Cellular mechanisms of somatostatin action in the gut
dc.contributor.author | DelValle, John | en_US |
dc.contributor.author | Park, Jung | en_US |
dc.contributor.author | Chiba, Tsutomu | en_US |
dc.contributor.author | Yamada, Tadataka | en_US |
dc.date.accessioned | 2006-04-10T13:37:20Z | |
dc.date.available | 2006-04-10T13:37:20Z | |
dc.date.issued | 1990-09 | en_US |
dc.identifier.citation | DelValle, John, Park, Jung, Chiba, Tsutomu, Yamada, Tadataka (1990/09)."Cellular mechanisms of somatostatin action in the gut." Metabolism 39(9, Supplement 2): 134-137. <http://hdl.handle.net/2027.42/28402> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B6WN4-4C2SHDV-76/2/f4fe050a806074a9b0ee0cd83b14322d | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/28402 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=1976208&dopt=citation | en_US |
dc.description.abstract | We have used isolated canine parietal cells to examine the receptor and postreceptor events mediating the inhibitory effects of somatostatin on acid secretion. Somatostatin-14 (S14) and somatostatin-28 (S28) dose dependently inhibited parietal cells stimulated by secretagogues that activate both the adenylate cyclase/cyclic adenosine monophosphate and the inositol phospholipid/protein kinase C cascades. The inhibitory action was mediated via a specific cell surface receptor that consists of a single subunit protein (molecular weight 99,000 d). This receptor recognized S14 and S28 equally well. Somatostatin inhibited parietal cell activity via mechanisms that are both dependent on and independent of a pertussis toxin-sensitive inhibitory guanine nucleotide binding protein. | en_US |
dc.format.extent | 543678 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | Cellular mechanisms of somatostatin action in the gut | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Medicine (General) | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, The University of Michigan Medical Center, Ann Arbor, MI, USA; Third Department of Internal Medicine, Kobe University School of Medicine, Kobe, Japan. | en_US |
dc.contributor.affiliationum | Third Department of Internal Medicine, Kobe University School of Medicine, Kobe, Japan; Department of Internal Medicine, The University of Michigan Medical Center, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationum | Third Department of Internal Medicine, Kobe University School of Medicine, Kobe, Japan; Department of Internal Medicine, The University of Michigan Medical Center, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationum | Third Department of Internal Medicine, Kobe University School of Medicine, Kobe, Japan; Department of Internal Medicine, The University of Michigan Medical Center, Ann Arbor, MI, USA | en_US |
dc.identifier.pmid | 1976208 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/28402/1/0000177.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0026-0495(90)90231-Z | en_US |
dc.identifier.source | Metabolism | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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