ArticleCell death & disease2017
CALCB splice region pathogenic variants leading to plasma cell neurotropic enrichment in type 1 autoimmune pancreatitis.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- CGRP: A New Endogenous Cell Stemness Maintenance Molecule.Oxidative medicine and cellular longevity · 2022Review
- CGRP-Mediated Prolactin Upregulation: a Possible Pathomechanism in IgG4-Related Disease.Inflammation · 2021Article
- DNA Methylation Pattern of CALCA and CALCB in Extremely Premature Infants with Monochorionic Triplets after Single-Embryo Transfer.Oxidative medicine and cellular longevity · 2021Article
- CALCB rs3829222 T/T Genotype and Low Expression of CALCB Are High-Risk Factors for Adenoid Cystic Carcinoma of Salivary Gland.Disease markers · 2021Article
- Methylation of CALCA and CALCB in Pancreatic Ductal Adenocarcinoma.Oxidative medicine and cellular longevity · 2021Article
- Impact of diet and genes on murine autoimmune pancreatitis.Journal of cellular and molecular medicine · 2020Article
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- Clinical and pathological characteristics of IgG4-related interstitial lung disease.Experimental and therapeutic medicine · 2018Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, we have demonstrated that PRSS1 mutations cause ectopic trypsinogen activation and thereby result in type 1 autoimmune pancreatitis (AIP). However, the molecules involved in inducing obliterative vasculitis and perineural inflammation in the pancreas are not well-described. The present study applied whole-exome sequencing (WES) to determine the underlying etiology and revealed novel missense splice region variants, CALCB c.88T>C (p.Ser30Pro) and IR [1]-mutants, in 2 of the 3 families and 2 of 26 unrelated patients with type 1 AIP. In vitro, both of the mutants displayed decreased βCGRP, ERK1/2 phosphorylation, and co-localized with endoplasmic reticulum and Golgi apparatus. The novel pathogenic variant identified in this case should contribute to our understanding of the expanding spectrum of AIP.
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