pubmed-article:6262331 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C0036536 | lld:lifeskim |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C0036537 | lld:lifeskim |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C0032019 | lld:lifeskim |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C0431085 | lld:lifeskim |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C0014242 | lld:lifeskim |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C0030956 | lld:lifeskim |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C1441547 | lld:lifeskim |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C1514468 | lld:lifeskim |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C0547044 | lld:lifeskim |
pubmed-article:6262331 | lifeskim:mentions | umls-concept:C1707511 | lld:lifeskim |
pubmed-article:6262331 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:6262331 | pubmed:dateCreated | 1981-7-20 | lld:pubmed |
pubmed-article:6262331 | pubmed:abstractText | The secretion of peptide products derived from pro-ACTH/endorphin was examined with several radioimmunoassays and with polyacrylamide gel analyses of immunoprecipitates of radioactively labeled peptides. In studies using a mouse pituitary tumor cell line the accumulation of each of the four molecular forms of adrenocorticotropic hormone (ACTH) in tissue culture medium was shown to be a linear function of time. No evidence for self inhibition of secretion by accumulated, secreted peptides (i.e., ultra-short feedback) was found. Furthermore, synthetic human ACTH and synthetic camel beta-endorphin did not alter secretion of peptides when added to the culture medium at levels up to 10,000 times physiological. Stimulation of the release of ACTH-, endorphin-, lipotropin-, and 16k fragment immunoreactive material by norepinephrine was fully blocked by cobalt; by this criterion, stimulated release was calcium dependent. All the smaller molecules derived from the pro-ACTH/endorphin common precursor were secreted in equimolar amounts under all circumstances tested, within the precision of these studies (+/- 11%). Norepinephrine and cobalt did not significantly alter the secretion of pro-ACTH/endorphin and ACTH biosynthetic intermediate. The stimulation of secretion by norepinephrine and inhibition of secretion by cobalt was restricted to the lower molecular weight products derived from pro-ACTH/endorphin: glycosylated and nonglycosylated ACTH(1-39); beta-lipotropin, beta-endorphin, and gamma-lipotropin; and 16k fragment. | lld:pubmed |
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pubmed-article:6262331 | pubmed:language | eng | lld:pubmed |
pubmed-article:6262331 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:6262331 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:6262331 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:6262331 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:6262331 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:6262331 | pubmed:month | Apr | lld:pubmed |
pubmed-article:6262331 | pubmed:issn | 0021-9525 | lld:pubmed |
pubmed-article:6262331 | pubmed:author | pubmed-author:EipperB ABA | lld:pubmed |
pubmed-article:6262331 | pubmed:author | pubmed-author:MainsR ERE | lld:pubmed |
pubmed-article:6262331 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:6262331 | pubmed:volume | 89 | lld:pubmed |
pubmed-article:6262331 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:6262331 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:6262331 | pubmed:pagination | 21-8 | lld:pubmed |
pubmed-article:6262331 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
pubmed-article:6262331 | pubmed:meshHeading | pubmed-meshheading:6262331-... | lld:pubmed |
pubmed-article:6262331 | pubmed:meshHeading | pubmed-meshheading:6262331-... | lld:pubmed |
pubmed-article:6262331 | pubmed:meshHeading | pubmed-meshheading:6262331-... | lld:pubmed |
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