The C-terminal peptide of the heavy chain of the rabbit immunoglobulin IgG.
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Amino Acid Sequence↗
Biomedical subjects
D Givol
Publications and source records attributed to D Givol.
A single gene and a pseudogene for the cellular tumour antigen p53.
The cellular tumour antigen p53 is a protein found in elevated levels in a great variety of transformed cells (reviewed in ref. 1). Overproduction of p53 was observed in cells transformed by a wide spectrum of agents as well as in embryonal carcinoma cells, and in spontaneous transformants. Although initially described in mice, similar p53-like proteins were also observed in cells of other species, including those derived from several human tumours. In non-transformed cells the protein turns over very rapidly and its levels appear to correlate with cell proliferation. Thus far, very little has been known about the precise nature of the protein and of the corresponding genes. We now provide evidence for the existence of a single functional gene for murine p53 and a processed pseudogene. The predicted amino acid sequence of murine p53 is also presented.
Amino Acid Sequence↗
Rearrangement of the oncogene c-mos in mouse myeloma NSI and hybridomas.
The activity and products of cellular oncogenes can be altered by various processes, such as the nearby integration of a retroviral genome, point mutation within the oncogene coding region, gene amplification, and chromosomal translocation (reviewed in ref. 1). Our work has provided an example of oncogene activation by yet a different process; the integration of an endogenous retrovirus-like DNA element (identified as an intracisternal A particle or IAP genome) within the coding region of the oncogene c-mos in a mouse plasmacytoma, XRPC 24. The rearranged c-mos gene of XRPC24 is actively transcribed and has transforming activity, suggesting some role for activated c-mos in the progression of the XRPC24 tumour. In this report we describe rearrangement of c-mos in a second mouse plasmacytoma, NSI, and in two hybridomas. In this case, as in XRPC24, c-mos was split by the insertion of a IAP genome. The rearranged c-mos genes (rc-mos) of NSI and XRPC24 differ in three major aspects: (1) The site of IAP integration in c-mos is in codon 30 in NSI but in codon 88 in XRPC24; (2) The orientation of the integrated IAP relative to c-mos is 'tail-to-head' in NSI and 'head-to-head' in XRPC24; and (3) transcriptional activity of rc-mos in NSI is much lower than in XRPC24. The two latter points suggest a correlation between the orientation of the long terminal repeat (LTR) of IAP relative to c-mos and its activity upon IAP integration.
Animals↗
Participation of p53 cellular tumour antigen in transformation of normal embryonic cells.
The cellular tumour antigen p53 is found at elevated levels in a wide variety of transformed cells (for reviews see refs 1, 2). Very little is yet known about the precise relationship of p53 to malignant transformation. Although the increase in p53 levels could be a secondary by-product of the transformed state, it is equally possible that p53 is actively involved in altering cellular growth properties, especially as it has been implicated in the regulation of normal cell proliferation. We sought to test whether p53 could behave in a manner similar to known genes in a biological test system, and we demonstrate here that p53 can cooperate with the activated Ha-ras oncogene to transform normal embryonic cells. The resultant foci contain cells of a markedly altered morphology which produce high levels of p53. Cell lines established from such foci elicit tumours in syngeneic animals.
Animals↗
Localization of gene for human p53 tumour antigen to band 17p13.
Recently the gene for the cellular tumour antigen p53, a phosphoprotein found in increased concentration in a variety of human cells, had been mapped to region 17q22 by in situ hybridization techniques and has been shown to translocate to the chromosome carrying the translocation [t(15; 17)] associated with acute promyelocytic leukaemia (APL). Based on this finding it has been postulated that this gene has a role in the pathogenesis of APL. Here we present evidence that the gene for p53 is not located on the long arm of chromosome 17, but maps to band 17p13. We therefore suggest that this gene is not directly involved in the chromosome translocation observed in APL.
Antigens, Neoplasm↗
Ligand binding by fibroblast growth factor receptors investigated using chimeric receptor molecules.
In order to map in detail the ligand binding sites of fibroblast growth factor receptor 2 (FGFR2) and keratinocyte growth factor receptor (KGFR), we have generated receptor molecules that are chimeric within the membrane proximal sequence that varies between them. The chimeric molecules are found to bind aFGF with a greater than 5-fold difference in affinity, indicating that there is coupling between the chimeric regions with respect to aFGF binding. Further, binding of bFGF and KGF is abolished in the chimeras, showing that the binding site for these ligands requires the whole of the 48- or 50- amino acid variable sequence to be intact. Direct interactions between the different regions exchanged in the chimeras are most probably involved in forming KGF or bFGF binding sites.
3T3 Cells↗
Combining site and antigenic determinants of the V regions.
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Animals↗