Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The regional distributions and relative frequencies of some gastrointestinal endocrine cells in the eight portions (fundus, pylorus, duodenum, jejunum, ileum, caecum, colon and rectum) of the gastrointestinal tract of SKH-1 hairless mice were investigated using immunohistochemical methods and seven types of specific antisera against somatostatin, serotonin, glucagon, cholecystokinin (CCK)-8, secretin, pancreatic polypeptide (PP) and gastrin. In this study, somatostatin-, serotonin-, glucagon-, CCK-8-, secretin- and gastrin-immunoreactive (IR) cells were identified. Most of these IR cells in the intestinal portion were generally spherical or spindle-shaped (open-type cell) while cells that were round in shape (close-type cell) were occasionally found in the stomach regions. Their relative frequencies were varied according to each portion of gastrointestinal tract. Somatostatin-IR cells were found throughout the gastrointestinal tract except for the large intestine. Serotonin-IR cells were detected throughout the whole gastrointestinal tract and were the most predominant endocrine cell types in this species of mouse. Glucagon-IR cells were restricted to the fundus, occurring rarely. CCK-8-IR cells were observed in the pylorus, duodenum and jejunum with frequencies that were numerous, moderate and few, respectively. Peculiarly, secretin-IR cells were demonstrated in the whole intestinal tract with either few or rare frequencies. Gastrin-IR cells were restricted to the pylorus and were numerous. However, no PP-IR cells were found in this study. In conclusion, some peculiar distributional patterns of gastrointestinal endocrine cells were found in SKH-1 hairless mouse.
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PMID:The regional distribution and relative frequency of gastrointestinal endocrine cells in SHK-1 hairless mice: an immunohistochemical study. 1204 43

Ptf1-p48 is a pancreas-specific bHLH transcriptional protein, which, in the normal adult pancreas, shows a restricted expression in acinar cells where it is predominantly localized in the nucleus and activates the transcription of exocrine-specific genes. Ptf1-p48 partners with two proteins to form the PTF1 active complex: a bHLH E-protein and suppressor of hairless RBP-J. Cytoplasmic mislocalization of Ptf1-p48 has been reported in pancreatic pathologies, suggesting its contribution in the early steps of pancreatic carcinogenesis. The aim of the our work was to elucidate the mechanisms regulating Ptf1-p48 subcellular localization. We hypothesized a role of Id proteins acting in a dominant-negative fashion by heterodimerizing with bHLH proteins. We reproduced Ptf1-p48 cytoplasmic mislocalization in acinar AR4-2J cells and demonstrated that a proliferative signal elicited by gastrin leads to increases in Id3 protein expression and levels of Id3/E47 and Id3/Ptf1-p48 interactions, and a decrease in the level of E47/Ptf1-p48 interaction. By contrast, Id3 silencing reversed the cytoplasmic mislocalization of Ptf1-p48 induced by gastrin. As E47 is responsible for the nuclear import of the PTF1 complex, disruption of this complex via Id3 interactions with both E47 and Ptf1-p48 appears to induce cytoplasmic mislocalization of Ptf1-p48. We then found that Ptf1-p48 is either absent or mislocalized in the cytoplasm and Id3 is overexpressed in human and murine pancreatic preneoplastic lesions. Our data provide novel insight into the regulation of Ptf1-p48 function and provide evidence that Ptf1-p48 cytoplasmic mislocalization and Id3 overexpression are early events in pancreatic cancer progression.
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PMID:Id3 modulates cellular localization of bHLH Ptf1-p48 protein. 2083 Jul 6