508 research outputs found
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
Tumour Suppressor Gene
No full textPATENT: D. F. Callen, S. A. Whitmore, G. Kremmidiotis, M. Kochetkova, J. Crawford, Joanna (Assignee: Bionomics Ltd). WO 2002/018592 A1 (PCT/AU2001/001097) filed Aug 31, 2001; published Mar 7, 2002.The invention provides an isolated DNA molecule comprising the nucleotide sequence set forth in SEQ ID NO: 1 or 2, or active fragments thereof, which encode a polypeptide active in suppressing cellular functions associated with cancer. In particular, the polypeptide (MTG16) functions as a tumour suppressor gene. It also provides variants of such DNA molecules which retain their function, polypeptides encoded by the DNA molecules and antibodies thereto, as well as the use of these molecules in diagnostic, prognostic and therapeutic procedures and other uses such as screening for candidate pharmaceuticals and animal model generation.Invented by D. F. Callen, S. A. Whitmore, G. Kremmidiotis, M. Kochetkova, J. Crawford, Joanna; Assigned to Bionomics Ltd; Griffith Hack agents for inventors
Tumour Suppressor Gene Identified on Chromosome 18
No full textPATENT: D. F. Callen, S. A. Whitmore, G. Kremmidiotis, M. Kochetkova, J. Crawford (Assignee: Bionomics Ltd). WO 2002/048354 A1 (PCT/AU2001-001623) filed Dec 14, 2001; published Jun 20, 2002.The invention provides an isolated nucleic acid molecule comprising the nucleotide sequence set forth in SEQ ID NO:1, or active fragment thereof, which encodes a polypeptide active in suppressing cellular proliferation. In particular, TSG18 functions as a tumour suppressor gene as well as having a role in immune/autoimmune/inflammatory disorders. It also provides variants of such DNA molecules which retain their function, polypeptides encoded by the DNA molecules and antibodies thereto, as well as the use of these molecules in diagnostic, prognostic and therapeutic procedures and other uses such as screening for candidate pharmaceuticals.Invented by D. F. Callen, S. A. Whitmore, G. Kremmidiotis, M. Kochetkova, J. Crawford; Assigned to Bionomics Ltd; Griffith Hack agents for inventors
Magnetic anisotropy in the cubic Laves REFe2 intermetallic compounds
No full textIn the past, the Callen–Callen (1965 Phys. Rev. 139 A455–71; 1966 J. Phys. Chem. Solids 27 1271–85) model has been highly successful in explaining the origin and temperature dependence of the magneto-crystalline anisotropy in many magnetic compounds. Yet, despite their high ordering temperatures of ~650 K, the Callen–Callen model has proved insufficient for the REFe2 compounds. In this paper, we show that it is possible to replicate the values of the phenomenological parameters K1, K2, and K3 given by Atzmony and Dariel (1976 Phys. Rev. B 13 4006–14), by extending the Callen–Callen model to second order in HCF. In particular, explanations are provided for (i) the unexpected changes in sign of K1 and K2 in HoFe2 and DyFe2, respectively, and (ii) the origin and behaviour of the K3 term. In addition, it is demonstrated that higher order terms are required, and that K4 exceeds K3 at low temperatures. Revised estimates of K1, K2, K3, K4, and K5 are given. Finally, an alternative 'multipolar' approach to the problem of magnetic anisotropy is also provided. It is shown that the latter confers significant advantages over the older phenomenological method. In particular, all the multipolar coefficients (\tilde {K}_N , N = 4, 6, 8, 10, 12) decrease monotonically with increasing temperature, with \tilde {K}_N decreasing faster than \tilde {K}_{N-2} etc. These observations are in accord with expectations based on the original Callen–Callen model
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
Assignment of the human beta tropomyosin gene (TPM2) to band 9p13 by fluorescence in situ hybridisation
No full textA sequence tagged site (STS) was developed for the human beta tropomyosin gene (TPM2). The STS was used to amplify DNA from somatic cell hybrids to localise TPM2 to human chromosome 9. Genomic clones isolated with the STS product were in turn used in fluorescence in situ hybridisation to metaphase chromosome spreads to further localise TPM2 to 9p13.Hunt, C C ; Eyre, H J ; Akkari, P A ; Meredith, C ; Dorosz, S M ; Wilton, S D ; Callen, D F ; Laing, N G ; Baker,
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
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
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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