Disease relevance of FAM48A

• In the 5% chromosomal environment of C13 we detected changes of the allelic status in 13 of 21 prostate cancers [1].
• In contrast, C13orf19 mRNA alterations in expression seemed to be random events in kidney cancers [2].
• Cisplatin (DDP)-resistant 2008 human ovarian carcinoma cells (C13*) have an elevated mitochondrial membrane potential that confers hypersensitivity to lipophilic cations [3].
• The elevated mitochondrial membrane potential and ensuing rhodamine 123 (Rh123) hypersensitivity of C13* cells provided a positive selection rationale [3].
• The membrane glycoproteins from control (BHK21/C13) and Rous sarcoma virus-transformed (C13/B4) baby hamster kidney cells grown in medium containing [14C]- or D-[3H]glucosamine have been separated into two distinct classes: a phenol-soluble fraction and an aqueous fraction [4].

High impact information on FAM48A

• Amino acid substitutions predicted to disrupt either the amphipathic or alpha-helical nature of C13 rendered the peptide inactive [5].
• An antiserum prepared against purified surface membranes of transformed BHK21/C13 cells (C13/B4) reversibly rounded and detached hamster cells from plastic tissue culture plates but did not affect cells of other species [6].
• It was found that luminamicin has the S, S, R, R, R, R, S, S, S, R, and S configurations at C2, C4, C7, C9, C10, C11, C12, C13, C16, C28, and C29, respectively [7].
• The hydrophobic region from C13 to C19 is also essential in binding and appears to act as an anchor in a hydrophobic domain of the glucose carrier [8].
• These changes can be observed with water-suppressed proton (H-1) and carbon-13 (C-13) nuclear magnetic resonance spectroscopy (NMR) and gas chromatography [9].

Chemical compound and disease context of FAM48A

• The membrane glycoproteins from control (BHK21/C13) and Rous sarcoma virus-transformed (C13/B4) baby hamster kidney cells labeled with D-[14C]- or D-[3H]glucosamine, respectively, were purified by means of polyacrylamide electrophoresis and gel electrofocusing [10].
• The limited induction of spermidine/spermine N1-acetyltransferase (SSAT) activity has been implicated as an important determinant of the reduced response to the spermine analogue N1,N12-bis(ethyl)spermine (BESpm) by the cisplatin or cis-diamminedichloroplatinum(II) (cDDP)-resistant human ovarian carcinoma cell line (C13*) [11].
• Comparisons of membrane glycopeptides from baby hamster kidney fibroblasts (BHK21/C13) and a clone transformed by Rous sarcoma virus (C13/B4) were made by using cells metabolically labeled with radioactive D-glucose and L-fucose [12].
• METHODS: H. pylori infected dyspepsia patients referred to our C13 urea breath testing laboratory between January 1999 to February 2002 were included [13].
• Spermine toxicity and glutathione depletion in BHK-21/C13 cells [14].

Biological context of FAM48A

• Quantitative real-time PCR was performed for C13orf19, a gene located on chromosome 13q and previously described to be down-regulated in prostate carcinoma, on different cancer cell lines, on matched prostate tissues from 61 patients with prostate carcinoma and on matched kidney tissues from 23 patients with renal clear cell carcinoma [2].
• However, an at least 1.5-fold C13orf19 mRNA downregulation was observed in samples from 28 patients (46%) and an at least 1.5-fold upregulation was observed in samples from 17 patients (28%) [2].
• In addition, in these samples the C-13 NMR spectra showed direct evidence of lipid peroxidation products [9].
• Cytokines, known to be released in response to malignant tumor cells and to affect lipid metabolism, were injected into normal mice and their effects on the H-1 and C-13 NMR spectra of plasma lipids were observed [9].
• The most prominent metabolite, termed M5, corresponded to an hydroxylation at the C6 position on the taxane ring, while the other metabolite, termed M4, corresponded to an hydroxylation at the para-position on the phenyl ring at the C3'-position of the C13 side chain [15].

Anatomical context of FAM48A

• BHK21/C13 and various BHK21 tumors all appeared to grow to concentration densities markedly higher than hamster embryo fibroblasts [16].
• A main docetaxel metabolite was generated by human liver microsomes in the presence of NADPH: retention time in high pressure liquid chromatography and its ion fragmentation in mass spectrometry were identical to those of the authentic derivative hydroxylated at the butyl group of the C13 side chain [17].
• Three human tumor cell lines made resistant to cis-diamminedichloroplatinum(II) (CDDP), SCC-25/CP, MCF-7/CP, and C13, are more sensitive to rhodamine-123 [tetrachloroplatinum(II)] [(PtCl4(Rh-123)2] than are the corresponding parental cell lines [18].
• A second enzymic activity detected in the oocytes (hydroperoxide lyase) cleaves specifically the (8R)-hydroperoxy substrate into C7 and C13 fragments, identified as the hydroxyacid, (5Z)-7-hydroxyheptenoic acid, and two aldehydes, (2E,4Z,7Z)-tridecenal and its 4E isomer [19].
• Human granulocyte colony stimulating factor (G-CSF) can support the survival and short term proliferation of the interleukin 3 (IL 3)-dependent diploid murine hemopoietic progenitor cell line 32D C13 [20].

Associations of FAM48A with chemical compounds

• These results indicate that the bypass response in the C13* line has some degree of specificity for cisplatin adducts [21].
• The DN reductase associated with CBR reduces the C13 methyl ketone group and does not metabolize the quinone ring of DN [22].
• RH4 cells displayed the same DDP accumulation defect, 2-fold elevated glutathione levels and 2-fold resistance to CdCl2 as C13* cells [3].
• We then examined the specificity of this enhanced bypass by repeating the steady-state assay with the 2008 and C13* lines using as damaging agents 1,2-diaminocyclohexanedichloroplatinum(II), UV radiation (producing pyrimidine dimers), and benzo(a)pyrene-7,8-diol-9,10-epoxide [21].
• We have investigated the inhibition of the recently identified family C13 cysteine peptidase, pig legumain, by human cystatin C [23].

Analytical, diagnostic and therapeutic context of FAM48A

• Fluorescence in situ hybridization, Southern blotting and radiation hybrid mapping demonstrated a chromosomal localization of C13 on 13q12-14 closest to the SHGC-34125 marker [1].
• A C13orf19 quantitative PCR (QPCR) showed the mRNA to be down-regulated in matched prostate tissues (P=0.007 and lower, paired Student's t-test) [2].
• 0. Our results show that the pronase glycopeptides of 20 out of 24 homologous membrane glycoproteins of equivalent molecular weight and isoelectric point from BHK21/C13 and C13/B4 cells are dissimilar as measured by Sephadex G-50 gel filtration [4].
• A number of aqueous and phenol-soluble glycoproteins from BHK21/C13 and C13/B4 cells were purified to near homogeneity by means of polyacrylamide electrophoresis and gel electrofocusing [4].
• We employed cDNA microarrays to identify the differentially expressed genes in a cisplatin-sensitive parental (2008) human ovarian carcinoma cell line and its cisplatin-resistant variant (2008/C13*) [24].

References