PINLYP

Last update 08 May 2025

Basic Info

Synonyms

phospholipase A2 inhibitor and LY6/PLAUR domain containing, phospholipase A2 inhibitor and Ly6/PLAUR domain-containing protein, PINLYP

Introduction-

100 Clinical Results associated with PINLYP

100 Translational Medicine associated with PINLYP

0 Patents (Medical) associated with PINLYP

Literatures (Medical) associated with PINLYP

05 Jan 2022·Proceedings of the National Academy of SciencesQ1 · CROSS-FIELD

Phospholipase A2 inhibitor and LY6/PLAUR domain-containing protein PINLYP regulates type I interferon innate immunity

Q1 · CROSS-FIELD

Article

Author: Jung, Jae U. ; Gao, Ying ; Lei, Zhangmengxue ; Liu, Mu ; Liang, Huaping ; Jiang, Congwei ; Huang, Chenxu ; Dong, Sihan ; Kuang, Linlin ; Liang, Xiaozhen ; Liu, Zhongshun ; Xiao, Hui ; Legembre, Patrick

Type I interferons (IFNs) are the first frontline of the host innate immune response against invading pathogens. Herein, we characterized an unknown protein encoded by phospholipase A2 inhibitor and LY6/PLAUR domain-containing (PINLYP) gene that interacted with TBK1 and induced type I IFN in a TBK1- and IRF3-dependent manner. Loss of PINLYP impaired the activation of IRF3 and production of IFN-β induced by DNA virus, RNA virus, and various Toll-like receptor ligands in multiple cell types. Because PINLYP deficiency in mice engendered an early embryonic lethality in mice, we generated a conditional mouse in which PINLYP was depleted in dendritic cells. Mice lacking PINLYP in dendritic cells were defective in type I IFN induction and more susceptible to lethal virus infection. Thus, PINLYP is a positive regulator of type I IFN innate immunity and important for effective host defense against viral infection.

01 Jul 2016·Molecular PsychiatryQ1 · MEDICINE

APOE*E2 allele delays age of onset in PSEN1 E280A Alzheimer’s disease

Q1 · MEDICINE

Article

Author: Wong, M L ; Easteal, S ; Rivera, D ; Chuah, A ; Creagh, P K ; Arkell, R ; Andrews, S J ; Licinio, J ; Mastronardi, C A ; Peng, K ; Tobón, C ; Villegas, A ; Arcos-Burgos, M ; Cai, Y ; Lopera, F ; Castellanos, F X ; de Leon, J ; Vélez, J I ; Silva Lara, M F ; Sepulveda-Falla, D ; Patel, H R ; Johar, A S

Alzheimer's disease (AD) age of onset (ADAOO) varies greatly between individuals, with unique causal mutations suggesting the role of modifying genetic and environmental interactions. We analyzed ~50 000 common and rare functional genomic variants from 71 individuals of the 'Paisa' pedigree, the world's largest pedigree segregating a severe form of early-onset AD, who were affected carriers of the fully penetrant E280A mutation in the presenilin-1 (PSEN1) gene. Affected carriers with ages at the extremes of the ADAOO distribution (30s-70s age range), and linear mixed-effects models were used to build single-locus regression models outlining the ADAOO. We identified the rs7412 (APOE*E2 allele) as a whole exome-wide ADAOO modifier that delays ADAOO by ~12 years (β=11.74, 95% confidence interval (CI): 8.07-15.41, P=6.31 × 10(-8), PFDR=2.48 × 10(-3)). Subsequently, to evaluate comprehensively the APOE (apolipoprotein E) haplotype variants (E1/E2/E3/E4), the markers rs7412 and rs429358 were genotyped in 93 AD affected carriers of the E280A mutation. We found that the APOE*E2 allele, and not APOE*E4, modifies ADAOO in carriers of the E280A mutation (β=8.24, 95% CI: 4.45-12.01, P=3.84 × 10(-5)). Exploratory linear mixed-effects multilocus analysis suggested that other functional variants harbored in genes involved in cell proliferation, protein degradation, apoptotic and immune dysregulation processes (i.e., GPR20, TRIM22, FCRL5, AOAH, PINLYP, IFI16, RC3H1 and DFNA5) might interact with the APOE*E2 allele. Interestingly, suggestive evidence as an ADAOO modifier was found for one of these variants (GPR20) in a set of patients with sporadic AD from the Paisa genetic isolate. This is the first study demonstrating that the APOE*E2 allele modifies the natural history of AD typified by the age of onset in E280A mutation carriers. To the best of our knowledge, this is the largest analyzed sample of patients with a unique mutation sharing uniform environment. Formal replication of our results in other populations and in other forms of AD will be crucial for prediction, follow-up and presumably developing new therapeutic strategies for patients either at risk or affected by AD.

International Journal of Molecular Sciences

Placenta Transcriptome Profiling in Intrauterine Growth Restriction (IUGR)

Article

Author: Jozwik, Marcin ; Majewska, Marta ; Lepiarczyk, Ewa ; Jastrzebski, Jan Pawel ; Majewski, Mariusz Krzysztof ; Szeszko, Karol ; Lipka, Aleksandra ; Paukszto, Lukasz ; Gowkielewicz, Marek

Intrauterine growth restriction (IUGR) is a serious pathological complication associated with compromised fetal development during pregnancy. The aim of the study was to broaden knowledge about the transcriptomic complexity of the human placenta by identifying genes potentially involved in IUGR pathophysiology. RNA-Seq data were used to profile protein-coding genes, detect alternative splicing events (AS), single nucleotide variant (SNV) calling, and RNA editing sites prediction in IUGR-affected placental transcriptome. The applied methodology enabled detection of 37,501 transcriptionally active regions and the selection of 28 differentially-expressed genes (DEGs), among them 10 were upregulated and 18 downregulated in IUGR-affected placentas. Functional enrichment annotation indicated that most of the DEGs were implicated in the processes of inflammation and immune disorders related to IUGR and preeclampsia. Additionally, we revealed that some genes (S100A13, GPR126, CTRP1, and TFPI) involved in the alternation of splicing events were mainly implicated in angiogenic-related processes. Significant SNVs were overlapped with 6533 transcripts and assigned to 2386 coding sequence (CDS), 1528 introns, 345 5’ untranslated region (UTR), 1260 3’UTR, 918 non-coding RNA (ncRNA), and 10 intergenic regions. Within CDS regions, 543 missense substitutions with functional effects were recognized. Two known mutations (rs4575, synonymous; rs3817, on the downstream region) were detected within the range of AS and DEG candidates: PA28β and PINLYP, respectively. Novel genes that are dysregulated in IUGR were detected in the current research. Investigating genes underlying the IUGR is crucial for identification of mechanisms regulating placental development during a complicated pregnancy.

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PINLYP

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