Disease relevance of TPD52L2

• Increased copy number (ICN) was measured using Southern blot analyses in 3/32 human breast carcinomas at hD52, and the related hD54 gene in 20q13.2-q13 [1].
• The magnitude of sensitization is cell type specific and is >10-fold for VP-16 in D54, a brain tumor cell line intrinsically resistant to topoisomerase II inhibitors [2].
• Three human glioma cell lines, U251 MG, U-87 MG and D54 MG, that did not express endogenous p16/CDKN2 gene and were easily infected with adenovirus vectors were selected for these experiments [3].
• Four glioma cell lines (D54, U251, U87MG, and EFC-2) were treated with fenretinide (1-100 microM) and showed dose- and time-dependent induction of cell death [4].
• EXPERIMENTAL DESIGN: We have used ZD6474 and/or ionizing radiation in human glioblastoma cell lines D54 and U251 in vitro and in nude mice bearing established xenografts [5].

High impact information on TPD52L2

• Specific small interference RNA (siRNA) transfection significantly inhibited Dynamin 2 expression in various tumor cell lines (LoVo, D54, and MCF-7) and abolished the radiation induction of Dynamin 2 [6].
• Three cell lines (U-251 MG, U-373 MG, and A-172) expressed endogenous mutant p53, and the other three (U-87 MG, EFC-2, and D54 MG) expressed wild-type p53 [7].
• EXPERIMENTAL DESIGN: Using our apoptosis imaging platform and diffusion magnetic resonance imaging (MRI), we monitored the antitumor effects of 5-FU, TRAIL, and 5-FU + TRAIL using D54 xenografts [8].
• In this study, we examined the use of 5-fluorouracil (5-FU) for sensitizing D54 tumors to tumor necrosis factor alpha-related apoptosis-inducing ligand (TRAIL) therapy by monitoring apoptotic activity in vivo using bioluminescence imaging [8].
• Sample D54 was a mixed infection of genotype 2i and 6h viruses [9].

Chemical compound and disease context of TPD52L2

• The human malignant glioma cell lines D54, U251, and U87 were maintained in normal or selenium-supplemented (30 nM sodium selenite) conditions [10].
• In this study, we investigated the function of anti-proliferative effects of HDAC inhibitors, N-butyric acid and trichostatin A, on human malignant glioma cell lines, U251-MG and D54 [11].
• The following experiments compare the original C6 rat glioma cell line with C6 cells transfected with the retroviral plasmid LacZ, and the human glioma cell lines GaMG, U373, U251, and D54 with cells stained with tracker dyes (Dil and DiO) [12].
• Subsequently, the expression level of MMPs and the serine protease uPA was investigated in 7 glioma cell lines (U373, GaMG, U251, GHE, SNB19, U138 and D54) by RT-PCR [13].

Biological context of TPD52L2

• Flow cytometric studies using D54 cells demonstrated no significant changes in the cell cycle distribution compared with untreated control, but a sub-G1 fraction consistent with apoptosis was detected [4].
• D54 MG cells were transfected with AdCMVCEA or an adenoviral vector encoding lacZ reporter gene as a control (AdCMVlacZ) [14].
• By using an in vitro assay of DNA fragmentation as a quantitative measure of apoptotic cell death, we sought to determine whether the sensitivity of two human glioma cell lines (D54 and U251) to drug-induced apoptosis could be inhibited by VN [15].
• Using alanine substitution mutagenesis, we established a functional role for aspartates D54 and D213 in solCD39 [16].

Associations of TPD52L2 with chemical compounds

• RESULTS: As single agents, ionizing radiation and ZD6474 caused a dose-dependent inhibition of soft agar growth in D54 and U251 cell lines, whereas a cooperative effect was obtained in combination [5].
• Treatment of rats by ICM with temozolomide 3 days after intracerebral challenge with D54 human MG xenograft increased median survival by 128% compared with rats treated by ICM with saline, by 113% compared with rats treated with i.p. saline, and by 100% compared with rats treated with i.p. temozolomide (P < 0.001) [17].
• GL261 and D54 cells were treated with 5 micromol/L of STI571 for 1 h and/or irradiated with 3 Gy [18].
• In U87, D54, GL261, and C6 tumors, AdZ.F(pK7) increased gene transfer by 10- to 100-fold compared with AdZ [19].

Other interactions of TPD52L2

• The identified hD54 cDNAs predicted three hD54 isoforms, suggesting that alternatively-spliced transcripts may be produced from D52-like genes [20].

Analytical, diagnostic and therapeutic context of TPD52L2

• The efficacy of transduction of recombinant AdCMVCEA by direct intratumoral injection into D54 MG xenografts was investigated by immunohistochemical analysis, immunofluorescence and by measuring 131I-labeled COL-1 uptake through external scintigraphic imaging and biodistribution studies [14].
• Immunofluorescence and immunohistochemistry assays employing unlabeled anti-CEA COL-1 monoclonal antibody demonstrated expression of CEA antigen on the cell surface of transduced D54 MG cells in culture [14].
• The structure of the identical sequence determined at 120 K involving somewhat different crystallization conditions has been reported previously [Harper et al. (1998), Acta Cryst. D54, 1273-1284] [21].
• HIV-1 gp120 binding proteins of the CD4-negative and Gal-C-negative, non-productively infectable human glioblastoma cell line D54 were purified by affinity chromatography over a gp120-conjugated sepharose column and identified by peptide microsequencing [22].
• Importantly, direct intratumoral injection of Delta-24, but not RA55, significantly suppresses tumor growth in intracranial (U-87 MG, U-251 MG) or subcutaneous (D54 MG) animal models [23].

References