Prohormone convertases PC1/3 and PC2 are expressed in autoimmune atrophic gastritis

Larkin, CJ; Curry, W.J.; Watson, R.; Johnston, C.F.; Ardill, Jes; Rhodes, Christopher; Buchanan, KD

doi:10.1016/s0016-5085(98)84707-0

Cited by 1 publication

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“…WE‐14 immunostaining was detected in 53% of medullary carcinomas of the thyroid21 and in 67% of nonfunctioning pituitary adenomas and was also observed in a range of functioning pituitary adenomas 22. Analysis of a spectrum of patients with autoimmune atrophic gastritis revealed that CgA was cleaved to generate WE‐14 and that this was more prevalent in those patients displaying micronodular ECL cell hyperplasia 23…”

Section: Pathologymentioning

confidence: 99%

WE‐14, a Chromogranin A‐Derived Neuropeptide

Curry

Barkatullah

Johansson

et al. 2002

Annals of the New York Academy of Sciences

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The neuropeptide WE-14 is derived from the posttranslational processing of chromogranin A (CgA). While CgA is expressed in a preponderance of neuroendocrine cells, WE-14 is generated in a distinct subpopulation of CgA-immunopositive cells, most notably in the adrenal, pituitary, and parathyroid glands. Physiological and pharmacological studies have demonstrated that CgA is cleaved to generate WE-14 in the adrenal chromaffin cell population and in the enterochromaffin-like (ECL) cells of the oxyntic mucosa. Pathological analyses of neuroendocrine tumors have revealed a heterogeneous pattern of WE-14 immunostaining, with variable concentrations quantified and chromatographically resolved in tissue extracts. Phylogenetic surveys have demonstrated that WE-14 exhibits an ancient lineage, while ontogenetic examination has shown that it is generated at an early stage during fetal development. Putative WE-14 receptor binding sites have been identified in several tissues; however, the physiological role of WE-14 remains enigmatic.

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Section: Pathologymentioning

confidence: 99%