Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal human sera were analyzed for the presence and molecular form of two human melanoma-associated antigens (MAAs), the 250 "melanoma-specific" glycoprotein and the 100 K "common tumor antigen". The 250 K MAA was not synthesized by any cultures other than human melanoma and was not detectable in normal human serum. In contrast, the 100 K MAA, which is present in spent medium of cultured human melanoma, carcinoma and fetal melanocytes but not of adult normal cells, was found in normal human serum in nanogram quantities. This serum form of the 100 K MAA was also found in pooled sera of higher apes but not of lower species. The cell-derived form of the 100 K MAA, present in spent culture medium, had a similar phylogenetic distribution. The molecule was produced by cultured brain glia from gorilla, but not by melanoma cells from miniature swine or dog. The 100 K MAA from gorilla glia had a mol. wt identical to the molecule produced by human melanoma cells. Molecular characterization of this MAA in normal human serum showed that it was heterogeneous in size and was present in fractions greater than 100 kd after analytical HPLC gel sieving under non-denaturing conditions. In contrast, MAA from spent culture medium of melanoma cells was 100 kd or less in chemically defined medium (CDM) with no protein supplement, but had a higher mol. wt in CDM with BSA or fetal calf serum supplement, similar to the serum form of the molecule. An association of the 100 K MAA with albumin was demonstrated by analytical HPLC gel sieving and SDS-PAGE analysis of monoclonal antibody immunoprecipitates. The 100 K MAA was dissociated from albumin in normal human serum by treatment with SDS and fractionation by gel sieving. Under these conditions 100 K MAA from serum co-migrated with similarly treated 100 K from melanoma cells. These results indicate that the 100 K MAA is a normal serum constituent which forms a strong, non-covalent association with albumin and is evolutionarily restricted to higher apes or humans.
Mol Immunol 1983 Dec
PMID:Monoclonal antibody defined-human melanoma-associated antigens: molecular and phylogenetic studies in normal serum. 665 76

A monoclonal antibody, 16B-13, derived from the immunization of BALB/c mice with a lung tumor line, immunoprecipitates a common tumor-associated molecule with an apparent mol. wt of 37,000 from lactoperoxidase-iodinated lung carcinoma, colon carcinoma, gastric carcinoma, brest carcinoma, melanoma and lymphoma cells, but not from normal fibroblasts. Analysis by two-dimensional gel electrophoresis of the cell surface-labeled 16B-13 antigen from a colorectal and a melanoma cell line reveals four components with similar mol. wts but with different isoelectric points. The antigen purified from a colorectal carcinoma cell line by immunoaffinity chromatography was shown to be a 37,000 mol. wt polypeptide similar to that obtained by the lactoperoxidase-labeling procedure. However, the purified antigen from the melanoma cell line shows the presence of a 65,000 mol. wt polypeptide and the loss of the 37,000 mol. wt component as detected by Coomassie blue staining and immunoprecipitation.
Mol Immunol 1983 Dec
PMID:Identification and isolation of a common tumor-associated molecule using monoclonal antibody. 665 79

We report that endogenous, as well as exogenous, interferon (IFN) regulates the growth of human melanoma cells in culture. When antibodies directed against human fibroblast IFN were incorporated into the media of high-density cells stimulated to proliferate with serum, the cells entered the cell cycle earlier than did the controls. In investigating the biochemical basis for this finding, we have found that there is an inverse relationship between the (2'-5')oligoadenylate synthetase levels and the percentage of cells in S in untreated cultures. Upon IFN treatment, the relationship is obliterated and (2'-5')oligoadenylate synthetase levels increase throughout all phases of the cell cycle. This increase in enzyme levels correlates well with the decreased probability of the IFN-treated cells to cycle. These findings suggest a biological role for IFN as a negative growth factor for cells in culture.
Mol Cell Biol 1983 May
PMID:Growth regulation of melanoma cells by interferon and (2'-5')oligoadenylate synthetase. 686 41

Tuftsin, a physiological tetrapeptide derived from the Fc region of leukophilic IgG possesses a variety of immunopotentiating properties including the ability to act as an immunotherapeutic agent against the experimental tumors, L1210 leukemia and Cloudman S-91 melanoma. Although the mechanism of action of tuftsin in vivo is not known, several types of leukocytes have been shown to become cytotoxic effector cells following activation with tuftsin. These cells presently include macrophages, natural killer cells, and granulocytes. The possibility that tuftsin can also activate other types of effector cells have not been ruled out. We feel this small peptide has a high potential (largely unrecognized) as an antitumor immunopotentiating agent. It is naturally occurring in man and appears to be relatively non-toxic. Its exact sequence (Thr-lys-Pro-Arg) is known and it can be chemically synthesized. Methods are also available to monitor the levels of tuftsin in body fluids. These properties along with its ability to control infectious disease make this agent one of the more promising immunopotentiators.
Mol Cell Biochem 1981 Dec 04
PMID:Antitumor effect of tuftsin. 689 73

The relationship between bromodeoxyuridine (BrdUrd) mutagenesis in mammalian cells and the effects of BrdUrd on deoxyribonucleoside triphosphate pools was analyzed. It was found that the exposure of Syrian hamster melanoma cells to mutagenic concentrations of BrdUrd resulted in the formation of a large bromodeoxyuridine triphosphate (BrdUTP) pool, which remained at a high level for several days. In contrast, the size of the deoxycytidine triphosphate (dCTP) pool dropped rapidly after the addition of BrdUrd, reached a minimum at about 6 h, and then expanded gradually to nearly its original level over the next 3 days. The addition of lower concentrations of BrdUrd, which had less of a mutagenic effect, resulted in the formation of a smaller BrdUTP pool and a slightly smaller drop in the dCTP pool. When a high concentration of deoxycytidine was added at the same time as a normally mutagenic concentration of BrdUrd, the drop in the dCTP pool was prevented, as was BrdUrd mutagenesis. In all of these experiments, mutagenesis was related to the ratio of BrdUTP to dCTP in the cells. In addition, it was shown that mutagenesis occurred primarily during the first 24 h of BrdUrd exposure, when the BrdUTP/dCTP ratio was at its highest level. It appears that there is a critical ratio of BrdUTP to dCTP that must be attained for high levels of mutagenesis to occur and that the extent of mutagenesis is related to the ratio of the BrdUrd and dCTP pools.
Mol Cell Biol 1981 Mar
PMID:Bromodeoxyuridine mutagenesis in mammalian cells is related to deoxyribonucleotide pool imbalance. 696 99

The pineal hormone melatonin modulates constitutive protein secretion from melanoma M2R cells. Nanomolar concentrations of melatonin inhibited protein secretion early after plating or at low cell density, but facilitated it late after plating or at high cell density. Inhibition by melatonin of adenylate cyclase is the best known downstream response to melatonin. We have therefore examined the involvement of cAMP in the melatonin-mediated modulation of protein secretion from the melanoma cells. Melatonin slightly but significantly reduced cell cAMP content when effecting inhibition and marginally increased cAMP levels when effecting facilitation of protein secretion. Dibutyryl cAMP abrogated the melatonin-mediated inhibition but not facilitation of protein secretion without affecting basal secretion. Accordingly, forskolin prevented the inhibitory action of melatonin on protein secretion without affecting basal secretion. The selective protein kinase A inhibitor H-89 did not alter the inhibitory effect of melatonin at low cell density and slightly facilitated secretion at high cell density with or without melatonin. Thus, melatonin's effects on protein secretion may not be mediated via cAMP. Nevertheless, changes in cAMP or protein kinase A activity can abrogate, or mask, the melatonin-mediated responses.
Mol Cell Endocrinol 1995 Aug 11
PMID:Modulation by melatonin of protein secretion from melanoma cells: is cAMP involved? 748 20

Colourimetric assays which rely on the conversion of metabolic dyes are becoming increasingly used for measuring cell proliferation and cytotoxicity. We developed a method for measuring cellular responsiveness to interferons based on the property of interferons to induce cell defenses to virus-mediated killing. The assay has several advantages over previous assays for measuring anti-viral activity and efficiently detected cytoprotective responses to human interferon of five human melanoma cell lines infected with Semliki Forest virus. The melanoma cell lines showed a varying cytoprotective response to interferons alpha 2, alpha 4, beta and gamma, in agreement with the results of previous assays for measuring melanoma cell responsiveness to interferons based upon the inhibition of cell growth (1).
Biochem Mol Biol Int 1993 Dec
PMID:A colourimetric dye assay to detect anti-viral activity of interferons: sensitivity for measuring cellular responsiveness to interferons. 751 20

Interstitial deletions of the short arm of chromosome 9 are associated with glioma, acute lymphoblastic leukemia, melanoma, mesothelioma, lung cancer, and bladder cancer. The distal breakpoints of the deletions (in relation to the centromere) in 14 glioma and leukemia cell lines have been mapped within the 400 kb IFN gene cluster located at band 9p21. To obtain information about the mechanism of these deletions, we have isolated and analyzed the nucleotide sequences at the breakpoint junctions in two glioma-derived cell lines. The A1235 cell line has a complex rearrangement of chromosome 9, including a deletion and an inversion that results in two breakpoint junctions. Both breakpoints of the distal inversion junction occurred within AT-rich regions. In the A172 cell line, a tandem heptamer repeat was found on either side of the deletion breakpoint junction. The distal breakpoint occurred 5' of IFNA2; the 256 bp sequenced from the proximal side of the breakpoint revealed 95% homology to long interspersed nuclear elements. One- and two-base-pair overlaps were observed at these junctions. The possible role of sequence overlaps, and repetitive sequences, in the rearrangement is discussed.
Mol Cell Biol 1994 Nov
PMID:Breakpoint junctions of chromosome 9p deletions in two human glioma cell lines. 752 63

Recently, we defined the antigenic epitope recognized by the human monoclonal antibody L94 to be a protein with a C-terminal sequence of alanine-proline (AP). An antigenic peptide no. 707 (RVAALARDAP), which was identified by the use of cDNA libraries of an antigen positive melanoma cell line M14, was evaluated for cellular immune responses in melanoma patients. PBMC from 16 of 19 melanoma patients were shown to lyse autologous B lymphoblastoid cell lines (BCL) pulsed with synthetic peptide no. 707 (hereafter no. 707). This specific cytotoxicity to the peptide significantly increased in 84% of melanoma patients after in vivo immunization with a melanoma cell vaccine (MCV). In contrast, peptide specific cytotoxicity was observed in only one of 19 normal volunteer donors. In vitro restimulation of MCV treated patients' PBMC with no. 707 augmented cytotoxicity against autologous no. 707-pulsed BCL. This cytotoxicity was specific to the C-terminal sequence AP, since the removal of C-terminal AP completely abolished the specific lysis. no. 707 restimulation of PBMC enhanced cytotoxicity against autologous melanomas. Autologous melanoma and peptide-pulsed BCL targets were lysed by CD8+CTL in a HLA class I-restricted manner. The strong cytotoxicity was obtained from patients of HLA A24. CTL lysis of autologous no. 707-pulsed BCL was partially blocked by unlabeled autologous melanomas in a cold target inhibition test. This suggested that the epitope identical or cross-reactive to no. 707 may be presented on the melanoma cell surface by HLA class I antigens. Our findings suggest that peptide no. 707 presented on human melanoma cells is recognized by CTL and that C-terminal AP plays a critical role in both antibody and T cell recognition.
Mol Immunol 1995 Jun
PMID:Cytotoxic T cell recognition of a human melanoma derived peptide with a carboxyl-terminal alanine-proline sequence. 754 91

The quantification of messenger RNA is central in studies of gene expression. We describe a quantitative assay for specific mRNAs (QASM) that measures mRNAs for insulin-like growth factor-I, IGF binding proteins (IGFBPs) -2, -3, -4, and -5, and beta-actin. The assay utilizes reverse transcription and polymerase chain reaction, followed by an ELISA based DNA assay technique. The use of internal (competitive) quantification standards gave poorly linear results, while external standards gave linear and reproducible results. QASM results correlated with IGFBP protein concentrations in conditioned medium and with mRNA levels determined by Northern blotting. QASM was used to study IGFBP expression in human malignant melanoma cells. Messenger RNA for IGFBP-2, -3, and -5 were present, while IGF-I and IGFBP-4 mRNAs were not detected. IGFBP-2 and -3 expression was increased in a dose dependent manner by treatment with IGF-I. Protein concentrations in conditioned media paralleled mRNA levels. QASM is a sensitive, specific, and reproducible approach to determining mRNA levels.
Mol Cell Endocrinol 1995 Apr 28
PMID:A quantitative assay for IGF-I and IGF binding protein mRNAs: expression in malignant melanoma cells. 754 21


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