Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.2.2.7 (heparinase)
 1,270 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether a recognition mechanism is involved in determination of sympathetic innervation patterns of various tissues, tissue-derived substances were applied to a restricted test surface region of dishes and the responses of cultured sympathetic neurites were examined. Sympathetic fibers exhibited a turning or ramifying response, resulting in a dense fiber growth on test regions coated with particulate (adheron) fractions of a conditioned-medium (CM) from expansor secundariorum, heart, peripheral blood vessel or abdominal aorta, whereas on test regions coated with those from lung, skeletal muscle or dorsal aorta the neurite growth was repelled and sparse fiber growth was observed. Particulate fractions of brain- or gizzard-CM had no effect. These patterns in vitro were in parallel with the dense sympathetic innervation in expansor secundariorum, heart, peripheral blood vessel and abdominal aorta, but little or no sympathetic innervation in lung, skeletal muscle and dorsal aorta in vivo. These results suggest that adheron particles may participate in determination of sympathetic innervation patterns. Activity which repels or promotes the sympathetic fiber growth was inactivated by pronase E or trypsin but not by DNase or neuraminidase. Repelling activity was lost after treatment with heparinase or heparitinase but not with chondroitinase ABC or hyaluronidase. Promoting activity was retained after treatment with these glycosidases. These results suggest that the factor(s) possessing a repellent effect is a heparan sulfate proteoglycan and one(s) possessing a promoting effect is a protein.
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PMID:Characterization of substances which promote or repel sympathetic fiber growth in vitro. 133 24

The localization of basic fibroblast growth factor (bFGF) in various cultured bFGF-producing cells, including bovine capillary endothelial (BCE) cells and human cholangiocellular carcinoma (HuCC-T1) cells, was determined by measuring binding of 125I-labeled specific monoclonal antibody against bFGF. bFGF on the cell surface and within the cells was determined by counting the radioactivity of the labeled monoclonal antibody bound to the cells before and after increasing their permeability by treatment with alcohol or Triton X-100. The radioactivity bound to these cells decreased with increase in the concentration of unlabeled monoclonal antibody. Scatchard analyses of these data suggested the quantitative localization of bFGF and Kd values showing the specific binding. This method was designated as in situ assay with radio-labeled antibody (ISARA). bFGF detected on the cell surface and within the cells could be partially removed by treatment with heparin or heparinase and with heparin or DNase, respectively. Exogenous bFGF bound to cells not producing bFGF was also quantified by ISARA. Measurements of bFGF in extracts of cells producing bFGF suggested that 8.3-13.3% of the bFGF associated with the cells was detected by ISARA. This method should be useful for quantitative confirmation of immunohistochemical results on bFGF.
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PMID:In situ assay of basic fibroblast growth factor in cultured cells with a specific monoclonal antibody. 751 65