 1C6, Canada 2 Chemistry, York University, Toronto, M3J 1P3, Center for Research in Mass Spectrometry, Medical Biophysics, M5G 1L, These authors have contributed equally to this work Correspondence to: Gunning, e-mail: patrick.gunning@utoronto.ca Keywords: STAT3, S3I-201, NSC 74859,...

10.18632/oncotarget.7838 article EN Oncotarget 2016-03-02

The activity of the transcription factor signal transducer and activator 3 (STAT3) is dysregulated in a number hematological solid malignancies. Development pharmacological STAT3 Src homology 2 (SH2) domain interaction inhibitors holds great promise for cancer therapy, novel class salicylic acid-based dimerization that includes orally bioavailable drug candidates has been recently developed. compounds SF-1-066 BP-1-102 are predicted to bind SH2 domain. However, given highly unstructured...

10.1074/jbc.m114.595454 article EN cc-by Journal of Biological Chemistry 2014-10-07

Evidence shows that signal transducer and activator of transcription 5 (Stat5) protein, a member the STAT family signalling proteins, plays pivotal role in progression many human cancers including acute myeloid leukemias prostate cancer. This mini-review outlines progress made towards identifying agents capable silencing aberrant Stat5 signalling.

10.1039/c1md00175b article EN MedChemComm 2011-10-03

Abstract MYC activity is regulated by a complex network of signaling cascades and protein interactions, some which result in post-translation modifications (PTMs). For example, phosphorylation the regulatory threonine 58 (T58) serine 62 (S62) plays pivotal role regulating stability activity. Loss this pathway cancer can lead to dysregulation contribute tumorigenesis. Despite their important role, majority PTMs arising downstream different consequences on remain largely unknown. To capture...

10.1158/1557-3125.myc15-a12 article EN Molecular Cancer Research 2015-10-01

Abstract The Myc family of transcription factors, c-Myc, N-Myc and L-Myc, are known to be deregulated in a large variety cancers. Mechanisms responsible for the deregulation activity members cancer not well understood. A number protein-protein interactions post-translational modifications have been suggested promote oncogenic Myc. Traditional biochemical approaches successful at mapping interactors due their tight association with chromatin labile nature proteins. Mapping that support...

10.1158/1538-7445.am2016-2010 article EN Cancer Research 2016-07-15

Abstract The oncogenic transcription factor c-MYC (MYC) is deregulated, and often overexpressed, in more than 50% of cancers. MYC deregulation associated with poor prognosis aggressive disease, suggesting that the development therapeutic inhibitors targeting would dramatically impact patient care outcome. a highly regulated factor, protein mRNA half-life approximately 30 min. most extensively studied pathway regulating stability involves ubiquitylation proteasomal degradation mediated by...

10.1158/1538-7445.am2018-5423 article EN Cancer Research 2018-07-01
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