CALCB splice region pathogenic variants leading to plasma cell neurotropic enrichment in type 1 autoimmune pancreatitis

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 stu...

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Published inCell death & disease Vol. 8; no. 2; p. e2591
Main Authors Liu, Qi-cai, Chen, Falin, Wu, Chao-yang, Gao, Feng, Zhuang, Ze-hao, Chen, Jin-tong, Cai, Bin, Zhang, Tianming, Guo, Ling, Lin, Li-qing, Zhao, Cheng-fei, Lin, Xin-hua
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 02.02.2017
Springer Nature B.V
Nature Publishing Group
Subjects
38/23
38/44
38/91
631/208/726/649
631/208/737
692/4020/1503/1712/1714/2755
692/420/2489
Antibodies
Autoimmune Diseases - genetics
Autoimmune Diseases - pathology
Biochemistry
Biomedical and Life Sciences
Calcitonin Gene-Related Peptide - genetics
Cell Biology
Cell Culture
Cell Line
Endoplasmic Reticulum - genetics
Female
Golgi Apparatus - genetics
HEK293 Cells
Humans
Immunology
Inflammation - genetics
Inflammation - pathology
Life Sciences
Male
MAP Kinase Signaling System - genetics
Mutation
Mutation - genetics
Original
original-article
Pancreas
Pancreas - pathology
Pancreatitis - genetics
Pancreatitis - pathology
Pathogens
Phosphorylation - genetics
Plasma
Plasma Cells - pathology
Trypsin - genetics
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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.
AbstractList 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.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.
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 beta CGRP, 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.
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.
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.
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.88T4C (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 CGRP, 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.
Author Chen, Falin
Zhao, Cheng-fei
Zhang, Tianming
Lin, Xin-hua
Wu, Chao-yang
Gao, Feng
Cai, Bin
Lin, Li-qing
Zhuang, Ze-hao
Chen, Jin-tong
Liu, Qi-cai
Guo, Ling
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Snippet Recently, we have demonstrated that PRSS1 mutations cause ectopic trypsinogen activation and thereby result in type 1 autoimmune pancreatitis (AIP). However,...
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pubmed
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springer
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StartPage e2591
SubjectTerms 38/23
38/44
38/91
631/208/726/649
631/208/737
692/4020/1503/1712/1714/2755
692/420/2489
Antibodies
Autoimmune Diseases - genetics
Autoimmune Diseases - pathology
Biochemistry
Biomedical and Life Sciences
Calcitonin Gene-Related Peptide - genetics
Cell Biology
Cell Culture
Cell Line
Endoplasmic Reticulum - genetics
Female
Golgi Apparatus - genetics
HEK293 Cells
Humans
Immunology
Inflammation - genetics
Inflammation - pathology
Life Sciences
Male
MAP Kinase Signaling System - genetics
Mutation
Mutation - genetics
Original
original-article
Pancreas
Pancreas - pathology
Pancreatitis - genetics
Pancreatitis - pathology
Pathogens
Phosphorylation - genetics
Plasma
Plasma Cells - pathology
Trypsin - genetics
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Title CALCB splice region pathogenic variants leading to plasma cell neurotropic enrichment in type 1 autoimmune pancreatitis
URI https://link.springer.com/article/10.1038/cddis.2017.32
https://www.ncbi.nlm.nih.gov/pubmed/28151472
https://www.proquest.com/docview/1863565650
https://www.proquest.com/docview/1865547927
https://www.proquest.com/docview/1868335834
https://pubmed.ncbi.nlm.nih.gov/PMC5386480
Volume 8
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