244 research outputs found
Mitochondrial genetics of yeast / by David F. Callen
No full textv, 100 leaves : ill., graphs, tables ; 30 cm.Thesis (Ph.D.) -- University of Adelaide, Dept. of Genetics, 197
Azobenzene-containing photoswitchable proteasome inhibitors with selective activity and cellular toxicity
No full textAccepted 8 June 2017Abstract not availableBeatriz Blanco, Kathryn A. Palasis, Alaknanda Adwal, David F. Callen, Andrew D. Abel
Absence of the Epstein-Barr virus genome in breast cancer-derived cell lines
No full text© 2003 Oxford University PressPeter Speck, David F. Callen, Richard Longnecke
Assignment of the Human CC Chemokine Gene TARC (SCYA17) to chromosome 16q13
No full textNomiyama, Hisayuki ; Imai, Toshio ; Kusuda, Jun ; Miura, Retsu ; Callen, David F. ; Yoshie, Osam
sj-docx-1-jad-10.1177_10870547231155875 – Supplemental material for Progress and Pitfalls in the Provision of Quality Care for Adults With Attention Deficit Hyperactivity Disorder in Primary Care
No full textSupplemental material, sj-docx-1-jad-10.1177_10870547231155875 for Progress and Pitfalls in the Provision of Quality Care for Adults With Attention Deficit Hyperactivity Disorder in Primary Care by Elisabeth F. Callen, Tarin L. Clay, Jillian Alai, David W. Goodman, Lenard A. Adler, Joel Shields and Stephen V. Faraone in Journal of Attention Disorders</p
sj-docx-1-jad-10.1177_10870547231218449 – Supplemental material for Measuring Quality Care for Adult ADHD Patients: How Much Does Gender and Gender Identity Matter?
No full textSupplemental material, sj-docx-1-jad-10.1177_10870547231218449 for Measuring Quality Care for Adult ADHD Patients: How Much Does Gender and Gender Identity Matter? by Tarin Clay, Elisabeth F. Callen, Jill Alai, David W. Goodman, Lenard A. Adler and Stephen V. Faraone in Journal of Attention Disorders</p
Ankrd11 is a chromatin regulator involved in autism that is essential for neural development
No full textAbstract not availableDenis Gallagher, Anastassia Voronova, Mark A. Zander, Gonzalo I. Cancino, Alexa Bramall, Matthew P. Krause, Clemer Abad, Mustafa Tekin, Paul M. Neilsen, David F. Callen, Stephen W. Scherer, Gordon M. Keller, David R. Kaplan, Katherina Walz, and Freda D. Mille
A template-based approach to inhibitors of calpain 2, 20S proteasome, and HIV-1 protease
No full textArticle first published online: 15 OCT 2013Specificity counts: A template-based approach to protease inhibitors is presented using a core macrocycle that presents a generic β-strand template for binding to protease active sites. This is then specifically functionalized at P2 , and the C and N termini to give inhibitors of calpain 2, 20S proteasome, and HIV-1 protease.Seth A. Jones, Paul M. Neilsen, Limei Siew, David F. Callen, Nathan E. Goldfarb, Ben M. Dunn, and Andrew D. Abel
Targeting the p53 pathway in Ewing Sarcoma
No full textExtent: 17p.The p53 tumour suppressor plays a pivotal role in the prevention of oncogenic transformation. Cancers frequently evade the potent antitumour surveillance mechanisms of p53 through mutation of the TP53 gene, with approximately 50% of all human malignancies expressing dysfunctional, mutated p53 proteins. Interestingly, genetic lesions in the TP53 gene are only observed in 10% of Ewing Sarcomas, with the majority of these sarcomas expressing a functional wild-type p53. In addition, the p53 downstream signaling pathways and DNA-damage cell cycle checkpoints remain functionally intact in these sarcomas. This paper summarizes recent insights into the functional capabilities and regulation of p53 in Ewing Sarcoma, with a particular focus on the cross-talk between p53 and the EWS-FLI1 gene rearrangement frequently associated with this disease. The development of several activators of p53 is discussed, with recent evidence demonstrating the potential of small molecule p53 activators as a promising systemic therapeutic approach for the treatment of Ewing Sarcomas with wild-type p53.Paul M. Neilsen, Kathleen I. Pishas, David F. Callen and David M. Thoma
New peptidomimetic boronates for selective inhibition of the chymotrypsin-like activity of the 26S proteasome
No full textPublication Date (Web): September 13, 2016Proteasome is a large proteinase complex that degrades proteins via its three catalytic activities. Among these activities, the “chymotrypsin-like” activity has emerged as the focus of drug discovery in cancer therapy. Here, we report new peptidomimetic boronates that are highly specific for the chymotrypsin-like catalytic activity of the proteasome. These new specific proteasome inhibitors were demonstrated to have higher in vitro potency and selective cytotoxicity for cancer cells compared to benchmark proteasome inhibitors: bortezomib and carfilzomib. In breast cancer cell lines, treatment with 1a or 2a induced accumulation of the high molecular weight polyubiqutinated proteins at similar levels observed for bortezomib and carfilzomib, indicating that cancer cell death caused by 1a/2a is chiefly due to proteasome inhibition.Xiaozhou Zhang, Alaknanda Adwal, Andrew G. Turner, David F. Callen, and Andrew D. Abel
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