Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A segment of the distal oesophagus lined with columnar epithelium (endobrachy oesophagus, Barrett's oesophagus), is very frequently seen in association with chronic reflux conditions. Usually, this entity is an asymmetrical columnar-cell metaplasia of varying extent, with an unsharp epithelial junction line cranial, and showing various large residual islands of squamous epithelium. In addition, usually well-developed peptic lesions are also found. More rarely seen are cases with a longer, symmetrical, cranially sharply delimited columnar-epithelial-lined segment, in which peptic lesions and strictures are usually either restricted to the proximal section, or are lacking altogether. Among more than 100 patients presenting with endobrachy-oesophagus, 14 cases had the latter form of the condition. Seven had a solitary, high peptic stricture, and only 50% unequivocal hiatus hernia. In four patients there were no inflammatory changes at all. In 8 patients, fundic glands were observed. Of particular interest was the segment-like arrangement of cardiac and fundic glands in 2 of the patients. In only a single case were scar formations seen in the columnar-lined segment. Considered from the point of view of our embryological knowledge, certain forms of endobrachy-oesophagus would appear to represent a congenital anomaly.
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PMID:Columnar-lined oesophagus (Barrett's syndrome) - congenital or acquired? 725 80

The pituitary cell-specific transcription factor Pit-1 has been show to trans-activate expression of the prolactin (PRL) promoter in non-pituitary cells. However, the cyclic AMP response element (CRE)-binding protein CREB is known to play a major role in cell-specific expression of hepatocyte-specific genes. Since the PRL promoter contains an asymmetrical form of a cyclic AMP response element (termed the CLE), we investigated whether CREB could also induce PRL promoter activity in non-pituitary cells. Transient expression in rat glial C6 cells of a constitutively active CREB-VP16 fusion protein strongly trans-activated expression of a co-transfected rat PRL promoter construct, (-187)PRL-CAT. Analysis by 5'-deletion showed that this response requires PRL promoter sequences between positions -113/-75. CREB-VP16 did not stimulate expression in C6 cells of any of three control promoter-CAT constructs, implying that the strong response of the PRL promoter to activated CREB is both promoter-specific, and is not due to non-specific transcriptional effects of the potent VP16 moiety of CREB-VP16. Surprisingly, mutations in the CLE only slightly reduced activation by CREB-VP16 of construct (-204)PRL-CAT, implying that the major action of CREB-VP16 on the PRL promoter does not involve a direct interaction with the CLE. CREB-VP16 stimulated PRL-CAT activity in C6 cells as strongly as, and synergistically with, Pit-1. These results imply that CREB can strongly and specifically activate expression of the PRL promoter in non-pituitary cells, via a mechanism different from that employed by Pit-1.
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PMID:A constitutively active form of CREB can activate expression of the rat prolactin promoter in non-pituitary cells. 939 71

The link of aneuploidy and heteroploidy in human solid tumours with early genetic events is poorly understood. The study of human preneoplastic precursor lesions, i.e., colorectal adenomas, chronic ulcerative colitis lesions, and Barrett's esophagus, as considered in this review, appears particularly useful to achieve this aim. Literature data examined here on aneuploidy were obtained by image and flow cytometry, classical cytogenetics, and in situ hybridization based cytogenetics. It appears that aneuploidy is linked with specific gene mutations, i.e., of the tumour suppressor gene p53 in chronic ulcerative colitis and in Barrett's esophagus, and of the protooncogene K-ras in colorectal adenomas. These data and data from experiments using in vitro and mouse models, suggest that chromosome instability, tetraploidization, and asymmetrical chromosome segregation during cell division are the result of deregulated cell cycle genes with multiple functions that normally exert active checks on the cell cycle processes including apoptosis and chromosome stability.
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PMID:Aneuploidy mechanisms in human colorectal preneoplastic lesions and Barrett's esophagus. Is there a role for K-ras and p53 mutations? 941 95

Several components of the gastrointestinal tract including the esophagogastric junction (EGJ) show circumferential asymmetry in the formation of pathological lesions, which is caused by the morphological and functional asymmetry of the gastrointestinal tract. Pressure in the lower esophageal sphincter (LES) is higher on the left posterior side as compared to the right anterior side, which may partly explain why Mallory-Weiss tears frequently occur on the right side wall of the EGJ. Lower LES pressure in the right anterior wall may not effectively prevent gastroesophageal reflux on this side and may be a reason why esophageal erosions in patients with reflux esophagitis, short segment Barrett's esophagus, and adenocarcinomas associated with short segment Barrett's esophagus are frequently found in the right anterior wall of the esophagus. In addition, acidic gastroesophageal reflux may also cause rupture of esophageal varices predominantly on that side. Thus, asymmetrical LES pressure may be a cause of the right anterior side predominance of diseases found in this part of the gastrointestinal tract.
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PMID:Asymmetrical circumferential distribution of esophagogastric junctional lesions: anatomical and physiological considerations. 1952 90