Biomedical subjects

D Bevec

Publications and source records attributed to D Bevec.

44 records · Page 3Linked to original sources

PubMed1991

Developmental and tissue-specific expression of the Q5k gene.

Expression of the Q5k gene was examined by northern blot analysis and polymerase chain reaction (PCR) in the AKR mouse and various cell lines, each of the H-2k haplotype. Our results show that Q5k mRNA is present during the whole postimplantational development of the AKR embryo/fetus (gestation day 6 to 15). In the juvenile mouse (week 2 to 4) transcription of the Q5k gene persisted in all organs examined. In contrast, in the adult animal expression of the Q5k gene was limited to the thymus and uterus of the pregnant mouse. Upon malignant transformation, the amount of Q5k-specific mRNA increased dramatically in thymus and could also be observed in the spleen of thymoma bearing animals. Expression of the Q5k gene was also detectable in several transformed mouse cell lines. Mitogen stimulation or treatment with cytokines induced Q5k expression in primary spleen cell cultures. A possible explanation for the tissue-restricted expression in the adult AKR mouse is discussed.

Aging↗

PubMed1991

trans-activation of the HIV-1 LTR by the HIV-1 Tat and HTLV-I Tax proteins is mediated by different cis-acting sequences.

Human immunodeficiency virus type 1 (HIV-1) gene expression is regulated by viral and cellular factors interacting with cis-elements located in the retroviral long terminal repeat (LTR). In this report we analyzed HIV-1 LTR-specific regulatory sequences responsive to the HIV-1 Tat and HTLV-I Tax trans-activator proteins. Our results indicate that the Sp1 binding sites in the HIV-1 LTR are crucially involved in Tat-mediated gene expression in human Jurkat T-cells whereas they are dispensable for HTLV-I Tax-induced activation. In contrast, the NF-kB binding sites within the HIV-1 LTR are essential for Tax-mediated transcription but had only marginal effect on Tat-induced reporter gene expression.

Animals↗

PubMed1989

Biosynthesis of complement C4 messenger RNA in normal human kidney.

Complementary DNA (cDNA) probes were used to investigate the extrahepatic production of the major histocompatibility complex (MHC)-linked complement components C4, factor B and C2 in various normal human tissues. The presence of the corresponding messenger RNA (mRNA) was tested by Northern blot analysis. Complement C4 mRNA was found in liver, and with high intensity also in normal kidneys. In contrast, no C2 mRNA and only very low amounts of factor B mRNA could be detected in the kidney. Slot blot hybridization was performed to quantitate the amount of C4 mRNA, and the intensity of C4 mRNA hybridization in the kidney samples was about 25% compared with liver RNA. C4-specific transcripts were not present in isolated glomeruli but in the renal interstitium. Other human tissues, such as tonsil, spleen, thymus, brain, lung and peripheral mononuclear cells, contained no C4 mRNA. Low amounts of C4 mRNA were found in colon, thyroid gland, lymph node and breast carcinoma. The results obtained with lung, where C2 mRNA was found but no C4 mRNA, further indicate an independent, tissue-specific regulation of the class III gene expression. The results, showing that the complement C4 genes are transcribed very efficiently in normal human kidney, suggest a direct role of complement C4 in renal pathogenesis.

Adult↗

PubMed1988

Sequence of the mouse Q4 class I gene and characterization of the gene product.

The Q4 class I gene has been shown to participate in gene conversion events within the mouse major histocompatibility complex. Its complete genomic nucleotide sequence has been determined. The 5' half of Q4 resembles H-2 genes more strongly than other Q genes. Its 3' end, in contrast, is Q-like and contains a translational stop signal in exon 5 which predicts a polypeptide with an incomplete membrane spanning segment. The presence of two inverted B1 repeats suggests that part of the Q4 gene may be mobile within the genome. Gene transfer experiments have shown that the Q4 gene encodes a beta 2-microglobulin associated polypeptide of Mr 41,000. A similar protein was found in activated mouse spleen cells. The Q4 polypeptide was found to be secreted both by spleen cells and by transfected fibroblasts and was not detectable on the cell surface. Antibody binding and two-dimensional gel electrophoresis indicate that the Q4 molecule is identical to a mouse class I polypeptide, Qb-1, which has been previously described.

Amino Acid Sequence↗

PubMed1985

Control of synthesis and expression of H-2 heavy chain and beta-2 microglobulin in AKR leukemias.

In a series of newly isolated AKR leukemias, some tumors expressed large amounts of both H-2K and H-2D molecules, while others had reduced levels of both antigens. The number of H-2 antigens expressed in steady state showed a consistent correlation with the rate of synthesis of the H-2 class I heavy chain and the beta-2 microglobulin (beta 2m) light chain, and with the amount of H-2- and beta 2m-specific mRNA present in the tumors. Stimulation of leukemic cells with interferon induced an increased transcription of both H-2 and beta 2m mRNA. These results suggest that there is a mechanism that regulates, at the transcriptional level, the coordinate expression of H-2K and H-2D heavy chains, and the beta 2m light chains encoded by genes on chromosomes 17 and 2, respectively.

Animals↗

PubMedDate not supplied

Aberrant MHC antigens in a sarcoma virus-induced mouse tumour.

From a series of mouse sarcomata, newly induced by Rous sarcoma virus (RSV), the DOH cell line was shown to lack expression of syngeneic H-2Kd and Dk antigens (Noll et al., 1986). It unexpectedly displayed determinants specific for H-2Kk molecules. Interferon treatment of DOH stimulated the expression of H-2Kk determinants and also the display of some, but not all, determinants of the syngeneic H-2Kd molecules. H-2Dk expression was not stimulated. Southern blot hybridization of genomic DNA digests from DOH cells confirmed the identity of the H-2K region with that from syngeneic C3H.OH liver cells, but also showed changes in the pattern of restriction fragments that contain class I genes from the D and Qa regions. These results suggest that aberrant MHC class I molecules that carry H-2Kd- and H-2Kk-like determinants are expressed by DOH sarcoma cells. These molecules may act as target antigens for tumour-specific cytotoxic T cells elicited by injection of DOH cells into syngeneic mice.

Animals↗

PubMedDate not supplied

Organization of the AKR Qa region: structure of a divergent class I sequence, Q5k.

We established the organization of the AKR Qa region and determined the sequence of the Q4 and Q5 genes. Restriction mapping and genomic Southern blot analysis revealed that the AKR strain codes for only three H-2K homologous genes in this region. The AKR Q5 gene is not homologous to the Q5 gene of the C57BL strain, but is presumably allelic to the Q5 gene isolated from Balb/c. The organization and structure of the AKR Qa family is virtually identical to the Qa genes of the C3H mouse. The AKR Q5 gene, in contrast to other H-2K homologous Qa region genes, codes for a typical transmembrane region, and upon transfection into BHK cells, a 1.6 kb Q5 transcript is detected.

Amino Acid Sequence↗

PubMedDate not supplied

Eukaryotic initiation factor 5A activity and HIV-1 Rev function.

Eukaryotic initiation factor 5A (eIF-5A) is the only cellular protein known to contain the unusual amino acid hypusine, a modification that appears to be required for cell proliferation. This hypusine-modified protein stimulates synthesis of methionyl-puromycin in an in vitro assay which mimics the formation of the first peptide bond during protein synthesis, although the exact role of eIF-5A in vivo is still unknown. The unexpected finding that eIF-5A is a cellular cofactor of the HIV-1 Rev trans-activator protein may, however, provide a novel opportunity to reveal precisely what function eIF-5A performs in eukaryotic cells. In this review article, we first present a brief description of HIV-1 Rev function, followed by an overview of the data that identified eIF-5A as a Rev cofactor and, finally, discuss novel findings with respect to cellular eIF-5A activities.

Amino Acid Sequence↗