Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.2 (focal adhesion kinase)
 44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We isolated overlapping cDNA clones corresponding to the major MET protooncogene transcript. The cDNA nucleotide sequence contained an open reading frame of 1408 amino acids with features characteristic of the tyrosine kinase family of growth factor receptors. These features include a putative 24-amino acid signal peptide and a candidate, hybrophobic, membrane-spanning segment of 23 amino acids, which defines an extracellular domain of 926 amino acids that could serve as a ligand-binding domain. A putative intracellular domain 435 amino acids long shows high homology with the SRC family of tyrosine kinases and within the kinase domain is most homologous with the human insulin receptor (44%) and v-abl (41%). Despite these similarities, however, we found no apparent sequence homology to other growth factor receptors in the putative ligand-binding domain. We conclude from these results that the MET protooncogene is a cell-surface receptor for an as-yet-unknown ligand.
Proc Natl Acad Sci U S A 1987 Sep
PMID:Sequence of MET protooncogene cDNA has features characteristic of the tyrosine kinase family of growth-factor receptors. 281 73

A serum-albumin-alprenolol conjugate was used to isolate beta-adrenergic receptors from the human A431 cell lysates. Three monoclonal antibodies were obtained from BALB/c mice immunized with these receptors. These antibodies: BRK-1, BRK-2, BRK-3, were respectively of the IgM, IgG2a and IgG3 classes. All three antibodies recognized photoaffinity-labelled receptors, immunoprecipitated ligand-binding activity and identified the 65-kDa and 55-kDa polypeptides corresponding to the beta 2-adrenergic receptors of A431 cells. BRK-2 and BRK-3 recognized both beta 1 and beta 2-adrenergic receptors of several mammalian cells. All three antibodies visualized, by immunofluorescence, the beta 2-adrenergic receptors at the surface of A431 cells. The monoclonal antibodies are directed against the protein portion of the beta-adrenergic receptors since partial or complete removal of the carbohydrate moieties by treatment with endoglycosidase such as endo-F (endo-beta-N-acetylglucosaminidase F) and periodate oxidation did not affect the immunoreactivity. These antibodies will be of value to immunopurify the beta-adrenergic receptors.
Eur J Biochem 1987 Sep 15
PMID:Monoclonal antibodies directed against the human A431 beta 2-adrenergic receptor recognize two major polypeptide chains. 282 Jul 27

The in vivo photosensitizing efficacy of mono-L-aspartyl chlorin has been studied by determining the percentage of BALB/c mice cured at varying doses of drug. Using an EMT-6 tumor model, animals received i.p. injections of mono-L-aspartyl chlorin (0.5-100 mg/kg) and then were subsequently exposed to light at 664 nm. Tumor biopsies were taken from selected animals sacrificed at 24 h after treatment and routine histopathological sections made. The other animals remained in the dark for a period of 6 weeks to determine the cure rate. Our results show that mono-L-aspartyl chlorin is an effective tumor localizer that brings about the selective degradation of tumor tissue following light exposure.
Cancer Res 1987 Sep 01
PMID:In vivo studies on the utilization of mono-L-aspartyl chlorin (NPe6) for photodynamic therapy. 295 47

We studied fundamentally subrenal capsule assay, using human tumor specimens (gastric, breast and pancreas cancers) serially transplanted in nude mice. Any prominent difference of host reaction was not found between the host of BALB/c-nu/+, BALB/c-+/+ and CDF1 mice. Using immunocompetent BALB/c-nu/+ mice, experimental chemotherapy with mitomycin C (MMC) and 5-fluorouracil (5-FU) was carried out. On day 6, macroscopic and histological findings corresponded relatively well with 5-FU effect but not with MMC. Using BALB/c-nu/nu mice, we tried 15-day SRC assay. When the sensitivity of anti-cancer drugs was compared between early and intermediate phase after inoculation, no obvious difference was found macroscopically and histologically. BALB/c-nu/nu mouse will be useful as a host of SRC assay, and could be applicable to clinical fresh cases.
Gan To Kagaku Ryoho 1987 Sep
PMID:[Subrenal capsule assay as a chemosensitivity test (III)--Comparison of host reaction, experimental chemotherapy and use of nude mice]. 311 83

The vast majority of pediatric RBC hypoplastic anemias are accounted for by red blood cell aplasia associated with chronic hemolysis, Diamond-Blackfan anemia, and transient erythroblastopenia of childhood. However, other causes of hypoplastic anemia occur in children, and some of these are similar to what is seen in adult RBC aplasia. For example, it has been reported that a 5-year-old girl with an aregenerative anemia had a thymoma and later developed pancytopenia. RBC aplasia also has been seen in children receiving anticonvulsant drug therapy, children recovering from severe protein malnutrition, children with hepatitis, and in children with leukemia during maintenance therapy. In addition, it is not uncommon for pediatric hematologists to observe children with RBC aplasia where there is no obvious diagnosis, although many are considered to be variants of Diamond-Blackfan anemia. Several important questions about RBC hypoplastic anemias in children need to be resolved; it is hoped that this will be accomplished in the next decade. Do RBC hypoplastic crises associated with hemolytic anemia occur with viral infections other than HPV? What is the cellular pathophysiology in DBA and TEC? Does the apparent heterogeneity of these disorders reflect limitations of laboratory techniques or are we looking at several different diseases? Is acute leukemia a real complication of Diamond-Blackfan anemia? Is TEC a completely benign entity or will we see other long-term problems in these children? Is the incidence of TEC actually increasing? Will TEC-like problems be seen in other aged children? As a case in point, we recently observed a 16-year-old girl who presented with pure RBC aplasia that required RBC transfusion support for 5 months; she also received prednisone therapy. After 7 months, however, this young lady had a spontaneous remission, and now 4 years later she is normal and free of any hematologic abnormalities. This was a most unusual event in our experience and, in view of the apparent increasing incidence of TEC in young children, we queried whether we were observing an adolescent equivalent of this disorder. During the next several years the answer to this and the other questions posed herein should be available.
Hematol Oncol Clin North Am 1987 Sep
PMID:Diagnosis and management of red cell aplasia in children. 312 94

The differential regulation of immunoactive FSH and LH secretion by endogenous GnRH was studied using a GnRH antagonist, [Ac-D2Nal1,D4FPhe2,DTrp3,DArg6]GnRH (the NAL-ARG antagonist), in normal women in the early follicular phase of the menstrual cycle, and their responses were compared to those in two groups of control women. Pulsatile LH secretion was examined as an index of the completeness of blockade of endogenous GnRH secretion. There was a dose-dependent decrease in both the frequency and amplitude of LH pulses. At the highest dose, LH pulses were completely abolished within 20 min after sc administration of the GnRH antagonist and for a minimum of 8 h in all women. The mean plasma LH levels were reduced within the first 4 h after antagonist administration at all doses (P less than 0.001). The duration of LH suppression was influenced by antagonist dose, with a continued effect 24 h after administration of the 500 micrograms/kg dose only. The maximum degree of LH suppression was 40% after 50 micrograms/kg (n = 6), 60% after 150 micrograms/kg (n = 6), and 59% after 500 micrograms/kg (n = 5). In contrast, plasma immunoreactive FSH levels did not change after these doses of the NAL-ARG GnRH antagonist. The maximum degree of FSH suppression was 16%, and the changes in plasma FSH concentrations were not dose dependent. Serum antagonist concentrations rose within 30 min after its administration to mean peak levels of 7.5 +/- 2.1 (+/- SE), 20.4 +/- 6.1, and 151 +/- 21 ng/mL after the 50, 150, and 500 micrograms/kg doses, respectively. The half-time of the disappearance of the NAL-ARG GnRH antagonist from plasma was 8.8 +/- 1.5 h. While there were no effects of antagonist administration on hematological, hepatic, or renal function, three women developed urticaria distant from the site of injection when administered the highest dose. We conclude that blockade of GnRH receptors by a GnRH antagonist 1) effectively antagonizes the action of GnRH, as assessed by its ability to block pulsatile LH secretion and reduce mean plasma LH levels; and 2) inhibits LH release to a considerably greater degree than FSH release, providing further evidence of possible GnRH-independent FSH secretion.
J Clin Endocrinol Metab 1988 Sep
PMID:Evidence of differential control of FSH and LH secretion by gonadotropin-releasing hormone (GnRH) from the use of a GnRH antagonist. 313 43

The expression, properties and relationship of two mouse embryonic antigens (TEC-1 and TEC-2), which are defined by monoclonal antibodies, were investigated in the epididymis of four rodent species. Absorption analysis, indirect immunofluorescence microscopy and immunohistochemistry revealed that all the species studied contained in their epididymides, but not in testes, either TEC-1 (Chinese hamster), TEC-2 (guinea pigs, rats) or both TEC-1 and TEC-2 (mice) antigens. In an indirect immunofluorescence assay, the antigens were found on spermatozoa isolated from caudae epididymides of guinea pigs, rats and Chinese hamsters but not mice. On the other hand, the TEC-2 antigen, which is expressed on mouse eggs, was not detected on eggs from the other species studied. Immunolabeling of epididymal extracts separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that both epididymal antigens have apparent molecular weights of greater than 200,000. In guinea pigs, rats and mice, the antigens were detected by a two-site sandwich radioantibody-binding assay in which the antigen is immobilized and detected with the same antibody; this indicates that several antigenic determinants were present on the same carrier. In mice, some carriers seem to express both TEC-1 and TEC-2 epitopes. In Chinese hamsters, TEC-1 antigen was only detected by the solid-phase assay, suggesting that in this species there are markedly fewer antigenic determinants per carrier molecule. Interspecies differences in the activities of epididymal glycosyltransferases and/or glycosidases appear to be the biochemical mechanism of the species-specific expression of these antigens.
Cell Differ 1987 Sep
PMID:Differential expression of mouse embryonic antigens TEC-1 and TEC-2 in the epididymis of four rodent species. 330 64

The Gardnerella vaginalis-infection of the urogenital tract is of clinical importance in females and of epidemiological importance in males. Females suffer from Bacterial Vaginosis, with a foul-smelling grey vaginal discharge with a pH of 5.0-5.5 which contains "clue cells", and from Sepsis. The isolation and identification of G. vaginalis i necessary in man. If G. vaginalis-infection is suspected, simultaneous infections with further STD-agents such as N. gonorrhoeae, C. trachomatis etc should be excluded. Metronidazole (1 g/day for 5 days) is the drug of choice in G. vaginalis-infection.
Urologe A 1987 Sep
PMID:[Gardnerella vaginalis infection. Clinical aspects, diagnosis and therapy]. 331 83

We assessed the use of a colorimetric assay for determination of radiosensitivity for cells taken directly from murine solid tumors. The assay uses microtier plates and measures the ability of viable cells to reduce a tetrazolium salt (MTT) to an insoluble form, a formazan salt. We established the dependency of the assay on the cell number and time of assay for two murine tumors (EMT-6 and RIF-1). We compared the MTT assay to the standard clonogenic assay and had good agreement of surviving fraction after radiation doses of 2 and 4 Gy. It is possible, therefore, to adapt the MTT assay for use with cell suspensions prepared directly from fresh murine tumors. This may provide a methodology for the determination of the clinical radiosensitivity of tumors including fresh clinical tumor specimens.
Int J Radiat Oncol Biol Phys 1988 Sep
PMID:Use of a colorimetric microtiter (MTT) assay in determining the radiosensitivity of cells from murine solid tumors. 341 90

4'-(9-acridinylamino) methanesulfon-m-anisidide (amsacrine or AMSA), an antitumor drug which has been tested in clinical trials, is known to bind to DNA by the intercalation of its 9-amino acridine moiety between DNA base pairs. Like AMSA, a peptidic derivative of 4-(9-acridinylamino) aniline, 4-(9-acridinylamino)-N-(lysylglycyl) aniline (ALGA) binds to DNA by intercalation and its affinity for the target was found to be higher than the parent drug. The antitumor effect of AMSA and ALGA has been monitored by drug exposure assays on EMT 6 cells. AMSA showed a slightly higher cytotoxic activity. The cell cycle effects of both drugs were studied using flow cytofluorimetry; an accumulation of cells in the S phase followed by a cycle arrest in the G2 phase, characteristic of intercalating drugs, was observed.
Cancer Biochem Biophys 1987 Sep
PMID:Cytotoxic action and cell cycle effects of ALGA, a peptidic derivative of the antileukemic drug amsacrine. 343 97


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