PIGZ

Last update 23 Jan 2025

Basic Info

Synonyms

FLJ12768, GPI mannosyltransferase 4, GPI mannosyltransferase IV

+ [9]

Introduction

Mannosyltransferase involved in glycosylphosphatidylinositol-anchor biosynthesis. Transfers a fourth mannose to some trimannosyl-GPIs during GPI precursor assembly. The presence of a fourth mannose in GPI is facultative and only scarcely detected, suggesting that it only exists in some tissues.

100 Clinical Results associated with PIGZ

100 Translational Medicine associated with PIGZ

0 Patents (Medical) associated with PIGZ

120

Literatures (Medical) associated with PIGZ

12 Jul 2024·Science Immunology

Initiator cell death event induced by SARS-CoV-2 in the human airway epithelium

Article

Author: Xie, Yuying ; Koller, Beverly H. ; Hsu, Martin ; Oguin, Thomas H. ; Karlsson, Amelia ; Blasi, Maria ; Ting, Jenny P.-Y. ; Lenschow, Deborah J. ; Barnett, Katherine C. ; Vannella, Kevin M. ; Chou, Wei-Chun ; Liang, Kaixin ; Nguyen, Tuong Thien ; Hewitt, Stephen M. ; Bais, Sachendra S. ; Sempowski, Gregory D. ; Chertow, Daniel S. ; Randell, Scott H. ; Riebe, Kristina

Virus-induced cell death is a key contributor to COVID-19 pathology. Cell death induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is well studied in myeloid cells but less in its primary host cell type, angiotensin-converting enzyme 2 (ACE2)–expressing human airway epithelia (HAE). SARS-CoV-2 induces apoptosis, necroptosis, and pyroptosis in HAE organotypic cultures. Single-cell and limiting-dilution analysis revealed that necroptosis is the primary cell death event in infected cells, whereas uninfected bystanders undergo apoptosis, and pyroptosis occurs later during infection. Mechanistically, necroptosis is induced by viral Z-RNA binding to Z-DNA–binding protein 1 (ZBP1) in HAE and lung tissues from patients with COVID-19. The Delta (B.1.617.2) variant, which causes more severe disease than Omicron (B1.1.529) in humans, is associated with orders of magnitude–greater Z-RNA/ZBP1 interactions, necroptosis, and disease severity in animal models. Thus, Delta induces robust ZBP1-mediated necroptosis and more disease severity.

01 Jun 2024·Zhongguo shi yan xue ye xue za zhi

[Whole Exome Sequencing Reveals Gene Mutation Characteristics of Primary Central Nervous System Lymphoma].

Article

Author: Zhang, Li-Tian ; Han, Ye ; Li, Cui-Cui ; Wu, Chong-Yang ; Jin, Qi-Qi ; Jiang, Hao-Yun

OBJECTIVETo investigate gene mutation characteristics of primary central nervous system lymphoma (PCNSL) through whole exome sequencing (WES) to 18 patients with PCNSL.METHODSTumor tissues from 18 patients with diffuse large B-cell lymphoma who were diagnosed with PCNSL in Department of Hematology, Lanzhou University Second Hospital from September 2018 to December 2020 and had normal immune function, no history of HIV or immunosuppressant therapy were collected. High-throughput-based WES was performed on the tumor tissues, with an average sequencing depth of >100×. After data processing and bioinformatics analysis of sequencing results, the mutation maps and mutation characteristics of 18 PCNSL patients were obtained.RESULTSObvious somatic mutations were detected in all 18 patients. The median number of somatic mutations was 321. Missense mutations were most prominent (accounting for about 90%), and the mutation type was dominated by C>T (50.2%), reflecting the age-related mutation pattern. Among the top 15 frequently mutated genes, PSD3, DUSP5, MAGEB16, TELO2, FMO2, TRMT13, AOC1, PIGZ, SVEP1, IP6K3, and TIAM1 were the driver genes. The enrichment results of driver gene pathways showed that RTK-RAS, Wnt, NOTCH, Hippo and Cell-Cycle pathways were significantly enriched. The tumor mutation burden was between 3.558 48/Mb and 8.780 89/Mb, and the average was 4.953 32/Mb, which was significantly higher than other cancer research cohorts in the TCGA database.CONCLUSIONSPCNSL occurs somatic missense mutations frequently, mainly point mutations, and the mutation type is mainly C>T. The driver genes are mainly involved in RTK-RAS, Wnt, NOTCH and Hippo pathways, indicating that the above pathways may be related to the pathogenesis of PCNSL. PCNSL has a significantly high tumor mutation burden, which may explain the efficacy of PD-1 inhibitors in PCNSL.

01 May 2024·Cell Reports

A ZBP1 isoform blocks ZBP1-mediated cell death

Article

Author: Zhang, Bo-Xin ; Wu, Puqi ; Li, Hongda ; Xie, Yu-Ze ; Yang, Zhang-Hua ; Cai, Zhi-Yu ; Mo, Wei ; Yang, Cong-Rong ; Liang, Hao ; He, Cai-Ling

ZBP1 is an interferon (IFN)-induced nucleic acid (NA) sensor that senses unusual Z-form NA (Z-NA) to promote cell death and inflammation. However, the mechanisms that dampen ZBP1 activation to fine-tune inflammatory responses are unclear. Here, we characterize a short isoform of ZBP1 (referred to as ZBP1-S) as an intrinsic suppressor of the inflammatory signaling mediated by full-length ZBP1. Mechanistically, ZBP1-S depresses ZBP1-mediated cell death by competitive binding with Z-NA for Zα domains of ZBP1. Cells from mice (Ripk1^D325A/D325A) with cleavage-resistant RIPK1-induced autoinflammatory (CRIA) syndrome are alive but sensitive to IFN-induced and ZBP1-dependent cell death. Intriguingly, Ripk1^D325A/D325A cells die spontaneously when ZBP1-S is deleted, indicating that cell death driven by ZBP1 is under the control of ZBP1-S. Thus, our findings reveal that alternative splicing of Zbp1 represents autogenic inhibition for regulating ZBP1 signaling and indicate that uncoupling of Z-NA with ZBP1 could be an effective strategy against autoinflammations.

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PIGZ

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